All Functions are Irreducibly Complex
Sean Pitman
quite common and usually involve some confusion about the definition
of IC. The following question posed by "sds" sparked my interest.
"sds" <bcno...@mindspring.com.leavethispartoff> wrote in message news:<bbcj98$t4d$1...@slb6.atl.mindspring.net>...
> Do you believe is it possible to show that an object or mechanism has an
> intelligent origin? Take the mousetrap again (for which I understand you
> *don't* find "irreducibly complex" to be a meaningful characterization).
> Can we show that a mousetrap probably could not exist without some
> intelligence to design it?
It seems to me that the concept of IC is quite helpful indeed. The
problem is that many, even Behe himself, seem to try to limit the
definition of IC to "very complex" systems of function in order to
show that IC systems cannot evolve.
As I see it all systems of function are IC. It is just that some
systems are more simple than other systems of function. There is a
spectrum of complexity, but all systems along this spectrum from
simple to more and more complex are all IC. In other words, not all
setups of a given number of parts or part types will be able to
perform a given function. The parts in any system of function can in
fact be altered, removed, or ordered in a different manner so that the
function of the system is completely destroyed. In fact, there are
vastly more non-functional potential arrangements of parts than there
are beneficially functional arrangements of parts in a particular
scenario.
Take, for example, Behe's famous mousetrap IC illustration. Many try
to argue that a mousetrap is not IC since parts can be removed or
changed and it still can catch mice. That is not the issue. If you
change the mousetrap, it may still catch mice, but not in the same
way. The changed mousetrap is a different mousetrap that catches mice
in a different way. Certainly there are many different kinds of
mousetraps that can catch mice, some more effectively than others.
However, all of these mousetraps are dependent upon a certain number
of parts that are all arranged in a very specific way in order for
these parts to work together to catch mice (i.e., To perform their
function). Clearly there are a lot more arrangements of mousetrap
parts for any given type of mousetrap that would not catch mice at
all. All mousetraps can in fact be reduced or changed in a way that
would destroy their function completely. And, these potential
non-functional mousetraps are far more numerous than those
comparatively few arrangements than can actually perform the mouse
catching function.
Of course, it is theoretically possible to arrange several of these
working mousetraps in sequential order so that very small steps seem
to exist as one moves from one type of trap to the other. Obviously
then, it is NOT impossible for IC systems to evolve via function-based
selection mechanisms since such an evolutionary path need not
necessarily cross wide neutral gaps in function or non-function. The
problem is that these gaps are often wider than one might initially
think.
http://naturalselection.0catch.com/Files/irreduciblemousetrap.html
Even functions that are based on the workings of single proteins, such
as the enzymatic functions of lactase or nylonase, are IC in that
there are a limited number of parts that are required to give rise to
that particular type of function. For more simple functions, such as
these single-protein-based functions, there might be a much higher
ratio of sequences of a given length or smaller that would be able to
perform a given function, like the lactase or nylonase function. For
example, given a sequence of amino acids 1,000aa in size, there are
about 1 x 10e1300 different possible protein sequences. This is an
absolutely huge number of different possibilities. It is a 1 with
1,300 zeros following it. Out of all of these possibilities, how many
would have the lactase function? Certainly there would be many of
these sequences that would have the lactase function, but certainly
not all of them or even most of them. Perhaps the ratio would be as
high as 1 in a trillion? If the ratio where 1 in a trillion, that
means that any given functional lactase AA sequence would be
surrounded by an average of 1 trillion non-lactase sequences. If a
particular functioning lactase sequence is changed or "reduced" beyond
a certain point, it will no longer function at all, not even a little
bit. This is the definition of IC. The lactase function, even though
based in the AA sequence of a single protein, is IC. Of course,
compared to other systems of function, the lactase and nylonase single
protein enzymes are not all that complex since there are is a
relatively high percentage of potential lactase sequences as compared
with the total number of possible sequences out there. Because of
this, these functions are relatively simple, requiring a relatively
short stretch of DNA to code for their function. Other systems of
function require multiple proteins all working together
simultaneously. Much more DNA real estate is necessary.
Before thinking about more complex systems function, such as bacterial
motility, consider that even the evolution of the relatively simple
lactase function is quite difficult. Barry Hall demonstrated this in
several experiments where he deleted the lacZ genes in E. coli
bacteria to see if they would evolve the lactase function back again
using some other genetic sequence. And, they did evolve the lactase
function in just one or two generations. As it turned out, a single
point mutation to a completely different DNA sequence was able to
produce a selectively advantageous lactase function in a lactose
environment. Hall called this "evolved" sequence the ebg gene
(evolved beta galactosidase gene). But, he started wondering, "If
this worked for the deletion of the lacZ gene, what will happen if I
delete the ebg gene too?" So, Hall deleted the ebg and lacZ genes in
certain colonies of E. coli. What happened next is very interesting.
These double mutant E. coli colonies never evolved the lactase
function back again despite high population numbers, high mutation
rates, 4 million base pairs of DNA each, positive selection pressure,
and tens of thousands of generations.
http://naturalselection.0catch.com/Files/galactosidaseevolution.html
Now, why didn't Hall's double mutant E. coli colonies evolve the
relatively simple lactase function back again? Hall himself described
this colonies as having, "limited evolutionary potential." What was
it that limited their ability to evolve the relatively simple lactase
function despite very positive benefits if they were to ever evolve
this helpful function?
It seems that neutral gaps existed between what was there and what was
needed. The genetic real estate of this huge population of E. coli
simply was not large enough to undergo the random walk across this
neutral gap in beneficial function despite being given thousands of
generations.
Obviously then, even such simple functions as the function of single
proteins are IC and this can and often does create difficulties for
mindless evolutionary processes. The problems only increase
(exponentially) as one moves up the spectrum of complex systems.
Sean Pitman
Matt Silberstein
seanpi...@naturalselection.0catch.com (Sean Pitman):
>Discussions concerning the concept of irreducible complexity (IC) are
>quite common and usually involve some confusion about the definition
>of IC. The following question posed by "sds" sparked my interest.
>
>"sds" <bcno...@mindspring.com.leavethispartoff> wrote in message news:<bbcj98$t4d$1...@slb6.atl.mindspring.net>...
>
>> Do you believe is it possible to show that an object or mechanism has an
>> intelligent origin? Take the mousetrap again (for which I understand you
>> *don't* find "irreducibly complex" to be a meaningful characterization).
>> Can we show that a mousetrap probably could not exist without some
>> intelligence to design it?
>
>It seems to me that the concept of IC is quite helpful indeed. The
>problem is that many, even Behe himself, seem to try to limit the
>definition of IC to "very complex" systems of function in order to
>show that IC systems cannot evolve.
>
>As I see it all systems of function are IC.
And, as such, there is no possibility of change in the world.
Thank you very much Zeno.
> It is just that some
>systems are more simple than other systems of function. There is a
>spectrum of complexity, but all systems along this spectrum from
>simple to more and more complex are all IC. In other words, not all
>setups of a given number of parts or part types will be able to
>perform a given function.
In actual words, each set of things in the world are different
from other sets of things. BFD.
>The parts in any system of function can in
>fact be altered, removed, or ordered in a different manner so that the
>function of the system is completely destroyed. In fact, there are
>vastly more non-functional potential arrangements of parts than there
>are beneficially functional arrangements of parts in a particular
>scenario.
Whatever you do, don't breath. You will alter your function.
>Take, for example, Behe's famous mousetrap IC illustration. Many try
>to argue that a mousetrap is not IC since parts can be removed or
>changed and it still can catch mice. That is not the issue. If you
>change the mousetrap, it may still catch mice, but not in the same
>way. The changed mousetrap is a different mousetrap that catches mice
>in a different way. Certainly there are many different kinds of
>mousetraps that can catch mice, some more effectively than others.
>However, all of these mousetraps are dependent upon a certain number
>of parts that are all arranged in a very specific way in order for
>these parts to work together to catch mice (i.e., To perform their
>function). Clearly there are a lot more arrangements of mousetrap
>parts for any given type of mousetrap that would not catch mice at
>all. All mousetraps can in fact be reduced or changed in a way that
>would destroy their function completely. And, these potential
>non-functional mousetraps are far more numerous than those
>comparatively few arrangements than can actually perform the mouse
>catching function.
Now all you have to do is show that there is some connection
between IC and evolution.
>Of course, it is theoretically possible to arrange several of these
>working mousetraps in sequential order so that very small steps seem
>to exist as one moves from one type of trap to the other. Obviously
>then, it is NOT impossible for IC systems to evolve via function-based
>selection mechanisms since such an evolutionary path need not
>necessarily cross wide neutral gaps in function or non-function. The
>problem is that these gaps are often wider than one might initially
>think.
And the problem for the ID/IC people is to make an actual case
that some actual gap is a problem. You make the assertion, you
provide the evidence.
[snip]
--
Matt Silberstein TBC HRL OMM
We are not here to judge other people,
we are just here to be better than they are.
Michael Painter
"Sean Pitman" <seanpi...@naturalselection.0catch.com> wrote in message
news:80d0c26f.03060...@posting.google.com...
Michael Painter
"Sean Pitman" <seanpi...@naturalselection.0catch.com> wrote in message
news:80d0c26f.03060...@posting.google.com...
> quite common and usually involve some confusion about the definition
> of IC. The following question posed by "sds" sparked my interest.
>
> "sds" <bcno...@mindspring.com.leavethispartoff> wrote in message
news:<bbcj98$t4d$1...@slb6.atl.mindspring.net>...
>
> > Do you believe is it possible to show that an object or mechanism has an
> > intelligent origin? Take the mousetrap again (for which I understand
you
> > *don't* find "irreducibly complex" to be a meaningful characterization).
> > Can we show that a mousetrap probably could not exist without some
> > intelligence to design it?
>
> It seems to me that the concept of IC is quite helpful indeed. The
> problem is that many, even Behe himself, seem to try to limit the
> definition of IC to "very complex" systems of function in order to
> show that IC systems cannot evolve.
>
> As I see it all systems of function are IC.
As soon as you change the definition then there is no way to continue the
argument.
You are calling a duck a dog and want to know why we don't see the wings.
Nobody cares if the base of the mousetrap is pure gold or cheap wood. It is
the design that he claims is irreducible.
Mark Isaak
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>It seems to me that the concept of IC is quite helpful indeed. The
>problem is that many, even Behe himself, seem to try to limit the
>definition of IC to "very complex" systems of function in order to
>show that IC systems cannot evolve.
>
>As I see it all systems of function are IC. [...]
So? We know very well that IC is not the least bit of an obstacle to
evolution.
--
Mark Isaak at...@earthlink.net
"Voice or no voice, the people can always be brought to the bidding of
the leaders. That is easy. All you have to do is tell them they are
being attacked, and denounce the pacifists for lack of patriotism and
exposing the country to danger." -- Hermann Goering
Lilith
> Discussions concerning the concept of irreducible complexity (IC) are
> quite common and usually involve some confusion about the definition
> of IC. The following question posed by "sds" sparked my interest.
>
> "sds" <bcno...@mindspring.com.leavethispartoff> wrote in message news:<bbcj98$t4d$1...@slb6.atl.mindspring.net>...
>
> > Do you believe is it possible to show that an object or mechanism has an
> > intelligent origin? Take the mousetrap again (for which I understand you
> > *don't* find "irreducibly complex" to be a meaningful characterization).
> > Can we show that a mousetrap probably could not exist without some
> > intelligence to design it?
>
> It seems to me that the concept of IC is quite helpful indeed. The
> problem is that many, even Behe himself, seem to try to limit the
> definition of IC to "very complex" systems of function in order to
> show that IC systems cannot evolve.
Behe relies on very complex systems because he realizes that an
argument as you use in the following paragraphs is too weak to hold up
under criticism.
As I see it, your argument depends on an unspoken assumption that
context (selective environment) stays fixed, but that is an assumption
that is not valid. In nature, there are few contexts so stable that
opportunities for improvement do not present themselves, and indeed in
those few cases, we can find ancient organisms who have been able to
sustain form and function as long as that context has been sustained.
Without selective context, evolution will happen only slowly in the
form of individual genetic arrangements and optimization.
But in an organism who has a great deal of "evolvability" --that is, a
systemic toolbox that is able to allow that organism entry into other
contexts, we should see appearence of function from existing parts
that are easily seen to be a result of co-option of existing pieces of
existing systems, OUT of their original context. In the case of a
mousetrap, the first step could only require a block of wood in a
completely different context. Then, nature sequentially rummages
through the vast "kitchen drawer" of biological tools and eventually
comes up with a mousetrap, as you've noted, in sequential steps.
At each step of parts generation, a new and different context (ie,
selective environment) was being answered to. A mousetrap was not
necessarily the item needed in predecessor contexts -- however, the
majority of the parts, from the spring to the board -- should have
existed in some early form before optimization. The predecessor parts
of the mousetrap, appeared not because of a need for a mousetrap, and
indeed if the mousetrap pieces were not already in existence, the
mousetrap would have never been assembled when the context for "need
mousetrap" arose.
From predecessor states of other existing systems (a pair of scissors,
a pen with a spring, a wire hanger), a mousetrap eventually is able to
be generated as the system's "kitchen drawer" became more and more
populated with evolved tools generated from other contexts. The main
driving force for such experimentation and shuffling is not only born
out of the "messy" assembly experiments that we find in nature, but
also the need FOR the appearence of the context demanding "mouse
trap". This isn't mere supposition, but is born out of observed
instance.
Nylonase, as you pointed out, is one such example of an utilization of
existing systems to process a substance in a new context (that of
man-made nylon abundance). Yet, we hear about the successes. There are
plenty of examples of life NOT being able to adapt. For instance,
these bacteria that generated nylonase were probably not able to
quickly generate an enzymatic system that can feed off of granite. In
order to evolve a function, an organism must have predecessor units
from other contexts. Additionally, the right context must be present.
Contexts and opportunities (such as a rich diet in nylon fiber) must
exist in which to allow selection.
Therefore, the problem for Intelligent Design is NOT trying to show
"irreducible complexity" because, despite what Behe says, "IC" can be
generated easily by adaptation and refinement of an already not-IC
system.
The true problem for ID is to show that any biological system is
unable to adapt to new contexts utilizing existing parts (except there
are already instances of this occuring in nature). Beyond denying
existing evidence, ID could show a certain "neatness" of biological
function. Except we find that biological systems are full of noise and
re-arrangements, as if these systems were constantly attempting to
produce a large playing field of adaptations in order for something to
select for advantage.
ID'ers must show that biological systems are perfect machines that
cannot move from one context to another context simply by adapting --
by evolutionary process as outlined -- their existing systems to other
contexts. Arguing that yeast cannot adapt to space conditions (as an
hypothetical example) is no argument, however, since evolution does
not require such great leaps. Evolution only requires reasonable
context jumps -- nylon instead of granite. The largest problem for ID
is, however, that they'd be arguing against observation.
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
On Sun, 1 Jun 2003 17:01:23 +0000 (UTC),
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>Discussions concerning the concept of irreducible complexity (IC) are
>quite common and usually involve some confusion about the definition
>of IC. The following question posed by "sds" sparked my interest.
Partially relevant to this, I've posted some replies to our last
exchange in the Ken Miller thread. It's over a weeklate, but
circumstances beyond my control and all that.
Cheers! Ian (snip rest)
=====================================================
Ian Musgrave Peta O'Donohue,Jack Francis and Michael James Musgrave
reyn...@werple.mira.net.au http://werple.mira.net.au/~reynella/
Southern Sky Watch http://www.abc.net.au/science/space/default.htm
Charlie Wagner
It is the evolutionists, not the ID'ers who are faced with
insurmountable difficulties. Evolutionists (especially darwinists) must
demonstrate that these functional adaptations can be discovered by
random, non-directed processes in spite of the fact that mathematical
analysis has shown a random search strategy to be highly inefficient.
For every functional system, the number of non-functional alternatives
is nearly infinite. To find these isolated "islands of function" from
within a "sea of noise" would be truly miraculous. Intelligent guidance
reduces the number of non-functional alternatives and directs the system
to optimum function is a much shorter time. To say that natural
selection is the operative equivalent of intelligent guidance and
accomplishes this task is blindly optimistic and not grounded in reality.
--
Regards, Charlie Wagner
http://www.charliewagner.com
Mark VandeWettering
> It is the evolutionists, not the ID'ers who are faced with
> insurmountable difficulties. Evolutionists (especially darwinists) must
> demonstrate that these functional adaptations can be discovered by
> random, non-directed processes in spite of the fact that mathematical
> analysis has shown a random search strategy to be highly inefficient.
What does random search have to do with evolution, Charlie?
> For every functional system, the number of non-functional alternatives
> is nearly infinite. To find these isolated "islands of function" from
> within a "sea of noise" would be truly miraculous.
Not miraculous at all, as genetic algorithms clearly and reliably demonstrate.
> Intelligent guidance reduces the number of non-functional
> alternatives and directs the system to optimum function is a much
> shorter time.
There is that "intelligent guidance" phrase you like so much. It's a pity
that you don't know what it is. Why not just call it "obfuscatonium"?
> To say that natural selection is the operative equivalent of
> intelligent guidance and accomplishes this task is blindly optimistic
> and not grounded in reality.
Mark
Frank Reichenbacher
"Charlie Wagner" <cha...@charliewagner.com> wrote in message
news:3EDB7443...@charliewagner.com...
How come? The question is not one that would apply to the theory of
evolution. Natural selection is not random, in fact, it is decidedly
non-random. I am afraid your mathematical analysis was unnecessary.
> For every functional system, the number of non-functional alternatives
> is nearly infinite. To find these isolated "islands of function" from
> within a "sea of noise" would be truly miraculous. Intelligent guidance
> reduces the number of non-functional alternatives and directs the system
> to optimum function is a much shorter time. To say that natural
> selection is the operative equivalent of intelligent guidance and
> accomplishes this task is blindly optimistic and not grounded in reality.
Demolish that strawman Charlie! Just whack at it. Hope it makes you feel
better.
Frank
dave e
>
> Take, for example, Behe's famous mousetrap IC illustration. Many try
> to argue that a mousetrap is not IC since parts can be removed or
> changed and it still can catch mice. That is not the issue. If you
> change the mousetrap, it may still catch mice, but not in the same
> way.
Mousetraps are not living organisms, and mousetrap parts are not
proteins. This analogy is a very poor one. In fact, I have yet to
see a GOOD analogy between living organisms, and any practical
invention which was intelligently designed by humans. I'm therefore
puzzled why the "appearance of design" argument is viewed as a
compelling arguement by so many creationists.
>
>
> http://naturalselection.0catch.com/Files/irreduciblemousetrap.html
>
> Even functions that are based on the workings of single proteins, such
> as the enzymatic functions of lactase or nylonase, are IC in that
> there are a limited number of parts that are required to give rise to
> that particular type of function.
Then how has it been possible for scientists to demonstrate the
evolution of similar enzyme functions in vitro, applying a variety of
selection strategies, and using random pools of protein, RNA,
antibodies or even DNA as the starting material?
Dave
Bobby D. Bryant
> It is the evolutionists, not the ID'ers who are faced with
> insurmountable difficulties. Evolutionists (especially darwinists) must
> demonstrate that these functional adaptations can be discovered by
> random, non-directed processes in spite of the fact that mathematical
> analysis has shown a random search strategy to be highly inefficient.
Who says evolution is anything other than highly inefficient?
How many pounds of ancestry have died to make your short life possible?
> For every functional system, the number of non-functional alternatives
> is nearly infinite. To find these isolated "islands of function" from
> within a "sea of noise" would be truly miraculous.
Actually, "island" solutions can be found even by dull-witted
hill-climbing algorithms, for some kinds of fitness landscapes.
Are you going to demonstrate that the fitness landscape provided by the
biosphere is not amenable to optimization by evolution?
> Intelligent guidance reduces the number of non-functional alternatives
> and directs the system to optimum function is a much shorter time.
Sure, our descendents will probably be able to do in a day what took
evolution billions of years. That's hardly an argument that evolution
didn't happen.
> To say that natural selection is the operative equivalent of intelligent
> guidance and accomplishes this task is blindly optimistic and not
> grounded in reality.
http://www.cs.utexas.edu/users/bdbryant/talk-origins/ga-on-tsp/index.html
Oh, and notice that scientists don't actually say that evolution (or
genetic algorithms) are "the operative equivalent of intelligent guidance".
Maybe you should be posting to talk.strawmen ?
--
Bobby Bryant
Austin, Texas
Mitchell Coffey
Natural selection is not a random search strategy, and it has been
found to be an efficient search strategy.
Mitchell Coffey
Boikat
1) How do you know they are "insurmountable"? Just because there is no
handy answer *now*? That is argument from ignorance/incredulity.
2) It is the very nature of science to attempt to answer these
"dificulties".
3) But I suppose you prefer the IDer's "Well, that's a complex process, and
since I can't figure itout, let's just close the lab, say some intelligent
designer (wink, wink, nudge, nudge) didit!"
> Evolutionists (especially darwinists) must
> demonstrate that these functional adaptations can be discovered by
> random, non-directed processes in spite of the fact that mathematical
> analysis has shown a random search strategy to be highly inefficient.
Nobody ever claimed that biological evolution or it's component theories was
highly effiecient (aside form the context of what you mena by "effiicient")
Viewed one way, it is mercylessly effieient, while viewed another it is
clumsy, time consuming and "hit or miss".
> For every functional system, the number of non-functional alternatives
> is nearly infinite.
And the "failures" never live long enough to reproduce in any numbers large
enough to make an impact on the population as a hole. That would be the
"mercylessly efficient" part.
> To find these isolated "islands of function" from
> within a "sea of noise" would be truly miraculous.
That would be the "clumsy, time consuming and "hit or miss" part.
> Intelligent guidance
> reduces the number of non-functional alternatives and directs the system
> to optimum function is a much shorter time.
The time could also be trimmed if there are large numbers of individuals in
the population too. It seems to me that the IDer's that follow your line of
reasoning think that there is only one "trial" going on at a time, when in
fact, every individual of a popultation is "on trial".
> To say that natural
> selection is the operative equivalent of intelligent guidance and
> accomplishes this task is blindly optimistic and not grounded in reality.
Actually, "optimistic" is relative (just like in an election year, the
Republicans are optimistic that their candidate will win, and eht Democrats
are just as optimistic that their candidate will win), and reality is where
the observed little bits of evidence that you ignore came from in the first
place. Or did you think that, as far as NS goes, Darwin just dreamed it up
out of the blue?
Get a grip chuckles. Just because you *want* there to be some alien guiding
force involved, does not mean that the modern synthysis of the ToE is wrong,
or that your desires are the answer.
Besides, *if* there were an alien designer (or whatever entity you are
pushing for) involved, how do you know it didn't design it's basic "starter
life's" genome to mutate at random in order to generate variations within
the population of the original "seed" of life on Earth?
But of course, any answer you can give to that question would be nothing
more than baseless speculation....
--
Boikat
"Hokey religions and ancient weapons
are no match for a good blaster
at your side, kid."
Han Solo, Star Wars, Episode IV
"I find your lack of faith disturbing"
Darth Vader, Star Wars, Episode IV
Howard Hershey
cha...@charliewagner.com wrote on 6/2/03 3:58 PM:
You know, humans are intelligent designers. They have designed many things
and even manufactured some of them. Including living organisms. It is
instructive to ask how (what mechanisms were used) humans designed living
organisms to better suit human needs. Did they build a "dachshund" factory
and construct "dachsunds" from scratch using a blueprint? Did they build
domestic chicken breeds from scratch? Did they build dairy cattle by
starting with horns and intestines and udders and randomly plugging them
together? Did they intelligently build maize?
Or did they use "selection" starting with previously existing organisms that
had some desired features? Did they take advantage of random mutations that
produced desired effects? Did they cull out thousands of individuals to get
breeding stock? What has been the mechanism by which humans have
intelligently designed 'living organisms' to suit their needs?
Sean Pitman
> > It is the evolutionists, not the ID'ers who are faced with
> > insurmountable difficulties. Evolutionists (especially darwinists) must
> > demonstrate that these functional adaptations can be discovered by
> > random, non-directed processes in spite of the fact that mathematical
> > analysis has shown a random search strategy to be highly inefficient.
>
> How come? The question is not one that would apply to the theory of
> evolution. Natural selection is not random, in fact, it is decidedly
> non-random. I am afraid your mathematical analysis was unnecessary.
> Demolish that strawman Charlie! Just whack at it. Hope it makes you feel
> better.
It seems to me, Frank, that you don't have a clue as to how natural
selection works. You are correct in saying that natural selection is
"not random". However, what you do not seem to realize is that there
are times when natural selection cannot selection between various
genetic changes that do in fact occur on a very regular basis. These
changes are called "neutral mutations". These neutral mutations are
purely *random* genetic mutations that do not result in phenotypic
changes. Natural selection cannot select between two *equally*
functional or nonfunctional genetic sequences. If such neutral
sequence gaps do exist between the genetic real estate that is
currently available and certain sequences that would in fact code for
certain complex beneficial functions, natural selection would not be
able to help in the crossing of such neutral gaps. Neutral gaps are
the death knell of natural selection. The only thing left as a force
for change is the force of purely *random* mutations. So you see,
neutral gaps make mindless processes of evolutionary change entirely
random. Charlie is right. This is no straw man here. This is
reality.
Now, your job would be to explain one of two things. Explain either
how these gaps are crossed without natural selection OR explain how
these gaps do not really exist. That is your job if you are thinking
to rescue the theory of mindless naturalistic evolution from this
neutral gap problem.
Perhaps a good place to start your explanations would be to explain
why Hall's mutant E. coli colonies were incapable of evolving a
relatively simple lactase function despite being given large
populations sizes, high mutation rates, adequate selection pressures,
and many thousands of generations of time? This is a very curious
finding. How is it explained? What, exactly, was the limiting factor
that prevented these bacteria from evolving a relatively simple
function that would in fact have been quite beneficial to them if they
ever were to evolve it?
> Frank
Sean
http://naturalselection.0catch.com/Files/galactosidaseevolution.html
Sean Pitman
snip
> ID'ers must show that biological systems are perfect machines that
> cannot move from one context to another context simply by adapting --
> by evolutionary process as outlined -- their existing systems to other
> contexts. Arguing that yeast cannot adapt to space conditions (as an
> hypothetical example) is no argument, however, since evolution does
> not require such great leaps. Evolution only requires reasonable
> context jumps -- nylon instead of granite. The largest problem for ID
> is, however, that they'd be arguing against observation.
Nylon instead of granite? Granite? Do you know of anything that can
eat granite? I was not aware that granite was such a potential energy
source for biological organisms. But hey, that isn't really the point
now is it?
I offered a simple example where certain E. coli colonies (lacking the
lacZ and ebgA genes) had been grown on a lactose rich
media/environment. They failed to evolve the lactase function despite
the obvious benefit to them if they ever did evolve this relatively
simple single protein based enzyme. These particular bacteria were
grown on this lactose rich media for tens of thousands of generations
with high mutation rates and large population sizes, and they still
never evolved this relatively simple lactase function. Really, we are
not talking about a dramatic shift in environment here. We aren't
talking about a lethal "outer space" environment either. The E. coli
bacteria grew just fine without the lactase function, but they would
have done much better in the lactose rich environment if they did have
this function. So, why didn't they evolve this function?
These very same bacteria would quickly evolve resistance to penicillin
if it were added to their environment. No more than a handful of
generations would be required. Why then is antibiotic resistance so
much easier for them to evolve than the lactase function? What is it
about the evolution of relatively simple enzymes that is so much more
difficult than the evolution of antibiotic resistance?
Also, we have actually seen a few relatively rare real time
demonstrations of enzyme evolution, to include the evolution of the
lactase function in some types of E. coli, but never in other types of
mutant E. coli and never in many other types of bacteria over the
course of 50+ years. However, we have never seen a bacterial function
evolve that requires multiple proteins working together at the same
time, such as would be required for the function of bacterial
motility. Why is this type of multi-protein function so difficult to
evolve in real time? Hmmmmm?
I look forward to finally hearing from someone in the know as to why
antibiotic resistance evolves so much faster than the functions of
enzymes and why enzymes evolve at least on some rare occasions, but
functions with multiple proteins working together at the same time,
never seem to evolve in real time. I mean, if it is so easy, as you
seem to be saying, then evolution should proceed rapidly, should it
not? If there were no neutral gaps to slow the process of evolution
down, then given the proper environment, the evolution of beneficial
functions, such as the lactase function in a lactose rich environment,
should proceed very quickly. This lactose environment ain't outer
space and it ain't granite you know. One little enzyme is all that is
needed to use this new environment in a more advantageous way. And
yet, many different types of bacteria seem unable to evolve the
lactase enzyme despite hundreds of thousands and even millions of
generations of time. What then, exactly, is slowing this process
down? Please, you seem so knowledgeable . . . what is the answer?
Sean
Bill Rogers
You are contrasting the ease with which a single mutation can lead to
gain of function (starting on the right background) with the problem
of evolving a new enzyme from scratch (or from an enzyme with
unrelated function). Yes. It is much faster if there is a gene
already there which needs just a single mutation to develop a new,
useful activity.
Here is a similar contrast from drug resistant malaria. Mefloquine is
a new anti-malarial drug that has been on the market for about 15
years. Mefloquine resistance began to appear in malaria parasites
within a few years of the release of the drug to the market and is now
a significant problem in treating malaria in southeast asia and the
amazon. One can start a culture of mefloquine-sensitive malaria
parasites in the lab (beginning with a single, cloned parasite) and,
by adding progressively higher concentrations of mefloquine select for
a mefloquine resistant population. A single mutation in a single gene
does the trick.
On the other hand, chloroquine resistance is diffferent. Chloroquine
resitance in malaria parasites appeared in the wild in the 60's and
spread throughout the world-wide malaria population over the following
30 years. However, no one has succeeded in starting with a chloroquine
sensitive parasite clone and selecting a chloroquine resistant
population in in vitro culture. Based on sequencing data from
chloroquine sensitive and chloroquine resistant strains it looks like
the problem is that chloroquine resistance requires the acquisition of
a series of 6 or 7 mutations in a particular order. No one has been
able to get this to happen in cultured parasites in the lab. But it
clearly happened in "real time" in nature as a result of widespread
use of chloroquine against malaria.
So... Both resistances evolved in nature in years to decades;
evolution of mefloquine resistance has been reproduced in the lab;
evolution of chloroquine resistance has not. Does this mean that the
"Designer" let P. falciparum handle mefloquine on its own, but
intervened to help P. falciparum deal with chloroquine?
>
> These very same bacteria would quickly evolve resistance to penicillin
> if it were added to their environment. No more than a handful of
> generations would be required. Why then is antibiotic resistance so
> much easier for them to evolve than the lactase function? What is it
> about the evolution of relatively simple enzymes that is so much more
> difficult than the evolution of antibiotic resistance?
Enzymes are really complicated. You are right. It almost certainly
takes more time than you have to watch to evolve a new enzyme from
scratch (or even from an unrelated enzyme). We all agree that
evolution takes a long time. Building enzymes from scratch is actually
more a part of abiogenesis than evolution, but most scientists would
agree, I think, that abiogenesis took a billion years or so, not a few
months, even with artificially boosted mutation rates.
It is possible to select for enzymatic activity in antibody molecules
(not originally enzymes at all) in the lab by cycles of mutation and
selection. That works pretty quickly. You can search in Medline under
Richard Lerner and/or Angray Kang to read about that system.
>
> Also, we have actually seen a few relatively rare real time
> demonstrations of enzyme evolution, to include the evolution of the
> lactase function in some types of E. coli, but never in other types of
> mutant E. coli and never in many other types of bacteria over the
> course of 50+ years. However, we have never seen a bacterial function
> evolve that requires multiple proteins working together at the same
> time, such as would be required for the function of bacterial
> motility. Why is this type of multi-protein function so difficult to
> evolve in real time? Hmmmmm?
>
> I look forward to finally hearing from someone in the know as to why
> antibiotic resistance evolves so much faster than the functions of
> enzymes and why enzymes evolve at least on some rare occasions, but
> functions with multiple proteins working together at the same time,
> never seem to evolve in real time.
Antiobiotic resistance is often easy because
(1) The gene already exists on plasmids in wild populations of the
bacterium in question and the plasmid is exchanged in the bacterial
populations (that is the case for some forms of penicillin
resistance). Remember, we've only been using penicillin for 60 or 70
years, but fungi have been using it for millions, so the bacteria have
had plenty of time to develop a suite of resistance genes.
or
(2) The action of the drug requires binding to some bacterial protein
and a simple mutation in the gene encoding the bacterial protein
destroys the binding site. This happens with other forms of penecillin
resistance, and with resistance to several antibiotic that bind to
bacterial ribosomes, like tetracycline.
So, yes, that's a lot easier than getting to a complex multi-enzyme
complex from scratch. No doubts.
I mean, if it is so easy, as you
> seem to be saying, then evolution should proceed rapidly, should it
> not?
Depends on what you mean by rapidly? It will not proceed rapidly if by
that you mean "right before my eyes."
Lenny Flank
<snip>
> Nylon instead of granite? Granite? Do you know of anything that can
> eat granite? I was not aware that granite was such a potential energy
> source for biological organisms. But hey, that isn't really the point
> now is it?
>
<snip>
Speaking of "the point", Dr, you seem to have not answered my simple
question. So I'll ask again.
As a medical dorctor, do you advise your patients to reject their
materialistic naturalistic atheistic biases when they get sick? Do
you advise them to seek non-naturalistic cures for the
non-naturalistic causes of their diseases -- such as evil spirits or
curses or The Evil Eye from local witches? Or do you use
materialistic naturalistic antibiotics to treat their materialistic
naturalistic diseases by killing their materialistic naturalistic
germs.
Are you just a materialistic natuiralisic atheist at heart, Dr?
===============================================
"There are no loose threads in the web of life"
Creation "Science" Debunked Website:
http://www.geocities.com/lflank
"DebunkCreation" email list at Yahoogroups:
http://groups.yahoo.com/group/DebunkCreation/join
Sean Pitman
> You are contrasting the ease with which a single mutation can lead to
> gain of function (starting on the right background) with the problem
> of evolving a new enzyme from scratch (or from an enzyme with
> unrelated function). Yes. It is much faster if there is a gene
> already there which needs just a single mutation to develop a new,
> useful activity.
Finally, someone who actually seems to understand what I am talking
about. There are clearly different levels of functional complexity.
The function of bacterial antibiotic resistance is extremely simple,
even in comparison to the most simple enzymatic functions. The reason
for this is that there is a dramatically higher ratio of functional
mutations as compared to neutral mutations in the development of
antibiotic resistance as compared to the evolution of a certain
enzymatic activities.
> Here is a similar contrast from drug resistant malaria. Mefloquine is
> a new anti-malarial drug that has been on the market for about 15
> years. Mefloquine resistance began to appear in malaria parasites
> within a few years of the release of the drug to the market and is now
> a significant problem in treating malaria in southeast asia and the
> amazon. One can start a culture of mefloquine-sensitive malaria
> parasites in the lab (beginning with a single, cloned parasite) and,
> by adding progressively higher concentrations of mefloquine select for
> a mefloquine resistant population. A single mutation in a single gene
> does the trick.
Exactly . . .
> On the other hand, chloroquine resistance is diffferent. Chloroquine
> resitance in malaria parasites appeared in the wild in the 60's and
> spread throughout the world-wide malaria population over the following
> 30 years. However, no one has succeeded in starting with a chloroquine
> sensitive parasite clone and selecting a chloroquine resistant
> population in in vitro culture. Based on sequencing data from
> chloroquine sensitive and chloroquine resistant strains it looks like
> the problem is that chloroquine resistance requires the acquisition of
> a series of 6 or 7 mutations in a particular order. No one has been
> able to get this to happen in cultured parasites in the lab. But it
> clearly happened in "real time" in nature as a result of widespread
> use of chloroquine against malaria.
The most likely reason why this has not been observed in the lab is
because the lab didn't use a large enough population size to overcome
the neutral gap created by 6 or 7 neutral mutations. A series of 7
neutral mutations in DNA would create a neutral gap or sea of 16,384
possibilities. In this case, only one of these possibilities is
"correct." In order to find this correct sequence out of all the
other possibilities, the given population of malaria parasites would
have to undergo random walk. This random walk takes time and this
time is dependent upon several factors. Lets see if we can figure out
a rough estimate based on these factors.
Let's say that the mutation rate was on the order of 10e-8 mutations
per base pair per generation. On average then, it would take around
10e7 generations to get just one mutation to one of our 7 base pairs
of interest. If a generation time is one day (I'm not exactly sure
what the generation time is for the malaria parasite), a steady state
population of 10e3 parasites would experience one mutation in these 7
base pairs every 10,000 days or 27 years on average. Given this
relatively small colony of parasites, it would take around 500,000
years to develop resistance to chloroquine. If the colony size were
increased to one million parasites, the time required to evolve
resistance would drop to around 5,000 years. If the colony size were
increased to one billion parasites, the time required would drop to
around 5 years.
These rough estimates based, on the time required to cross a known
neutral gap, are very much in line with what we have seen in the
evolution of chloroquine resistance in the wild and they also explain
why this resistance has never been demonstrated in the lab. The lab
experiments simply didn't use a large enough population size or didn't
carry on the experiments for enough generations.
In any case, it is a great example that demonstrates very nicely the
limits that neutral gaps put on the theory of evolution. This only
strengthens my theory.
> So... Both resistances evolved in nature in years to decades;
> evolution of mefloquine resistance has been reproduced in the lab;
> evolution of chloroquine resistance has not. Does this mean that the
> "Designer" let P. falciparum handle mefloquine on its own, but
> intervened to help P. falciparum deal with chloroquine?
You don't seem to understand the statistics involved here. Obviously,
a neutral gap in function of 6 or 7 base pairs can easily be crossed
by random walk alone given the much larger population sizes of the
malaria parasites (P. falciparum) that exist in the wild as compared
to the relatively limited population size that was most likely used in
the laboratory experiments. No ID is needed to explain the evolution
of chloroquine resistance in either case. The average time required
is well within reason.
> > These very same bacteria would quickly evolve resistance to penicillin
> > if it were added to their environment. No more than a handful of
> > generations would be required. Why then is antibiotic resistance so
> > much easier for them to evolve than the lactase function? What is it
> > about the evolution of relatively simple enzymes that is so much more
> > difficult than the evolution of antibiotic resistance?
>
> Enzymes are really complicated. You are right. It almost certainly
> takes more time than you have to watch to evolve a new enzyme from
> scratch (or even from an unrelated enzyme).
I'm glad that you realize this because many people think that the
evolution of antibiotic resistance is something very significant
and/or complex. What many do not realize or admit is that even the
relatively simple function of a single protein based enzyme, is far
more complex than the function of antibiotic resistance.
Obviously more time is required to evolve the enzymatic functions than
the functions of antibiotic resistance. That question is, "Why?" Why
is more time required to evolve functions of increasing complexity? I
am proposing that neutral gaps are the reason for this observed
phenomenon. What is your explanation?
> We all agree that
> evolution takes a long time. Building enzymes from scratch is actually
> more a part of abiogenesis than evolution, but most scientists would
> agree, I think, that abiogenesis took a billion years or so, not a few
> months, even with artificially boosted mutation rates.
Oh, so the evolution of even one little protein sequence is based on
"abiogenesis" not on evolution? Really?! This is *most* interesting.
This is exactly my whole point. Abiogenesis is based on neutral
drift/random walk. Natural selection really is limited when it comes
to ideas on abiogenesis since by far most of the changes in
abiogenesis are functionally neutral as far as a mindless nature is
concerned. This is why scientists think that abiogenesis took
billions of years to produce the first self-replicating cell. But
why? Why does abiogenesis take so long? Because of the neutral gaps.
When you actually start plugging in the numbers and doing some real
estimates based on the idea of neutral gaps, you quickly find that the
abiogenesis of much of anything would take far longer than a few
billion or even many trillions or zillions or googols of years.
> It is possible to select for enzymatic activity in antibody molecules
> (not originally enzymes at all) in the lab by cycles of mutation and
> selection. That works pretty quickly. You can search in Medline under
> Richard Lerner and/or Angray Kang to read about that system.
Yes, this works pretty quickly because it is not based on the needs,
mutation rates, or genetic capabilities of any given life form, but on
the ability of a human scientist to recognize some sort of specific
enzymatic activity from a random pool of proteins. And, even in these
experiments, nothing more than the functions of single proteins are
demonstrated. These functions are still relatively simple compared to
those cellular functions that require multiple proteins all working
together at the same time (i.e., bacterial motility systems like the
flagellum).
> > Also, we have actually seen a few relatively rare real time
> > demonstrations of enzyme evolution, to include the evolution of the
> > lactase function in some types of E. coli, but never in other types of
> > mutant E. coli and never in many other types of bacteria over the
> > course of 50+ years. However, we have never seen a bacterial function
> > evolve that requires multiple proteins working together at the same
> > time, such as would be required for the function of bacterial
> > motility. Why is this type of multi-protein function so difficult to
> > evolve in real time? Hmmmmm?
> >
> > I look forward to finally hearing from someone in the know as to why
> > antibiotic resistance evolves so much faster than the functions of
> > enzymes and why enzymes evolve at least on some rare occasions, but
> > functions with multiple proteins working together at the same time,
> > never seem to evolve in real time.
>
> Antiobiotic resistance is often easy because
>
> (1) The gene already exists on plasmids in wild populations of the
> bacterium in question and the plasmid is exchanged in the bacterial
> populations (that is the case for some forms of penicillin
> resistance). Remember, we've only been using penicillin for 60 or 70
> years, but fungi have been using it for millions, so the bacteria have
> had plenty of time to develop a suite of resistance genes.
That is a nice "just-so" story that many use to explain the origin of
rather complex enzymes like the penicillinase enzyme. It may be true,
but until it can be demonstrated or until some real statistical
calculations can be made to estimate the number of neutral gaps that
would need to be crossed, it is just a story without any real backing
in actual evidence.
In any case, I do thank you for pointing out that the gain of
information via plasmid from some other bacterium, is not the same
thing as the evolution of this information to begin with. Penicillin
resistance that is the result of the penicillinase enzyme is not the
evolution of anything much since the enzyme code was already there.
It did not evolve de novo in these resistant colonies.
> or
>
> (2) The action of the drug requires binding to some bacterial protein
> and a simple mutation in the gene encoding the bacterial protein
> destroys the binding site. This happens with other forms of penecillin
> resistance, and with resistance to several antibiotic that bind to
> bacterial ribosomes, like tetracycline.
Exactly. Practically all examples of antibiotic resistance involve
the destruction of a pre-established interaction of a target sequence
with the antibiotic. The destruction of this interaction is
relatively easy to do with one or two of several different possible
mutations that would do the same thing. Antibiotic resistance that
arises via mutation is based on the simple concept that it is far
easier to break or interfere with a pre-established function than it
is to make a new function from scratch. It is much like the
children's rhyme about Humpty Dumpty. It is far easier to break
something than it is to create something new.
> So, yes, that's a lot easier than getting to a complex multi-enzyme
> complex from scratch. No doubts.
Thank-you for making this so clear.
> > I mean, if it is so easy, as you
> > seem to be saying, then evolution should proceed rapidly, should it
> > not?
>
> Depends on what you mean by rapidly? It will not proceed rapidly if by
> that you mean "right before my eyes."
If there were no neutral gaps, then yes. Rapidly would mean, "right
before my eyes." The mutation rates are high enough to achieve such
rapid evolution if there were no neutral gaps or random walks to take
up the time in the travel toward new functions.
> > If there were no neutral gaps to slow the process of evolution
> > down, then given the proper environment, the evolution of beneficial
> > functions, such as the lactase function in a lactose rich environment,
> > should proceed very quickly. This lactose environment ain't outer
> > space and it ain't granite you know. One little enzyme is all that is
> > needed to use this new environment in a more advantageous way. And
> > yet, many different types of bacteria seem unable to evolve the
> > lactase enzyme despite hundreds of thousands and even millions of
> > generations of time. What then, exactly, is slowing this process
> > down? Please, you seem so knowledgeable . . . what is the answer?
> >
> > Sean
Thanks again for your most helpful and enlightening post.
Sean
Lane Lewis
> Lilith wrote in message
news:<75200cbc.03060...@posting.google.com>...
>
> snip
> > ID'ers must show that biological systems are perfect machines that
> > cannot move from one context to another context simply by adapting --
> > by evolutionary process as outlined -- their existing systems to other
> > contexts. Arguing that yeast cannot adapt to space conditions (as an
> > hypothetical example) is no argument, however, since evolution does
> > not require such great leaps. Evolution only requires reasonable
> > context jumps -- nylon instead of granite. The largest problem for ID
> > is, however, that they'd be arguing against observation.
>
> Nylon instead of granite? Granite? Do you know of anything that can
> eat granite? I was not aware that granite was such a potential energy
> source for biological organisms. But hey, that isn't really the point
> now is it?
>
snip
> Sean
Not sure about granite, but
http://www.google.com/search?hl=en&ie=UTF-8&oe=UTF-8&q=Rock+eating+bacteria
http://makeashorterlink.com/?G370238E4
Lane
Lane Lewis
> bro...@noguchi.mimcom.net (Bill Rogers) wrote in message
news:<8984713a.03061...@posting.google.com>...
>
>
> > We all agree that
> > evolution takes a long time. Building enzymes from scratch is actually
> > more a part of abiogenesis than evolution, but most scientists would
> > agree, I think, that abiogenesis took a billion years or so, not a few
> > months, even with artificially boosted mutation rates.
>
> Oh, so the evolution of even one little protein sequence is based on
> "abiogenesis" not on evolution? Really?! This is *most* interesting.
> This is exactly my whole point. Abiogenesis is based on neutral
> drift/random walk. Natural selection really is limited when it comes
> to ideas on abiogenesis since by far most of the changes in
> abiogenesis are functionally neutral as far as a mindless nature is
> concerned. This is why scientists think that abiogenesis took
> billions of years to produce the first self-replicating cell. But
> why? Why does abiogenesis take so long? Because of the neutral gaps.
> When you actually start plugging in the numbers and doing some real
> estimates based on the idea of neutral gaps, you quickly find that the
> abiogenesis of much of anything would take far longer than a few
> billion or even many trillions or zillions or googols of years.
>
snip
>
> Sean
>
In fact scientist do not believe abiogenesis took billions of years.
According to the evidence it took a very short period of time, in the
millions at the most.
And again what numbers are you talking about that produce the "trillions or
zillions or googols of years" it would take for abiogenesis to happen, you
seem to be avoiding supplying these numbers as I have asked you before.
It seems this is the point you are trying to make in all of your post but we
have yet to see any of the math supporting your argument. Without the math
you are not doing science but instead just PREACHING what is most likely
nonsense.
Time to put up or shut up.
Lane
Von Smith
> bro...@noguchi.mimcom.net (Bill Rogers) wrote in message news:<8984713a.03061...@posting.google.com>...
>
> > You are contrasting the ease with which a single mutation can lead to
> > gain of function (starting on the right background) with the problem
> > of evolving a new enzyme from scratch (or from an enzyme with
> > unrelated function). Yes. It is much faster if there is a gene
> > already there which needs just a single mutation to develop a new,
> > useful activity.
>
> Finally, someone who actually seems to understand what I am talking
> about. There are clearly different levels of functional complexity.
Really? How is it clear that mefloquine resistance is less complex
than chloroquine resistance? Could you have predicted this before the
fact based on a description of the function involved, or before an
identification of the probable evolutionary pathway? Can you say
anything meaningful about their respective complexities without
peeking?
> The function of bacterial antibiotic resistance is extremely simple,
> even in comparison to the most simple enzymatic functions.
Except of course for the cases in which antibiotic resistance *is* an
enzyme function, as in the case of, say vancomycin or cefotaxime
resistance.
> The reason
> for this is that there is a dramatically higher ratio of functional
> mutations as compared to neutral mutations in the development of
> antibiotic resistance as compared to the evolution of a certain
> enzymatic activities.
So, how do you determine complexity without *first* knowing what
evolutionary changes are involved?
Not really. No one ever denied that there were evolutionary
constraints, nor that the majority of mutations are functionally
neutral. Nor did anyone ever suggest that *any* arbitrarily selected
function would evolve quickly from *any* given precursor. That is
your strawman.
But your theory isn't simply that "neutral gaps" exist. That would be
fairly uninteresting, and of no real importance to the theory of
common descent at all. Your theory is that they are so pervasive as
to preclude evolution of life as we see it today in the available
history of the world. The fact that chloroquine resistance may take a
large population several years to evolve hardly supports such a
generalization.
>
> > So... Both resistances evolved in nature in years to decades;
> > evolution of mefloquine resistance has been reproduced in the lab;
> > evolution of chloroquine resistance has not. Does this mean that the
> > "Designer" let P. falciparum handle mefloquine on its own, but
> > intervened to help P. falciparum deal with chloroquine?
>
> You don't seem to understand the statistics involved here.
Neither do you, apparently. You have argued that the density of
sequences for antibiotic resistance may be as high as 1 in 3; you have
suggested elsewhere that the density for functional enzyme sequences
is about 1 per 1e12, or is it 1e24? In a different context you argued
that the density of functional sequences for a 100aa long protein
might be as low as 1 per 1e106 (and the logic you used in that post
could be extended to arbitrarily long sequences to get arbitrarily low
densities such as ~1e-1277 for a 1000aa sequence). Now here you argue
that the density of (genetic) sequences conferring chloroquine
resistance may be about 1e-4.
So obviously you have no idea what the sequence density for any given
function is ahead of time, although you are good at saying: "See, I
knew that!" after the fact. Nor do you know what the available
evolutionary pathways were, nor what sort of fitness landscapes they
traversed. Nonetheless, you are sure that there are enough neutral
gaps around to prevent evolution of many of the functions we observe
in life today; you base your confidence on the "statistics involved",
which enable you to predict with confidence that the density for
functional sequences in a sequence space is somewhere between 1 in 3
and 1 in 1e106 (or perhaps even as low as 1e1277).
> Obviously,
> a neutral gap in function of 6 or 7 base pairs can easily be crossed
> by random walk alone given the much larger population sizes of the
> malaria parasites (P. falciparum) that exist in the wild as compared
> to the relatively limited population size that was most likely used in
> the laboratory experiments. No ID is needed to explain the evolution
> of chloroquine resistance in either case. The average time required
> is well within reason.
OK, so at least you are smart enough not to deny the evolvability of
something that has been observed to evolve.
>
> > > These very same bacteria would quickly evolve resistance to penicillin
> > > if it were added to their environment. No more than a handful of
> > > generations would be required. Why then is antibiotic resistance so
> > > much easier for them to evolve than the lactase function? What is it
> > > about the evolution of relatively simple enzymes that is so much more
> > > difficult than the evolution of antibiotic resistance?
> >
> > Enzymes are really complicated. You are right. It almost certainly
> > takes more time than you have to watch to evolve a new enzyme from
> > scratch (or even from an unrelated enzyme).
>
> I'm glad that you realize this because many people think that the
> evolution of antibiotic resistance is something very significant
> and/or complex. What many do not realize or admit is that even the
> relatively simple function of a single protein based enzyme, is far
> more complex than the function of antibiotic resistance.
Except, again, when the antibiotic resistance in question *is* an
enzyme activity.
>
> Obviously more time is required to evolve the enzymatic functions than
> the functions of antibiotic resistance. That question is, "Why?" Why
> is more time required to evolve functions of increasing complexity? I
> am proposing that neutral gaps are the reason for this observed
> phenomenon. What is your explanation?
My explanation is that you claim with hindsight a level of complexity
based on what you already know about the evolutionary pathway, so that
your "theory" is basically a circular argument that lacks the
predictive value you need for it to be pose much of a challenge to
evolution.
>
> > We all agree that
> > evolution takes a long time. Building enzymes from scratch is actually
> > more a part of abiogenesis than evolution, but most scientists would
> > agree, I think, that abiogenesis took a billion years or so, not a few
> > months, even with artificially boosted mutation rates.
>
> Oh, so the evolution of even one little protein sequence is based on
> "abiogenesis" not on evolution? Really?! This is *most* interesting.
> This is exactly my whole point. Abiogenesis is based on neutral
> drift/random walk. Natural selection really is limited when it comes
> to ideas on abiogenesis since by far most of the changes in
> abiogenesis are functionally neutral as far as a mindless nature is
> concerned. This is why scientists think that abiogenesis took
> billions of years to produce the first self-replicating cell. But
> why? Why does abiogenesis take so long? Because of the neutral gaps.
> When you actually start plugging in the numbers and doing some real
> estimates based on the idea of neutral gaps, you quickly find that the
> abiogenesis of much of anything would take far longer than a few
> billion or even many trillions or zillions or googols of years.
Actually, the oldest accepted unicellular fossils are about 3.6 Gya,
indicating that life arose within no more than a couple hundred
million years after conditions on earth made it possible. And I would
love to see you "start plugging in the numbers and doing some real
estimates". All you need is a detailed model of what the likely
precursor molecules were, what their population size and composition
was like, what their mutation and replication rate was like (both
probably much faster initially than that we typically see in life
forms today), what the environment was, what the fitness landscape
looked like over the sequence space and what evolutionary constraints
there were (since the earliest replicators would have had few
functions, there was almost no place to go but up, as someone quoted
Maynard Smith as saying elsewhere). I'm sure you'll be able to
estimate the length of time it would take to within about, oh, 106
orders of magnitude (given that error, what you estimate to take
googles of years could actually have taken place within a few minutes
or even seconds)
>
> > It is possible to select for enzymatic activity in antibody molecules
> > (not originally enzymes at all) in the lab by cycles of mutation and
> > selection. That works pretty quickly. You can search in Medline under
> > Richard Lerner and/or Angray Kang to read about that system.
>
> Yes, this works pretty quickly because it is not based on the needs,
> mutation rates, or genetic capabilities of any given life form, but on
> the ability of a human scientist to recognize some sort of specific
> enzymatic activity from a random pool of proteins.
Exactly, and a pool of simple replicators that hadn't already evolved
complex cellular functions might be similarly free of constraints.
We already know that enzymes of comparable sequence lengths can evolve
in real time. Ian Musgrave pointed out to you elsewhere that many
different novel cefotaxime-resistant strains using extended spectrum
b-lactamases have evolved in just the last 20 years or so. I would
think that if beta-lactamase is a complex enzyme, then ESBLs are even
more complex, wouldn't you?
I'm guessing that, no, *you* probably wouldn't think that, because you
would already have "peeked" at the evolutionary pathways from known
precursors and asserted that the evolution of ESBLs from an ancestor
was "trivial". Of course, if you didn't already know the pathway, you
would have no way of making such an argument. In spite of this, it
doesn't seem to bother you in the least to make pronouncements about
the complexity of a function in the *absence* of such extrinsic
knowledge about the evolutionary history of penicillinase: you are
somehow convinced that it must be unevolvably complex by default until
it is proven otherwise.
> It may be true,
> but until it can be demonstrated or until some real statistical
> calculations can be made to estimate the number of neutral gaps that
> would need to be crossed, it is just a story without any real backing
> in actual evidence.
As is *any* talk about neutral gaps, including yours. Funny, when I
first pointed out that one needed such detailed knowledge of the
evolutionary pathways involved to meaningfully estimate neutral gaps,
you seemed to consider this an unreasonable burden of proof on you.
But here you lay down exactly the same requirement (for exactly the
same reason) without blinking when it suits your argument.
>
> In any case, I do thank you for pointing out that the gain of
> information via plasmid from some other bacterium, is not the same
> thing as the evolution of this information to begin with. Penicillin
> resistance that is the result of the penicillinase enzyme is not the
> evolution of anything much since the enzyme code was already there.
> It did not evolve de novo in these resistant colonies.
>
> > or
> >
> > (2) The action of the drug requires binding to some bacterial protein
> > and a simple mutation in the gene encoding the bacterial protein
> > destroys the binding site. This happens with other forms of penecillin
> > resistance, and with resistance to several antibiotic that bind to
> > bacterial ribosomes, like tetracycline.
>
> Exactly. Practically all examples of antibiotic resistance involve
> the destruction of a pre-established interaction of a target sequence
> with the antibiotic. The destruction of this interaction is
> relatively easy to do with one or two of several different possible
> mutations that would do the same thing. Antibiotic resistance that
> arises via mutation is based on the simple concept that it is far
> easier to break or interfere with a pre-established function than it
> is to make a new function from scratch. It is much like the
> children's rhyme about Humpty Dumpty. It is far easier to break
> something than it is to create something new.
Right, and the history of life is certainly replete with such losses
of function. The loss of fins in early amphibians was certainly a
loss of function; critters like ichthyostega were no longer as
efficient swimmers as their fish counterparts, because their fins had
been replaced by deformed protrusions that were fit for little more
than scudding along the bottom of shallow waters. Mammals have
"broken" reptilian jaw hinges which have lost their function; now they
do nothing more than rattle around in our middle ear, creating these
annoying vibrations inside our heads. Humans and other apes have
"broken" claws that are useless for fighting. All we have are these
stupid flat cuticled fingernails. If we want to scare off a lion, we
have to resort to something like a rock or a pointed stick.
>
> > So, yes, that's a lot easier than getting to a complex multi-enzyme
> > complex from scratch. No doubts.
>
> Thank-you for making this so clear.
>
> > > I mean, if it is so easy, as you
> > > seem to be saying, then evolution should proceed rapidly, should it
> > > not?
> >
> > Depends on what you mean by rapidly? It will not proceed rapidly if by
> > that you mean "right before my eyes."
>
> If there were no neutral gaps, then yes. Rapidly would mean, "right
> before my eyes." The mutation rates are high enough to achieve such
> rapid evolution if there were no neutral gaps or random walks to take
> up the time in the travel toward new functions.
>
>
> > > If there were no neutral gaps to slow the process of evolution
> > > down, then given the proper environment, the evolution of beneficial
> > > functions, such as the lactase function in a lactose rich environment,
> > > should proceed very quickly. This lactose environment ain't outer
> > > space and it ain't granite you know. One little enzyme is all that is
> > > needed to use this new environment in a more advantageous way. And
> > > yet, many different types of bacteria seem unable to evolve the
> > > lactase enzyme despite hundreds of thousands and even millions of
> > > generations of time. What then, exactly, is slowing this process
> > > down? Please, you seem so knowledgeable . . . what is the answer?
> > >
> > > Sean
>
> Thanks again for your most helpful and enlightening post.
...which, for some odd reason, you seem to think supports your views.
Von Smith
Fortuna nimis dat multis, satis nulli.
>
> Sean
Bill Rogers
> bro...@noguchi.mimcom.net (Bill Rogers) wrote in message news:<8984713a.03061...@posting.google.com>...
>
> > You are contrasting the ease with which a single mutation can lead to
> > gain of function (starting on the right background) with the problem
> > of evolving a new enzyme from scratch (or from an enzyme with
> > unrelated function). Yes. It is much faster if there is a gene
> > already there which needs just a single mutation to develop a new,
> > useful activity.
>
> Finally, someone who actually seems to understand what I am talking
> about.
That I understand you does not mean that you are correct.
>There are clearly different levels of functional complexity.
> The function of bacterial antibiotic resistance is extremely simple,
> even in comparison to the most simple enzymatic functions. The reason
> for this is that there is a dramatically higher ratio of functional
> mutations as compared to neutral mutations in the development of
> antibiotic resistance as compared to the evolution of a certain
> enzymatic activities.
Why do you say that. Some antibiotic resistance genes encode enzymes.
How could you possibly know anything about a "dramatically higher
ratio of functional
mutations as compared to neutral mutations in the development of
antibiotic resistance as compared to the evolution of a certain
enzymatic activities" without specifying in a whole lot more detail
what genes you are talking about and without doing experiments to
determine which changes are or are not functional or neutral?
Everything depends on the starting material and the "fitness
landscape" around the point you start from. In some cases you pretty
clearly even "cannot get there from here," e.g., not many feathered
bats, or gilled whales, even though such creatures might be at finess
optima if they existed.
Yeah, that's tricky; in nature when you take into account the
likelihood of the parasite actually getting out one host, into a
mosquito, and then into another host, the effective generation time is
about 6 months, which is completely different than the 48-72 hours it
takes for one erythrocytic stage cycle of the parasite.
> a steady state
> population of 10e3 parasites would experience one mutation in these 7
> base pairs every 10,000 days or 27 years on average. Given this
> relatively small colony of parasites, it would take around 500,000
> years to develop resistance to chloroquine. If the colony size were
> increased to one million parasites, the time required to evolve
> resistance would drop to around 5,000 years. If the colony size were
> increased to one billion parasites, the time required would drop to
> around 5 years.
In fact the "colony" sizes people use are on the order of 5,000,000
parasites per culture, though it is possible to grow 10 fold larger
amounts easily enough.
>
> These rough estimates based, on the time required to cross a known
> neutral gap, are very much in line with what we have seen in the
> evolution of chloroquine resistance in the wild and they also explain
> why this resistance has never been demonstrated in the lab. The lab
> experiments simply didn't use a large enough population size or didn't
> carry on the experiments for enough generations.
>
> In any case, it is a great example that demonstrates very nicely the
> limits that neutral gaps put on the theory of evolution. This only
> strengthens my theory.
But how do you know that even these gaps are neutral? Your own example
of the evolution of lactase makes it clear that you cannot make ad hoc
calculations to tell you how long it will take for something to
evolve. Everything depends on the available starting materials, the
relative fitness of intermediates, changes in the environment, etc.
Multiplying the number of genetic differences between two sequences in
related organisms by the estimated population size, mutation rate, and
generation time, is pretty irrelevant. No one thinks that evolution
works entirely by neutral mutation and random walks.
>
> > So... Both resistances evolved in nature in years to decades;
> > evolution of mefloquine resistance has been reproduced in the lab;
> > evolution of chloroquine resistance has not. Does this mean that the
> > "Designer" let P. falciparum handle mefloquine on its own, but
> > intervened to help P. falciparum deal with chloroquine?
>
> You don't seem to understand the statistics involved here. Obviously,
> a neutral gap in function of 6 or 7 base pairs can easily be crossed
> by random walk alone given the much larger population sizes of the
> malaria parasites (P. falciparum) that exist in the wild as compared
> to the relatively limited population size that was most likely used in
> the laboratory experiments. No ID is needed to explain the evolution
> of chloroquine resistance in either case. The average time required
> is well within reason.
We know what the "average time" is, not because of your post hoc
statistics, but because we observed the evolution of chloroquine
resistance in nature.
I have no idea why you think this. Most ideas about abiogenesis (apart
from creationist, junkyard to B727, strawmen) are based on selection.
We all agree that a random walk through all possible chemical
structures to cytochrome c is not what happened.
> This is why scientists think that abiogenesis took
> billions of years to produce the first self-replicating cell. But
> why? Why does abiogenesis take so long? Because of the neutral gaps.
> When you actually start plugging in the numbers and doing some real
> estimates based on the idea of neutral gaps, you quickly find that the
> abiogenesis of much of anything would take far longer than a few
> billion or even many trillions or zillions or googols of years.
Please, show your model. But it isn't a random walk.
And so we should conclude that God created beta-lactamase?
>
> In any case, I do thank you for pointing out that the gain of
> information via plasmid from some other bacterium, is not the same
> thing as the evolution of this information to begin with. Penicillin
> resistance that is the result of the penicillinase enzyme is not the
> evolution of anything much since the enzyme code was already there.
> It did not evolve de novo in these resistant colonies.
>
> > or
> >
> > (2) The action of the drug requires binding to some bacterial protein
> > and a simple mutation in the gene encoding the bacterial protein
> > destroys the binding site. This happens with other forms of penecillin
> > resistance, and with resistance to several antibiotic that bind to
> > bacterial ribosomes, like tetracycline.
>
> Exactly. Practically all examples of antibiotic resistance involve
> the destruction of a pre-established interaction of a target sequence
> with the antibiotic.
That is incorrect. Many of them involve degradation of the antibiotic
or enhanced transport of the antibiotic out of the target cell.
>The destruction of this interaction is
> relatively easy to do with one or two of several different possible
> mutations that would do the same thing. Antibiotic resistance that
> arises via mutation is based on the simple concept that it is far
> easier to break or interfere with a pre-established function than it
> is to make a new function from scratch. It is much like the
> children's rhyme about Humpty Dumpty. It is far easier to break
> something than it is to create something new.
>
> > So, yes, that's a lot easier than getting to a complex multi-enzyme
> > complex from scratch. No doubts.
>
> Thank-you for making this so clear.
It was already clear. Why you think it helps your argument is beyond
me. No one thinks that the ribosome arouse from a random walk through
the space of all possible chemical compounds, or even a random walk
though the space of all possible combinations of protein and RNA
sequences.
>
> > > I mean, if it is so easy, as you
> > > seem to be saying, then evolution should proceed rapidly, should it
> > > not?
> >
> > Depends on what you mean by rapidly? It will not proceed rapidly if by
> > that you mean "right before my eyes."
>
> If there were no neutral gaps, then yes. Rapidly would mean, "right
> before my eyes." The mutation rates are high enough to achieve such
> rapid evolution if there were no neutral gaps or random walks to take
> up the time in the travel toward new functions.
>
>
> > > If there were no neutral gaps to slow the process of evolution
> > > down, then given the proper environment, the evolution of beneficial
> > > functions, such as the lactase function in a lactose rich environment,
> > > should proceed very quickly. This lactose environment ain't outer
> > > space and it ain't granite you know. One little enzyme is all that is
> > > needed to use this new environment in a more advantageous way. And
> > > yet, many different types of bacteria seem unable to evolve the
> > > lactase enzyme despite hundreds of thousands and even millions of
> > > generations of time. What then, exactly, is slowing this process
> > > down? Please, you seem so knowledgeable . . . what is the answer?
> > >
> > > Sean
>
> Thanks again for your most helpful and enlightening post.
Alas, it does not seem to have enlightened you.
>
> Sean
Sean Pitman
snip
> > There are clearly different levels of functional complexity.
> > The function of bacterial antibiotic resistance is extremely simple,
> > even in comparison to the most simple enzymatic functions. The reason
> > for this is that there is a dramatically higher ratio of functional
> > mutations as compared to neutral mutations in the development of
> > antibiotic resistance as compared to the evolution of a certain
> > enzymatic activities.
>
> Why do you say that. Some antibiotic resistance genes encode enzymes.
Yes, penicillinase is an enzyme that destroys the antibiotic function
of penicillin. However, there are a lot of other ways to gain
penicillin resistance that are a lot less complex than the evolution
of a fairly complex enzyme like the penicillinase enzyme.
> How could you possibly know anything about a "dramatically higher
> ratio of functional mutations as compared to neutral mutations in
> the development of antibiotic resistance as compared to the evolution
> of a certain enzymatic activities" without specifying in a whole lot
> more detail what genes you are talking about and without doing
> experiments to determine which changes are or are not functional or
> neutral? Everything depends on the starting material and the "fitness
> landscape" around the point you start from. In some cases you pretty
> clearly even "cannot get there from here," e.g., not many feathered
> bats, or gilled whales, even though such creatures might be at finess
> optima if they existed.
If cow-like creatures could turn into whales and reptiles into birds,
then why do you think it would be so hard to get bats to evolve
feathers or whales to evolve gills if they would in fact benefit from
such structures? Really, the theory of evolution has proposed that
such dramatic changes have occurred that practically anything is
possible given enough time. The starting point really has little to
do with it. All that is needed is the right environment and enough
time.
Knowledge of the starting point is only important if neutral gaps do
in fact exist and if random walk would in fact pose a problem for
evolution. An argument based on the idea of a starting point is
really one that is based on the validity of my position.
So anyway, you suggest that there is no way to know where the starting
point is, and this is true. However, one can get a pretty good idea
that a random starting point will be a certain distance away from a
given function in a particular creature like a bacterium. Certainly
it is true that when Hall deleted the lacZ genes in various colonies
of E. coli, these E. coli happened to be just one step away from a
different lactase sequence. What where the odds? How fortunate for
them! We know that this was quite a stroke of luck indeed when we
consider how very difficult it is for many other bacteria to evolve
the lactase function. Granted, on occasion some life forms might just
happen upon a particular complex sequence, like the lactase enzyme,
because of the luck of their starting point. However, how long will
this luck hold out? What are the odds that they will not only just
happen to be close to one of the fairly rare lactase sequences out
there, but also close to one of the fairly rare penicillinase
sequences as well? I mean, look at how many different complex enzymes
and other functional proteins that an E. coli bacterium can produce.
What are the odds that its original ancestral genetic real estate was
that close to all of these various functional sequences? And we are
only talking about the function of single proteins here. We haven't
even started talking about the relative rarity of more complex
multi-protein systems of function as are required for bacterial
motility and the like.
snip
> > a steady state
> > population of 10e3 parasites would experience one mutation in these 7
> > base pairs every 10,000 days or 27 years on average. Given this
> > relatively small colony of parasites, it would take around 500,000
> > years to develop resistance to chloroquine. If the colony size were
> > increased to one million parasites, the time required to evolve
> > resistance would drop to around 5,000 years. If the colony size were
> > increased to one billion parasites, the time required would drop to
> > around 5 years.
>
> In fact the "colony" sizes people use are on the order of 5,000,000
> parasites per culture, though it is possible to grow 10 fold larger
> amounts easily enough.
Well then, the larger the colony size, the faster the evolution across
this gap of 6 or 7 mutations.
> > These rough estimates based, on the time required to cross a known
> > neutral gap, are very much in line with what we have seen in the
> > evolution of chloroquine resistance in the wild and they also explain
> > why this resistance has never been demonstrated in the lab. The lab
> > experiments simply didn't use a large enough population size or didn't
> > carry on the experiments for enough generations.
> >
> > In any case, it is a great example that demonstrates very nicely the
> > limits that neutral gaps put on the theory of evolution. This only
> > strengthens my theory.
>
> But how do you know that even these gaps are neutral?
First off, this is your illustration. You were the one who said that
6 or 7 point mutations were required in a particular order for the
evolution of Chloroquine resistance to be realized. I just went with
your estimates here in my calculations.
Another reason why I think that they had to be neutral mutations is
because if they were selectable in some functional way, the evolution
would have proceeded much faster than it did. In just a handful of
generations a gap of 6 or 7 mutations would be crossed if each step
were selectable in some advantageous way. The fact that the evolution
of Chloroquine resistance took so long means that the gap was indeed a
neutral gap that required a random walk to get across it. In fact,
this is the reason given for the problems with the demonstration of
Chloroquine resistance in the lab.
In light of this question, lets take a look at how Chloroquine works:
In human red blood cells, P. falciparum supports its growth by taking
up host cell cytoplasm in an acidic digestive food vacuole. Toxic
heme, in its hematin form, is released in the vacuole by hemoglobin
digestion and is crystallized into innocuous hemozoin, or "malaria
pigment". Chloroquine (CQ) interferes with this process by complexing
with hemozoin. This complex prevents hematin from crystallizing into
the innocuous hemozoin form. The "toxic" effects of free hematin are
caused by hematin's ability to increase membrane permeability which
lead to cell lysis and death. Hematin also is known to inhibit
parasite enzymes.
Chloroquine resistant strains of P. falciparum show a reduced
accumulation of CQ in the digestive vacuole. The genetic mutations
associated with this reduced accumulation have been isolated to the
PfCRT (P. falciparum chloroquine resistance transporter) gene. The
gene contains 13 exons that cover 3.1 kb. The PfCRT gene product is a
423 amino acyl ten-transmembrane channel or transporter protein that
catalyzes chloroquine flux and H+ equilibrium across the digestive
vacuole membrane. Many different point mutations have been isolated
in resistant CQR strains of malaria (M74I, N75E, K76T, A220S, Q271E,
N326S, I356T, and R371I). Of these, only the K76T and the A220S
mutations are shared in common between resistant malaria strains on
various affected continents of Asia, Africa, and S. America. The K76T
mutation in particular seems to be the most important marker of CQR.
What is interesting is that the K76T mutation is never seen by itself,
but is always associated with a few other point mutations. However,
in some CQ resistance strains the K76T mutation is absent. One such
strain is the "106/1" strain that has the K76I mutation instead. This
strain has six of the other point mutations, but is has the K76I
instead of the K76T mutation at position 76. Even without the K76T
mutation the 106/1 strain does have a fairly high level of CQR.
However, the level of resistance is not as high as those strains that
do have the K76T mutation. Interestingly enough, Fidock et al.,
performed an experiment with the 106/1 strain where stepwise CQ
pressure was added to the population. The result was a fairly rapid
change at position 76 from the K76I to the more resistant K76T
mutation.
The results of such observations suggest that the K76T mutation is not
selectively advantageous by itself. the A220S may fulfill a
particular requirement in the development of CQR since this mutation
has consistently been found to accompany the K76T mutation in CQR
parasites from the different New and Old World foci. "The suggestion
that K76T cannot occur in the absence of other PfCRT point mutations
may also explain the slow genesis of CQ resistance in the field as
well as the difficulties that have been experienced with attempts to
select CQ resistance in the laboratory."
http://www.dbbm.fiocruz.br/class/Lecture/d24/drug_resistance/mc4404.pdf
> Your own example
> of the evolution of lactase makes it clear that you cannot make ad hoc
> calculations to tell you how long it will take for something to
> evolve.
What Hall's experiments with lactase evolution in E. coli tell us is
that the lactase function is much harder to evolve than many types of
bacterial antibiotic resistance. Certainly it is true that I do not
know exactly how many potential lactase enzymes exist in the potential
space of 10e1300 potential amino acid sequences of an equivalent size
or less. However, Hall's experiment made it pretty clear that the
ratio of lactase enzymes as compared with non-lactase sequences is not
high enough to eliminate fairly significant neutral gaps. If the
ratio of lactase enzymes to non-lactase sequences were as high as 1 in
10, then one would expect that the evolution of the lactase function
would be easily demonstrable in just about any type of bacteria. In
fact, just about 1 in 10 DNA sequences and/or genes in all bacteria
would have some sort of lactase function. If this ratio were the real
ratio, Hall would have discovered sequence after sequence with the
lactase function. Every time he deleted another sequence with lactase
function (as he did with the lacZ genes), a new one would quickly
evolve (as happened with the ebg gene - but with no other gene after
the ebg gene was deleted). The fact that no other lactase gene
evolved after the ebg gene was deleted means that the ratio of
sequences with the lactase function is low enough so that not very
many lactase sequences can can be evolved by a fairly large population
even with tens of thousands of generations of time. Based on this
lack of evolution one can reasonable calculate the average neutral gap
involved, at least to the extent that the gap is most likely *larger*
than a particular ratio (Since any function with a higher ratio of
representation in the total number of potential sequences should be
realized after a given amount of time).
> Everything depends on the available starting materials, the
> relative fitness of intermediates, changes in the environment, etc.
This is true. However, consider a hypothetical situation where there
are five potentially beneficial functions that would benefit a
particular organism in its current environment. Let us say that all
of these functions are coded for by 100aa sequences and that all of
them have 10e50 different sequence solutions (about the flexibility
allowed by certain proteins such as cytochrome c). The total space
created by 100aa is 10e129 potential sequences. How long, on average,
will it take our colony of organisms to get all 5 beneficial
functions? By sheer luck, our organism may be just one point mutation
away from one of these 5 beneficial functions, but what are the odds
that it would be so close to *all* of the 5 beneficial functions? Not
so good seeing as how the average beneficial sequence in this scenario
is surrounded by 10e79 non-beneficial sequences. Finding one of them
would be like finding one particular subatomic particle in the whole
universe. By some sort of astronomically fortunate twist of fate, a
random sequence might be just one step away from one of these winning
sequences, but what are the odds that all 5 of the winning sequences
that you are looking for would be right next to each other in this
vast universe of potential? Also, what are the odds that some
particular shift in environment will place you all that much closer to
any other correct sequence in such a vast pile of junk?
Really, explain to me how all this evolution would work when there is
very clear evidence that the "junk" is far more common than the
"gold." In order for your scenarios to work, the ratio of beneficial
sequences as compared to junk sequences would have to be extremely
high. You yourself admit that the ratios do in fact go down as
complexity increases. Well then, please explain to me where this
ratio levels off so that evolution can keep up with these
exponentially expanding neutral gaps.
> Multiplying the number of genetic differences between two sequences in
> related organisms by the estimated population size, mutation rate, and
> generation time, is pretty irrelevant. No one thinks that evolution
> works entirely by neutral mutation and random walks.
Oh really? Evolution works by other mechanisms than random mutation
and natural selection? If there is a neutral gap, clear this gap
destroys the power of natural selection. So, how is this gap crossed?
What other evolutionary mechanisms do you know of that are capable of
crossing such gaps?
> > > So... Both resistances evolved in nature in years to decades;
> > > evolution of mefloquine resistance has been reproduced in the lab;
> > > evolution of chloroquine resistance has not. Does this mean that the
> > > "Designer" let P. falciparum handle mefloquine on its own, but
> > > intervened to help P. falciparum deal with chloroquine?
> >
> > You don't seem to understand the statistics involved here. Obviously,
> > a neutral gap in function of 6 or 7 base pairs can easily be crossed
> > by random walk alone given the much larger population sizes of the
> > malaria parasites (P. falciparum) that exist in the wild as compared
> > to the relatively limited population size that was most likely used in
> > the laboratory experiments. No ID is needed to explain the evolution
> > of chloroquine resistance in either case. The average time required
> > is well within reason.
>
> We know what the "average time" is, not because of your post hoc
> statistics, but because we observed the evolution of chloroquine
> resistance in nature.
Yes, we have observed the average time required and the mutations that
are required first, before any calculations. However, based on the
required mutations we can figure out how long these required mutations
would take to evolve if they were in fact neutral mutations. We can
then see if these calculations are consistent with what we actually
saw in nature. If the calculations are consistent, then we can know
that the evolution that we saw take place in nature was in fact the
result of random walk across a certain number of neutral steps. We
can also know what would be required to evolve this function in the
lab. Much better estimates on the needed population size could be
pre-determined in order to achieve success in a given span of time.
The reason why this example of CQR is helpful to me is because it
shows that wider neutral gaps in function do in fact translate into
longer spans of time due to the fact that random walk was involved in
the process. There is no way around this conclusion that I can see.
Why else would the evolution of the few steps involved in CXR have
taken so long and why else is CXR not easily demonstrated in vitro?
Oh really? What happened then? Specifically? Detail a scenario for
the evolution of cytochrome c where each mutation is selectively
advantageous. You even get to use an already established life form
capable of self-replication. Getting this life form to begin with
(via abiogenesis) is a whole different ball game. In fact, this is
whole idea that abiogenesis could have given rise to the first living
cell is what drove many like Sir Frederick Hoyle to other theories of
living coming from outer space. Then, once you have the first living
cell, using the idea of random mutation and mindless selection to get
other functions of increasing complexity is still an astronomical task
that really is no easier than explaining the origin of the first life
form to begin with.
> > This is why scientists think that abiogenesis took
> > billions of years to produce the first self-replicating cell.
Actually you and I stand corrected on this point. Somehow scientists
think that abiogenesis happened relatively quickly in a few millions,
not billions, of years.
> > But
> > why? Why does abiogenesis take so long? Because of the neutral gaps.
> > When you actually start plugging in the numbers and doing some real
> > estimates based on the idea of neutral gaps, you quickly find that the
> > abiogenesis of much of anything would take far longer than a few
> > billion or even many trillions or zillions or googols of years.
>
> Please, show your model. But it isn't a random walk.
My model is based on random walk. What is your model? If random walk
is not involved, then even millions of years are not required.
Without random walk to slow things down, evolution would happen right
before your very eyes. It would be a snap. Without random walk, the
first cell would self-assemble in a matter of seconds in the right
environment (one with all the required parts). Then, without random
walk, this first cell would quickly go multi-cellular in just a few
generations. A few years down the road and fish would be crawling out
onto the land. A few thousand years later and Survivor would be a hit
television show.
Random walk slows things down. Without random walk, evolution would
be very fast. The fact that evolution seems to be very slow must mean
that random walk is a real limiting force of nature. The problem is
that random walk limits things too much for evolution to produce much
of anything in the blink of an eye that is 4 or 5 billion years.
I'm not ready to say that beta-lactamase specifically had to have been
intelligently designed. I don't know enough about the gaps to say
this. The point is that beta-lactamase seems to be even more complex
than other single protein enzymes like lactase or nylonase. Perhaps
it is to a point were 4 billion years would not be long enough, but I
really can't say this. What seems to be clear though is that the
function of beta-lactamase is just another step up the ladder of
complexity. The ladder gets much taller however. Beta-lactamase, as
complex as it apparently is and as separated by neutral gaps as it
apparently is from all known bacterial genetic real estate, is still a
very simple function when compared to other functions that require
multiple parts all working together at the same time (i.e., bacterial
motility systems). I am much more confident in suggesting that
bacterial motility systems are so complex that the neutral gaps
involved would in fact require more time than the theory of evolution
has time for. ID is certainly a very reasonable explanation for such
multi-protein functions as bacterial motility.
> > In any case, I do thank you for pointing out that the gain of
> > information via plasmid from some other bacterium, is not the same
> > thing as the evolution of this information to begin with. Penicillin
> > resistance that is the result of the penicillinase enzyme is not the
> > evolution of anything much since the enzyme code was already there.
> > It did not evolve de novo in these resistant colonies.
> >
> > > or
> > >
> > > (2) The action of the drug requires binding to some bacterial protein
> > > and a simple mutation in the gene encoding the bacterial protein
> > > destroys the binding site. This happens with other forms of penecillin
> > > resistance, and with resistance to several antibiotic that bind to
> > > bacterial ribosomes, like tetracycline.
> >
> > Exactly. Practically all examples of antibiotic resistance involve
> > the destruction of a pre-established interaction of a target sequence
> > with the antibiotic.
>
> That is incorrect. Many of them involve degradation of the antibiotic
> or enhanced transport of the antibiotic out of the target cell.
I'm talking about examples of real time evolution of antibiotic
resistance here. There are no real time demonstrations of the
evolution of the ability to degrade an antibiotic (i.e., via
penicillinase etc). Also, enhanced transport of an antibiotic is the
result of single point mutations that up-regulate an existing
function. Many different point mutations to the transporting
apparatus are capable of enhancing antibiotic transport. The ratio of
beneficial to non-beneficial is high. The evolution is rapid since the
gaps are very small and the random walk is practically non-existent.
> >The destruction of this interaction is
> > relatively easy to do with one or two of several different possible
> > mutations that would do the same thing. Antibiotic resistance that
> > arises via mutation is based on the simple concept that it is far
> > easier to break or interfere with a pre-established function than it
> > is to make a new function from scratch. It is much like the
> > children's rhyme about Humpty Dumpty. It is far easier to break
> > something than it is to create something new.
> >
> > > So, yes, that's a lot easier than getting to a complex multi-enzyme
> > > complex from scratch. No doubts.
> >
> > Thank-you for making this so clear.
>
> It was already clear. Why you think it helps your argument is beyond
> me. No one thinks that the ribosome arouse from a random walk through
> the space of all possible chemical compounds, or even a random walk
> though the space of all possible combinations of protein and RNA
> sequences.
Of course no one thinks that random walk had to be involved, or at
least no one actually admits this. I mean, if they did admit this,
then clearly evolution would not be possible. No evolutionist can
admit that random walk is required. Evolutionists must rest their
faith on the possibility, however remote, that random walk was
overcome by some as yet undetected path around all the myriad of junk
sequences. But, faith is great in the scientific community. Even
though no one seems to know exactly how functions of higher and higher
complexity evolved, evolutionists have great faith that someday the
functional evolutionary paths will be revealed. Certainly many
"just-so stories" have been proposed but they have never made it off
the paper they were written on and into real life tests that are
required by the scientific method. They are just like so many fantasy
stories that really have no backing by testable predictions.
> > > > I mean, if it is so easy, as you
> > > > seem to be saying, then evolution should proceed rapidly, should it
> > > > not?
> > >
> > > Depends on what you mean by rapidly? It will not proceed rapidly if by
> > > that you mean "right before my eyes."
> >
> > If there were no neutral gaps, then yes. Rapidly would mean, "right
> > before my eyes." The mutation rates are high enough to achieve such
> > rapid evolution if there were no neutral gaps or random walks to take
> > up the time in the travel toward new functions.
> >
> >
> > > > If there were no neutral gaps to slow the process of evolution
> > > > down, then given the proper environment, the evolution of beneficial
> > > > functions, such as the lactase function in a lactose rich environment,
> > > > should proceed very quickly. This lactose environment ain't outer
> > > > space and it ain't granite you know. One little enzyme is all that is
> > > > needed to use this new environment in a more advantageous way. And
> > > > yet, many different types of bacteria seem unable to evolve the
> > > > lactase enzyme despite hundreds of thousands and even millions of
> > > > generations of time. What then, exactly, is slowing this process
> > > > down? Please, you seem so knowledgeable . . . what is the answer?
> > > >
> > > > Sean
> >
> > Thanks again for your most helpful and enlightening post.
>
> Alas, it does not seem to have enlightened you.
I disagree. I have found what you have had to say very enlightening.
Sean
John Harshman
Sean Pitman wrote:
> bro...@noguchi.mimcom.net (Bill Rogers) wrote in message news:<8984713a.03061...@posting.google.com>...
[snip]
> If cow-like creatures could turn into whales and reptiles into birds,
And they did too, though you are never interested in confronting the
evidence for that.
> then why do you think it would be so hard to get bats to evolve
> feathers or whales to evolve gills if they would in fact benefit from
> such structures? Really, the theory of evolution has proposed that
> such dramatic changes have occurred that practically anything is
> possible given enough time. The starting point really has little to
> do with it. All that is needed is the right environment and enough
> time.
I think other people have covered this "problem". I just preserved the
rest of your paragraph to avoid an incomplete quotation.
[snip]
> My model is based on random walk. What is your model? If random walk
> is not involved, then even millions of years are not required.
> Without random walk to slow things down, evolution would happen right
> before your very eyes. It would be a snap. Without random walk, the
> first cell would self-assemble in a matter of seconds in the right
> environment (one with all the required parts). Then, without random
> walk, this first cell would quickly go multi-cellular in just a few
> generations. A few years down the road and fish would be crawling out
> onto the land. A few thousand years later and Survivor would be a hit
> television show.
>
> Random walk slows things down. Without random walk, evolution would
> be very fast. The fact that evolution seems to be very slow must mean
> that random walk is a real limiting force of nature. The problem is
> that random walk limits things too much for evolution to produce much
> of anything in the blink of an eye that is 4 or 5 billion years.
There's a simple solution for that problem, even in your own terms.
Since you have no way to determine the actual sizes of neutral gaps
between functions, why not just suppose they are exactly the right size
to slow selection down to the observed (from the fossil record and
inferred phylogenies) rate of evolution? That is, if unimpeded selection
is too fast and big gaps make evolution too slow, what keeps there from
being a combination of selection and gap size that makes evolution just
right? We can call this the Baby Bear (BB) theory.
[snip the rest}
By the way, were you ever intending to respond to any of my other posts,
or are you just uninterested in the objective evidence favoring common
descent?
Bigdakine
>From: "Lane Lewis" lanej...@hotmail.com
>Date: 6/12/03 6:55 AM Hawaiian Standard Time
>Message-id: <Eg2Ga.67616$cm4.1...@twister.tampabay.rr.com>
Granite may or may not be eaten by bacteria, but certain plants and lichens use
it for breakfast, lunch and dinner.
I suggest "Dr." Pittman do some field work in and examine what he finds growing
on granites. Oh. I forgot, Dr. Pittman, doesn't do field work. Pity.
The truth will set you free Dr. Pittman.
http://www.frankdan.com/oct00/pages/oct17.htm
http://dennis.flaherty.com/Port/20.htm
Dr. Pittman, do you ever get tired of looking foolish?
Ever?
Stuart
Dr. Stuart A. Weinstein
Ewa Beach Institute of Tectonics
"To err is human, but to really foul things up
requires a creationist"
Sean Pitman
> > > You are contrasting the ease with which a single mutation can lead to
> > > gain of function (starting on the right background) with the problem
> > > of evolving a new enzyme from scratch (or from an enzyme with
> > > unrelated function). Yes. It is much faster if there is a gene
> > > already there which needs just a single mutation to develop a new,
> > > useful activity.
> >
> > Finally, someone who actually seems to understand what I am talking
> > about. There are clearly different levels of functional complexity.
>
> Really? How is it clear that mefloquine resistance is less complex
> than chloroquine resistance?
Why do you think? More neutral mutations are needed to produce
chloroquine resistance.
> Could you have predicted this before the
> fact based on a description of the function involved, or before an
> identification of the probable evolutionary pathway?
I could not have predicted which one of the two (mefloquine vs.
chloroquine) would be more complex ahead of time. However, I could
have predicted, based on the description of the function involved,
that only a very few mutations would be needed to establish resistance
to either one of them. And, this is in fact true. Mefloquine
resistance requires just one point mutation. Chloroquine resistance
(CQR) is a bit more vague, but seems to require at least a few
mutations (as many as 6), perhaps only two mutations, before at least
some beneficial level of resistance can be realized. It turns out that
several of the mutations seen in CQR are selectively advantageous once
the initial two or three are realized.
The resistance to both mefloquine and chloroquine is achieved via the
blocking or interference of the pre-established interaction of these
drugs with specific target proteins. Again, my prediction that such
interferences are relatively easy to achieve holds up in these cases
as well. No new protein or enzyme is evolved in these cases. The
only thing that happens is a disruption of a specific interaction that
was pre-established (It is just a different way of breaking Humpty
Dumpty, but still relatively easy to do.). Such disruptions are
relatively easy to achieve and are almost always based on one or two
point mutations, or at most a handful of such mutations as is the case
with chloroquine resistance. Also, chloroquine resistance has been
very difficult to reproduce in the lab and has taken a bit longer to
evolve in the wild than mefloquine resistance. However, the
difference in complexity between the two drugs is really is rather
negligible considering that the mutations responsible for this
difference in complexity can be counted on one hand. This evidence
fits very well with my predictions for the required time needed to
evolve this very low level of complexity.
> Can you say
> anything meaningful about their respective complexities without
> peeking?
Yes. I can say that both of them have a very low level of complexity
since their actions are both very specific and would most likely be
easily disrupted by one or two point mutations. . . perhaps a few more
point mutations might be needed, but I wouldn't have predicted that
more than a handful of mutations would be needed to produce a
selectable advantageous disruption of their specified functions. This
prediction continues to hold true, even for chloroquine resistance.
> > The function of bacterial antibiotic resistance is extremely simple,
> > even in comparison to the most simple enzymatic functions.
>
> Except of course for the cases in which antibiotic resistance *is* an
> enzyme function, as in the case of, say vancomycin or cefotaxime
> resistance.
When most think of penicillin-type antibiotic resistance, the enzyme
penicillinase comes to mind. However, there are several other ways
that bacteria become resistant to penicillin. A notable example is
occurs S. pneumoniae. b-lactamases have never been identified in S.
pneumoniae, and yet they are capable of penicillin antibiotic
resistance due to modification of its penicillin binding proteins
(PBPs).
As far as vancomycin resistance is concerned it is not always the
result of a penicillinase-type enzyme. The complex between vancomycin
and D-Ala-D-Ala involves a set of five crucial hydrogen bonds between
the elongated backbone of vancomycin and the stem peptide. As would be
expected then, vancomycin resistance involves a single point mutation
in which the D-Ala-D-Ala portion is replaced with D-ala-D-Lactate.
This inclusion of an ester instead of an amide bond in the stem
peptide structure profoundly alters its interaction with the
vancomycin "backbone" structure in that there is a loss of one of the
five hydrogen bonds. The resulting binding affinity is three orders of
magnitude lower than it was with D-Ala-D-Ala and bacterocidal activity
is lost.
In several bacterial species, such as in enterococcal species,
vancomycin resistance is achieved through the function of a five-gene
operon that is located on a transposon (mobile genetic element). The
mobility of this element suggests that this resistance mechanism could
be acquired by a large number of pathogenic bacteria. The five genes
include three structural genes named, vanH, vanA, and van X. VanH
converts pyruvate to D-lactate. VanA takes the D-lactate produced by
vanH and synthesizes D-Ala-D-Lactate with it. VanX selectively
hydrolyzes all D-Ala-D-Ala peptides that are naturally produced by the
host. Without the availability of D-Ala-D-Ala, the concentration of
D-Ala-D-Lactate builds up in the cell and thus the resulting
peptidoglycan is made entirely of D-Ala-D-Lactate. Of course, this
gives the host resistance to vancomycin.
Further mutagenesis efforts identified that single point mutation of
"Gln 552" into a glutamate residue caused a severe reduction in
acylation efficiency for both cefotaxime and penicillin G, probably
due to electrostatic effects between the incoming antibiotic and the
residue, which borders the active site.
So you see, the ability to produce the comparably complex
penicillinase enzyme is by no means the only way for bacteria to gain
resistance to beta-lactam antibiotics such as vancomycin and
cefotaxime. And in fact, if these bacteria did not have ancestral
access to a pre-formed code for such enzymes as penicillinase, they
never do evolve it as a means of achieving antibiotic resistance.
Instead, they rely on some of the other methods of interfering
mutations described briefly here. In comparison, it is far more
difficult or complex to evolve entire enzymes from scratch, like the
penicillinase enzyme, as compared to one or two interfering point
mutations that do give basically the same result without the cost of
having to maintain a gene for an enzyme in the genetic real estate.
Such maintenance costs extra energy, but it doesn't cost any extra
energy to maintain one or two interfering mutations in a target
sequence.
> > The reason
> > for this is that there is a dramatically higher ratio of functional
> > mutations as compared to neutral mutations in the development of
> > antibiotic resistance as compared to the evolution of a certain
> > enzymatic activities.
>
> So, how do you determine complexity without *first* knowing what
> evolutionary changes are involved?
We know enough about specified interactions to know that it is
relatively easy to interfere with such interacting functions. The
interactions of antibiotics and target sequences or transport
sequences are in fact quite specific. No need to know ahead of time
the specific mutations that would be needed to interfere with such
specific interactions. The odds are clearly in favor of betting that
just one or two or rarely a handful of mutations is all that will be
needed to interfere with such an interaction in a selectable manner.
The more specific and/or delicate the interaction, the easier it would
be to mess up this interaction with a random mutation. You can bet on
it. It is a law of nature (entropy).
Obviously then, those functions that are not based on the disruption
of other functions, but upon the building of a specified order of
parts/amino acids in proteins, are obviously more complex since not
just any order will do. A very specific order is required. Only a
relatively few sequences out of all the potential sequences, will be
able to be of the "right" order to achieve a specified function like
an enzymatic-type function.
Take for example the human genome of around 6 or 7 billion base pairs
(diploid). There is still some argument, but lets say that there are
around 40,000 genes. How many of these genes or genetic sequences are
capable of producing a protein with the lactase function? Not too
many. You see, if the lactase function were really common, just about
any protein, regardless of its usual job, could produce the lactase
function as well. The fact is that only a tiny fraction of all the
known proteins out there are capable of hydrolyzing lactose. This
means that the lactose function is relatively rare. This relatively
rarity means that there is a sizable gap that exists between sequences
with the lactase function. Odds are that a sequence chosen at random
will be a fair distance from the closest sequence with the lactase
function.
This seems to be a well-supported observation, even without Hall's
experiments to back it up. I mean, before Hall did his experiments I
would have bet a lot of money on the prediction that his E. coli would
not be able to evolve more than a handful of different lactase enzymes
even over the course of tens of thousands of generations per try. It
turns out that this is exactly what happened. The E. coli bacteria
were only capable of evolving one lactase enzyme. And, without this
ebg gene, they weren't capable of evolving any more of them.
I would bet the same way for many other enzymes, like the
penicillinase enzyme. If one were to completely delete the
penicillinase gene in a colony of bacteria, I would bet that this
colony would not have too much genetic real estate close enough to any
other penicillinase sequence that could be reached in hundreds of
thousands of generations. Perhaps a rare colony would come up with at
least one penicillinase enzyme, but if this were taken away, I am
betting that the odds of it happening a second time would be much
worse than the odds of lightening hitting the same place twice or the
same person winning the California lottery twice in a lifetime. Why?
Because enzymes of such complexity seem rather widely separated in the
potential space of the junk-pile. Hall's E. coli experiments only
highlighted this obvious conclusion.
snip
All the functions that we see in living things are claimed to have
evolved in less than 4 or 5 billion years. This is an extremely short
time for mindless processes to have produced all that we see around us
if in fact the vast "majority of mutations are functionally neutral."
For you to suggest that there are in fact limits on what evolution can
do depending on what evolution has to work with is simply misguided.
You need to check back with what your theory is claiming the power to
do.
Your theory claims that starting with a few organic molecules the
mindless processes of nature were able to assemble these randomly
interacting molecules into the first living cell of no more complexity
than the most simple of bacterial life forms. I would say that this
original life form was quite limited in genetic real estate and
function. And yet, your theory claims that in just a few billion
years this life form, with its apparently limited and humble
resources, was capable of giving rise to all that we see around us.
How then are you trying to support this claim of yours that
evolutionists do not "suggest" that anything can evolve from anything?
I mean, it seems like, given the proper shifts in environment, a cow
could evolve into a bat or a chicken could evolve into an elephant.
Certainly this is what you believe. If you truly think that some
starting points do in fact have significant limits, how on earth do
you explain evolution? And, what is it exactly that creates these
supposed limits for the process of evolution? I mean, starting with
the very first cell, what were its limits? Was it impossible for that
cell to evolve a flagellar apparatus? Certainly not since it is here.
Was it impossible for that cell to evolve a camera type eye? Nope.
How about a bat or a pigeon or a pine tree? Nope. So then, where are
the limits?
You just don't like the fact that these limits do in fact seem to
exist and so you try to claim that your theory has already taken all
this into account. . . when it really hasn't. These limits really
are significant enough to destroy your theory. That is the problem
and that is why you are trying to blow smoke over this whole mess.
> But your theory isn't simply that "neutral gaps" exist. That would be
> fairly uninteresting, and of no real importance to the theory of
> common descent at all. Your theory is that they are so pervasive as
> to preclude evolution of life as we see it today in the available
> history of the world. The fact that chloroquine resistance may take a
> large population several years to evolve hardly supports such a
> generalization.
There is plenty of evidence to support the idea that neutral gaps are
extremely pervasive. The experiments of Hall and the evidence
supplied by chloroquine resistance are only parts of the puzzle. They
support this position very well. It is actually you and your position
who have very little evidence to suggest that these gaps are not very
pervasive or that they do not really interfere too much with the
evolution of new and increasingly complex functions. What evidence do
you have to counter my position? What examples of evolution can you
point out to prove me wrong?
As far as I can tell, the best you have is antibiotic resistance,
chloroquine resistance and other types of drug resistance, and the
occasional new single protein enzyme. Is that it? What kind of
evidence is that? All it is based on is the idea that it is easier to
break something that it is to create something from scratch and
occasionally, one might actually make something that does not really
on breaking something else, as long as this new function is extremely
simple and relatively common. You call that evidence?
> > > So... Both resistances evolved in nature in years to decades;
> > > evolution of mefloquine resistance has been reproduced in the lab;
> > > evolution of chloroquine resistance has not. Does this mean that the
> > > "Designer" let P. falciparum handle mefloquine on its own, but
> > > intervened to help P. falciparum deal with chloroquine?
> >
> > You don't seem to understand the statistics involved here.
>
> Neither do you, apparently. You have argued that the density of
> sequences for antibiotic resistance may be as high as 1 in 3; you have
> suggested elsewhere that the density for functional enzyme sequences
> is about 1 per 1e12, or is it 1e24? In a different context you argued
> that the density of functional sequences for a 100aa long protein
> might be as low as 1 per 1e106 (and the logic you used in that post
> could be extended to arbitrarily long sequences to get arbitrarily low
> densities such as ~1e-1277 for a 1000aa sequence). Now here you argue
> that the density of (genetic) sequences conferring chloroquine
> resistance may be about 1e-4.
You don't seem to understand the difference between the function of an
enzyme, like lactase, and the function of chloroquine resistance.
Chloroquine resistance is based on the interference of a previously
established interaction. As such, it is relatively easy to create
this function since the ratio of potential mutations that could
deliver this particular function is quite high. For certain types of
antibiotic resistance it might be extremely high indeed since some
interactions are extremely specific and can easily be disrupted. The
function of enzymes is not like this. Enzymatic function is *not*
based on the interference of a pre-established function. Do you
understand the difference and why the "densities" for specific
enzymatic functions are much much less than the "densities" for
specific antibiotic resistance functions?
> So obviously you have no idea what the sequence density for any given
> function is ahead of time,
Actually I do have a very good idea about sequence densities ahead of
time. You tell me the type of function and I can predict for you,
with a fair degree of accuracy, how easy that function will be to
evolve. Functions that are based on the interference of
pre-established interactions will take a lot longer to evolve than
those functions that are not based on the interference of other
functions. Some enzymes are more simple than others. More or less
densities might be involved. However, as a rule, the functions of
enzymes are far less dense than the functions of various types of
antibiotic resistance described above (the ones that do not involve
enzymes obviously).
> Although you are good at saying: "See, I
> knew that!" after the fact.
Not after the fact at all. You come up with a new antibiotic, I will
predict right now that resistance to that antibiotic will happen real
quick like. You come up with a new enzymatic function, and I am
betting right now that this new enzymatic function will not be
realized by very many life forms if any. You come up with a new
function that requires a dozen or so proteins all working together at
the same time and I am betting right now that no life form will evolve
this function or anything equivalent in your lifetime or by the time
your offspring have reached a billion generations.
> Nor do you know what the available
> evolutionary pathways were, nor what sort of fitness landscapes they
> traversed.
Certainly not, and neither do you. I don't believe that these
pathways exist, so why would I even hope to know what they were? I
think the evidence clearly supports this position. You have no
evidence about how your supposed fitness landscapes did change or
could have changed in a way that could have even theoretically produce
the variety that we see in the world today. You have faith that such
pathways and landscape changes did exist and did in fact give rise to
what we find today, but you really have no clue as to how it worked or
could have worked. You have a bunch of just so stories, but no real
evidence to back your stories up. All you have is a bunch of hopeful
people on your side with a very great faith and an overactive
imagination. You expect me to give you far more evidence than you are
willing to produce yourself. You have nothing to support these
imagined evolutionary pathways and tree of yours. Truly, the
important missing links are not those missing from the fossil record,
they are the missing genetic links from the imagined phylogenetic
trees of life.
> Nonetheless, you are sure that there are enough neutral
> gaps around to prevent evolution of many of the functions we observe
> in life today; you base your confidence on the "statistics involved",
> which enable you to predict with confidence that the density for
> functional sequences in a sequence space is somewhere between 1 in 3
> and 1 in 1e106 (or perhaps even as low as 1e1277).
Depending on the type of function in question, this range is quite
easily supported. But this is not the worst of it. The range gets
far worse when you start including those functions that are based on
multiple proteins all working together at the same time. For such
levels of complexity, the "density" might be as low as 10e1000e1000.
And then, it gets worse. . .
> > Obviously,
> > a neutral gap in function of 6 or 7 base pairs can easily be crossed
> > by random walk alone given the much larger population sizes of the
> > malaria parasites (P. falciparum) that exist in the wild as compared
> > to the relatively limited population size that was most likely used in
> > the laboratory experiments. No ID is needed to explain the evolution
> > of chloroquine resistance in either case. The average time required
> > is well within reason.
>
> OK, so at least you are smart enough not to deny the evolvability of
> something that has been observed to evolve.
If the numbers make sense, and they do, then such an observation is
not a mystery at all.
> > > > These very same bacteria would quickly evolve resistance to penicillin
> > > > if it were added to their environment. No more than a handful of
> > > > generations would be required. Why then is antibiotic resistance so
> > > > much easier for them to evolve than the lactase function? What is it
> > > > about the evolution of relatively simple enzymes that is so much more
> > > > difficult than the evolution of antibiotic resistance?
> > >
> > > Enzymes are really complicated. You are right. It almost certainly
> > > takes more time than you have to watch to evolve a new enzyme from
> > > scratch (or even from an unrelated enzyme).
> >
> > I'm glad that you realize this because many people think that the
> > evolution of antibiotic resistance is something very significant
> > and/or complex. What many do not realize or admit is that even the
> > relatively simple function of a single protein based enzyme, is far
> > more complex than the function of antibiotic resistance.
>
> Except, again, when the antibiotic resistance in question *is* an
> enzyme activity.
The type of antibiotic resistance in question here was *not* an
enzymatic activity. Enzymes that do produce antibiotic resistance do
not often evolve. In fact, I really can't think of even one example.
Certainly the penicillinase enzyme has never been shown to evolve in
nature or in the lab. Obviously then, this finding supports my
position.
> > Obviously more time is required to evolve the enzymatic functions than
> > the functions of antibiotic resistance. That question is, "Why?" Why
> > is more time required to evolve functions of increasing complexity? I
> > am proposing that neutral gaps are the reason for this observed
> > phenomenon. What is your explanation?
>
> My explanation is that you claim with hindsight a level of complexity
> based on what you already know about the evolutionary pathway, so that
> your "theory" is basically a circular argument that lacks the
> predictive value you need for it to be pose much of a challenge to
> evolution.
All hypotheses are based on "hindsight". All observations happened in
the past. Based on these "hindsight" observations one makes
hypothesis or predictions about the future. I predict that enzymes
have been and will always be harder to evolve than antibiotic
resistance functions. This is not a circular argument at all. It is
hypothesis that is based on past experience and past evidence that
makes a prediction based on this evidence that can be tested in a way
that will give it predictive power.
> > > We all agree that
> > > evolution takes a long time. Building enzymes from scratch is actually
> > > more a part of abiogenesis than evolution, but most scientists would
> > > agree, I think, that abiogenesis took a billion years or so, not a few
> > > months, even with artificially boosted mutation rates.
> >
> > Oh, so the evolution of even one little protein sequence is based on
> > "abiogenesis" not on evolution? Really?! This is *most* interesting.
> > This is exactly my whole point. Abiogenesis is based on neutral
> > drift/random walk. Natural selection really is limited when it comes
> > to ideas on abiogenesis since by far most of the changes in
> > abiogenesis are functionally neutral as far as a mindless nature is
> > concerned. This is why scientists think that abiogenesis took
> > billions of years to produce the first self-replicating cell. But
> > why? Why does abiogenesis take so long? Because of the neutral gaps.
> > When you actually start plugging in the numbers and doing some real
> > estimates based on the idea of neutral gaps, you quickly find that the
> > abiogenesis of much of anything would take far longer than a few
> > billion or even many trillions or zillions or googols of years.
>
> Actually, the oldest accepted unicellular fossils are about 3.6 Gya,
> indicating that life arose within no more than a couple hundred
> million years after conditions on earth made it possible.
That is the theory anyway . . . which is quite amazing indeed. A few
million years is all that is needed to get random molecules to self
assemble themselves into a living organism. Amazing speed isn't it?
In any case, I only used the "billion years" figure because Bill used
it. It wasn't an important point to challenge him on.
> And I would
> love to see you "start plugging in the numbers and doing some real
> estimates". All you need is a detailed model of what the likely
> precursor molecules were, what their population size and composition
> was like, what their mutation and replication rate was like (both
> probably much faster initially than that we typically see in life
> forms today), what the environment was, what the fitness landscape
> looked like over the sequence space and what evolutionary constraints
> there were (since the earliest replicators would have had few
> functions, there was almost no place to go but up, as someone quoted
> Maynard Smith as saying elsewhere).
Almost no place to go but up? Amazing! I thought you said that
depending on your starting point there could be a lot of restrictions
to evolution? In any case, I'll give you every benefit of the doubt.
Start with a relatively advanced E. coli bacterium as your first
creature. E. coli have a relatively rapid generation time, as fast as
20 minutes or so. Give these E. coli all the food and building blocks
they need to grow and massively reproduce to cover the entire globe
and every available square millimeter of water on earth. They still
would never get across a gap of just 30aa in 4 billion years.
Now, you explain this same scenario and detail to me how these E. coli
could evolve new functions of increasing complexity. Make your
description a genetic description and not a morphologic description as
is so often done. You must explain using genetics or even other coded
systems like the letters of the alphabet and comparisons to the
English language system as to how this evolution could have taken
place.
> I'm sure you'll be able to
> estimate the length of time it would take to within about, oh, 106
> orders of magnitude (given that error, what you estimate to take
> googles of years could actually have taken place within a few minutes
> or even seconds)
Oh really? A few seconds? How so? Explain your marvelous hypothesis
to me. I'll even give you access to a ball of bacteria with a
diameter the size of the galaxy. . . . and you still couldn't do much
in just 4 billion years.
> > > It is possible to select for enzymatic activity in antibody molecules
> > > (not originally enzymes at all) in the lab by cycles of mutation and
> > > selection. That works pretty quickly. You can search in Medline under
> > > Richard Lerner and/or Angray Kang to read about that system.
> >
> > Yes, this works pretty quickly because it is not based on the needs,
> > mutation rates, or genetic capabilities of any given life form, but on
> > the ability of a human scientist to recognize some sort of specific
> > enzymatic activity from a random pool of proteins.
>
> Exactly, and a pool of simple replicators that hadn't already evolved
> complex cellular functions might be similarly free of constraints.
So, the less there is, the easier it is to evolve new stuff? Is that
it? You have got to be joking!
There are always constraints that are dependent upon the current
genetic functions and environment of the life form in question. A
pool of simple "replicators" would still be constrained. Some
sequences would make them replicate less well while others might make
them replicate better, but the vast majority would be neutral as far
as a help to their replication abilities. A lactase enzyme might not
be any help at all to a very simple "replicator" that did not yet have
a glycolytic pathway set up. What good would a cytochrome c protein
be without all the other proteins in the electron chain? All new
sequences must be able to fit in with and compliment what is already
there. This creates a significant constraint to what can and what
cannot be used in a beneficial way.
snip
> > > Antiobiotic resistance is often easy because
> > >
> > > (1) The gene already exists on plasmids in wild populations of the
> > > bacterium in question and the plasmid is exchanged in the bacterial
> > > populations (that is the case for some forms of penicillin
> > > resistance). Remember, we've only been using penicillin for 60 or 70
> > > years, but fungi have been using it for millions, so the bacteria have
> > > had plenty of time to develop a suite of resistance genes.
> >
> > That is a nice "just-so" story that many use to explain the origin of
> > rather complex enzymes like the penicillinase enzyme.
>
> We already know that enzymes of comparable sequence lengths can evolve
> in real time. Ian Musgrave pointed out to you elsewhere that many
> different novel cefotaxime-resistant strains using extended spectrum
> b-lactamases have evolved in just the last 20 years or so. I would
> think that if beta-lactamase is a complex enzyme, then ESBLs are even
> more complex, wouldn't you?
When I started reading this paragraph I thought you claimed that you
were going to point me to an example of an "enzyme of comparable
sequence length" that could or did "evolve in real time." You did
nothing of the sort. Your example is not a sequence of "comparable
length" at all. Your example is an example of an alteration of an
existing enzyme, not its original evolution. So, how do we know that
such enzymes of comparable length and complexity "can evolve in real
time"?
These bacteria did not evolve these enzymes from scratch. They were
already making these beta-lactamases to begin with. When the new
synthetic antibiotics came along, all that they did to combat the new
antibiotics was to alter their pre-existing enzymes with one or two
point mutations so that the interaction with the antibiotics would be
enhanced. No beta-lactamases were evolved without a prior existence
of the code for such enzymes. The ESBL's are hardly more complex than
the original beta-lactamase enzyme. In fact, I would say that they
are really no more complex. It would be just as hard to evolve the
ESBL's as it would be to evolve the original beta-lactamase enzyme to
begin with, starting from scratch.
Come on man . . . Don't you have anything better than this?
> I'm guessing that, no, *you* probably wouldn't think that, because you
> would already have "peeked" at the evolutionary pathways from known
> precursors and asserted that the evolution of ESBLs from an ancestor
> was "trivial".
It was trivial and that is only to be expected. A series of
sequentially selectable variants is quite trivial. No neutral gaps
need be involved or would be expected to be involved in such a
scenario. Try getting an ESBL from scratch however, and we'll just
see how easy it is. Delete the original beta-lactamase from the
genome and then see if you can ever demonstrate the de novo evolution
of an ESBL or even a regular beta-lactamase for that matter. You
can't. That is certainly curious.
> Of course, if you didn't already know the pathway, you
> would have no way of making such an argument.
Certainly I would. There are many "generations" of beta-lactams now.
I expect that there would be more "generations" coming along in the
future. I predict that with just a few mutations the current
beta-lactams will be able to adjust to these new antibiotics in short
order. It isn't so complicated you know.
> In spite of this, it
> doesn't seem to bother you in the least to make pronouncements about
> the complexity of a function in the *absence* of such extrinsic
> knowledge about the evolutionary history of penicillinase: you are
> somehow convinced that it must be unevolvably complex by default until
> it is proven otherwise.
Can you demonstrate it or explain it? The best you can come up with
are variations on a theme, but you can't come up with the theme
itself? Please, what do you have that makes you so sure you are
right?
> > It may be true,
> > but until it can be demonstrated or until some real statistical
> > calculations can be made to estimate the number of neutral gaps that
> > would need to be crossed, it is just a story without any real backing
> > in actual evidence.
>
> As is *any* talk about neutral gaps, including yours. Funny, when I
> first pointed out that one needed such detailed knowledge of the
> evolutionary pathways involved to meaningfully estimate neutral gaps,
> you seemed to consider this an unreasonable burden of proof on you.
> But here you lay down exactly the same requirement (for exactly the
> same reason) without blinking when it suits your argument.
The fact is that the current evidence for neutral gaps is
overwhelming. In order to overcome this evidence, you must present
something that at least explains how they really aren't all that
significant. What have you done to do this? You have to have at
least *some* evidence you know. You are the one claiming that
bacteria turned into trees, bears, bugs, and humans. That is an
impressive, counterintuitive statement. What genetic evidence do you
have for this? Where are your demonstrations? Where are your
calculations of probability? Where are your predictions for the paths
and time involved for the crossing of these imagined paths of yours?
You want me to prove you wrong, but you don't really want to have to
come up with any evidence to support yourself. You make up stories
that really cannot be falsified and then you say, "prove me wrong."
You say, "You can't prove beyond all question that a path could have
existed somewhere." Well no I can't, but neither can I prove beyond
all question that there is no elevator to the moon. It is the weight
of evidence, not the providing of absolute evidence, that is important
here. You have yet to provide convincing evidence that an
evolutionary path even possibly existed. The evidence is that such a
path most likely did not exist. There are no absolutes. What you
have to do is to show that such a path *probably* did exist. Good
luck.
snip
> > Practically all examples of antibiotic resistance involve
> > the destruction of a pre-established interaction of a target sequence
> > with the antibiotic. The destruction of this interaction is
> > relatively easy to do with one or two of several different possible
> > mutations that would do the same thing. Antibiotic resistance that
> > arises via mutation is based on the simple concept that it is far
> > easier to break or interfere with a pre-established function than it
> > is to make a new function from scratch. It is much like the
> > children's rhyme about Humpty Dumpty. It is far easier to break
> > something than it is to create something new.
>
> Right, and the history of life is certainly replete with such losses
> of function. The loss of fins in early amphibians was certainly a
> loss of function; critters like ichthyostega were no longer as
> efficient swimmers as their fish counterparts, because their fins had
> been replaced by deformed protrusions that were fit for little more
> than scudding along the bottom of shallow waters. Mammals have
> "broken" reptilian jaw hinges which have lost their function; now they
> do nothing more than rattle around in our middle ear, creating these
> annoying vibrations inside our heads. Humans and other apes have
> "broken" claws that are useless for fighting. All we have are these
> stupid flat cuticled fingernails. If we want to scare off a lion, we
> have to resort to something like a rock or a pointed stick.
LOL - too funny. This is classic. Often when I ask for examples of
evolution in action, all I get are a bunch of examples detailing the
loss of previous functions. Certainly this is a type of evolution,
but you must admit that breaking Humpty Dumpty is a far cry from
explaining how Humpty Dumpty got put together to begin with! ; )
snip
> > Thanks again for your most helpful and enlightening post.
>
> ...which, for some odd reason, you seem to think supports your views.
I am equally mystified by your conclusions. . .
> Von Smith
> Fortuna nimis dat multis, satis nulli.
Lenny Flank
<snip>
> LOL - too funny. This is classic. Often when I ask for examples of
> evolution in action, all I get are a bunch of examples detailing the
> loss of previous functions. Certainly this is a type of evolution,
> but you must admit that breaking Humpty Dumpty is a far cry from
> explaining how Humpty Dumpty got put together to begin with! ; )
>
How dreadful.
As a medical dorctor, do you advise your patients to reject their
materialistic naturalistic atheistic biases when they get sick? Do
you advise them to seek non-naturalistic cures for the
non-naturalistic causes of their diseases -- such as evil spirits or
curses or The Evil Eye from local witches? Or do you use
materialistic naturalistic antibiotics to treat their materialistic
naturalistic diseases by killing their materialistic naturalistic
germs.
Are you just a materialistic naturalisic atheist at heart, Dr?
Robin Levett
Without wishing to sound too stupid, Sean, wouldn't it help
if you demonstrated that there was a problem before claiming
that the problem was insoluble?
Just one example where for an existing structure to have
evolved, it had to cross a neutral gap, please.
--
I don't trust camels - or anyone else that can go for a week
without a drink.
(Use rle...@ibmrlevett.uklinux.net - deleting big blue -
for email)
Frank J
Let's see, he's apparently "uninterested" that the founder of IC,
Michael Behe, has no problem with common descent, and of course an old
earth (that Dr, Sean also tries to refute).
This is as good a place as any to cue the American Physics Society
quip: "So much for the pretense that the debate is over the science."
Howard Hershey
seanpi...@naturalselection.0catch.com wrote on 6/13/03 7:23 PM:
> bro...@noguchi.mimcom.net (Bill Rogers) wrote in message
> news:<8984713a.03061...@posting.google.com>...
>
> snip
>>> There are clearly different levels of functional complexity.
>>> The function of bacterial antibiotic resistance is extremely simple,
>>> even in comparison to the most simple enzymatic functions. The reason
>>> for this is that there is a dramatically higher ratio of functional
>>> mutations as compared to neutral mutations in the development of
>>> antibiotic resistance as compared to the evolution of a certain
>>> enzymatic activities.
>>
>> Why do you say that. Some antibiotic resistance genes encode enzymes.
>
> Yes, penicillinase is an enzyme that destroys the antibiotic function
> of penicillin. However, there are a lot of other ways to gain
> penicillin resistance that are a lot less complex than the evolution
> of a fairly complex enzyme like the penicillinase enzyme.
Just as there are a lot of mutations that can interfere with and protect
individuals from malaria as well. Sickle cell is merely one of these.
There are thalassemias, and favism, and several other forms of Hb changes,
including HbC. So, yes, there can be simple single mutations that can
affect complex systems.
But no one except you ever claimed that a complex enzyme, like
penicillinase, evolved from *absolutely* random sequences with *no*
intermediate steps having *any* selectable activity or function of *any*
sort. Just the opposite. All the evolutionary claims are constrained to
producing changes that have selectable function *of some sort* after each
step or few steps. Evolution is *descent with modification*, not *invention
of a needed product from nothing*. The latter process is called
"creationism" of some sort. That *necessarily* means that some organisms,
those that lack the appropriate precursor capable of being modified to form
a new functionality (or that lacks the redundancy to allow modification of a
redundant copy without losing the original activity) *will not* evolve the
end product. That is why there are bacteria today that cannot evolve
"lactase" activity in the short time frame you allow. They lack the
necessary precursor protein (which need not itself have lactase activity and
may serve some related function in the cell) capable of being modified to
"lactase" activity. Of course evolution by natural selection will easily
work only in those organism that, by the chance vagaries of their historical
past, chance to have a 'precursor' capable of being modified to the new
functionality. Other organisms, that lack this exaptive 'precursor' will
simply either die or not grow as well in media that has lactose as a major
or sole ingredient. Evolution is constrained by the structure of the
organism being put under selective pressure (or selective opportunity -- as
in the opportunity to exploit a resource, like lactose, that your neighbors
cannot).
No one but you claims that *any* organism, put in *any* new environment
*somehow*, according to evolutionary (due to selection) ideas, *must* be
able to evolve a function that allows it to survive. Nor has anyone but you
ever claimed that selection is a teleological process which "knows" what
specific end point must be reached. Evolution by natural selection is a
blind process working to adapt organisms to local conditions. There is no
guarantee that *all* organisms will be able to evolve to *any* arbitrarily
stated conditions. If there is no pathway from the current state of an
organism to the end state that includes regular useful functionality at
intermediate points, evolution by natural selection will not occur. If
there are useful intermediates from which a single (or a few) changes can
produce a new functionality, it can occur. All the "story-telling" pathways
that we present wrt to flagella are pointing out just such pathways *and*
the evidence to support those pathways.
We fully *recognize* that bacterial flagella (or any complex function)
cannot evolve by a mechanism in which you start with no useful function
whatsoever, randomly produce products with no functional utility whatsoever,
and only get functionality when the final chance step is complete. That is
precisely why it is necessary that the proteins involved in flagella
formation must have other utilities or utility as subsets of the final
flagella. They do. In short, evolution by natural selection specifically
rejects your stated premise that systems evolve by a random walk through a
sea of totally useless intermediate steps. You have yet to show that any
biological system appeared by such a system.
>
>> How could you possibly know anything about a "dramatically higher
>> ratio of functional mutations as compared to neutral mutations in
>> the development of antibiotic resistance as compared to the evolution
>> of a certain enzymatic activities" without specifying in a whole lot
>> more detail what genes you are talking about and without doing
>> experiments to determine which changes are or are not functional or
>> neutral? Everything depends on the starting material and the "fitness
>> landscape" around the point you start from. In some cases you pretty
>> clearly even "cannot get there from here," e.g., not many feathered
>> bats, or gilled whales, even though such creatures might be at finess
>> optima if they existed.
>
> If cow-like creatures could turn into whales and reptiles into birds,
> then why do you think it would be so hard to get bats to evolve
> feathers or whales to evolve gills if they would in fact benefit from
> such structures?
Future evolution is constrained by past history. It may be possible to
evolve something functionally "similar" to feathers (in bats) or gills (in
whales), but it is unlikely that it will occur by the same mechanism because
of historical constraint. Evolution is not teleological, Sean. It cannot
magically poof whatever an organism needs into existence like your
"intelligent designer" could have done. It has to work via a chain of
events constrained by history and by the necessity of intermediate
functionality.
> Really, the theory of evolution has proposed that
> such dramatic changes have occurred that practically anything is
> possible given enough time. The starting point really has little to
> do with it. All that is needed is the right environment and enough
> time.
Evolutionary theory does not say this. You do. Evolution via variation and
selection *also* needs for there to be a pathway of intermediate
functionality working within the structural and functional constraints of
the organism. It needs what you assert (since you have presented no
evidence) cannot ever exist, pathways of intermediacy with functional
utility (not necessarily the end function, since that would be a
teleological pathway, not an evolutionary one).
>
> Knowledge of the starting point is only important if neutral gaps do
> in fact exist and if random walk would in fact pose a problem for
> evolution. An argument based on the idea of a starting point is
> really one that is based on the validity of my position.
Knowledge of the entire pathway by which a system arose is important if the
evolutionary idea is valid, precisely because of the need for functional
utility in intermediate states. This is why it is important that there be
'eyes' with intermediate ability of focusing images in the animal world --
they demonstrate that the structural intermediate states in a pathway
between a light sensitive spot and a camera eye (which is similar to what is
seen during organogenesis) can have functional utility.
That is why the fact that bacterial flagella also function as protein export
machinery in ways that suggest utility of an incomplete subset of the enzyme
complex involved in its formation (also shown in the organogenesis of the
flagella) is important.
*You* are the one who has to demonstrate a *pathway* in which there is what
you misleadingly call "neutral" steps (actually, what you are proposing is
not 'neutral', but what I call 'keystone' or 'group' selection -- that a
function does not appear until a final 'keystone' mutation plus a bunch of
completely inutile changes have occurred) that lead to the formation of new
functions that only appear at the end point.
>
> So anyway, you suggest that there is no way to know where the starting
> point is, and this is true. However, one can get a pretty good idea
> that a random starting point will be a certain distance away from a
> given function in a particular creature like a bacterium. Certainly
> it is true that when Hall deleted the lacZ genes in various colonies
> of E. coli, these E. coli happened to be just one step away from a
> different lactase sequence. What where the odds? How fortunate for
> them!
Yet that is precisely how evolution works. E. coli did "just happen" to
have a protein, which served a different but dispensible function, which
could be modified to serve a "lactase" functionality in one or a few
mutational steps. If the function were not dispensible, then there would
have to be two steps, one of which would truely be "neutral" -- namely
generating redundancy.
> We know that this was quite a stroke of luck indeed when we
> consider how very difficult it is for many other bacteria to evolve
> the lactase function.
That is, other bacteria did not have a gene serving this other process, or
this other protein was not redundant or dispensible. SFW? How does this
mean that the evolution of lactase activity is impossible? It merely means
that evolution of lactase activity is contingent upon the existence of an
evolvable step.
> Granted, on occasion some life forms might just
> happen upon a particular complex sequence, like the lactase enzyme,
> because of the luck of their starting point.
So what? That merely means that, if the environment, which usually contains
more than one bacterial species has lactose (not as the sole carbon source)
and no bacteria which can use it, that the bacteria with the shortest
pathway to generating a "lactase" function from one of its other current
'functional' enzymes -- some of which may have rudimentary b-galactosidase
activity -- will be the probable winner in the race to utilize this
previously unuseable resource. At that point, however, since bacteria do
have mechanisms for horizontal transfer, it is likely that this gene will
spread horizontally from that point, with selection merely deciding which of
the bacteria that get it will retain it for any length of time. How does
this obviate evolution by natural selection? It merely shows that descent
with modification requires a pathway where there is no long chain of
completely inutile, but absolutely necessary, random mutational events. On
that both you and I agree. But, other than assertion, I have not seen you
present any evidence other than your personal incredulity that such long
chains of completely inutile, but absolutely necessary, random mutations are
actually involved in the formation of complex structures. In every case
where there *is* evidence, there are intermediate stages with utility.
> However, how long will
> this luck hold out? What are the odds that they will not only just
> happen to be close to one of the fairly rare lactase sequences out
> there, but also close to one of the fairly rare penicillinase
> sequences as well?
Quite good, actually. Most enzymes have a range of substrates that they can
use other than the one that is ordinarily considered to be the 'substrate'
that the enzyme works on. And there are a limited number of types of
biochemical activities: hydrolases, dehydrogenases, hydrogenases, etc.
That, in fact, is why one can find medicines and drugs and venoms and toxins
that can be used by existing enzymes and why simple mutations can alter
substrate specificities. Something that does not interact with some
biochemical is unlikely to have any biological effect. If it does interact
with some biochemical, then somewhere, somehow, a change in biochemistry can
alter that effect. That does not mean that some *particular* arbitrarily
chosen organism will *necessarily* be able to modify an effect or organ to a
predetermined end point (for that would be teleological).
> I mean, look at how many different complex enzymes
> and other functional proteins that an E. coli bacterium can produce.
> What are the odds that its original ancestral genetic real estate was
> that close to all of these various functional sequences? And we are
> only talking about the function of single proteins here. We haven't
> even started talking about the relative rarity of more complex
> multi-protein systems of function as are required for bacterial
> motility and the like.
The above is a hand-waving argument of no utility or evidence at all, other
than personal incredulity. *Most* proteins, even in E. coli, are not
*necessary*, they are *dispensible* (and are dispensed with in other
organisms). There are only a few *necessary* genes and enzymatic functions,
and one can even dispense with many of these if you posit RNA-based genomes.
Modification of duplications (redundancy) of *necessary* genes seem to be
the source of many *dispensible* genes, whose functions are, in fact, often
related to that of the *necessary* genes.
>
[snip argument about chloroquine resistance that actually undercuts Sean's
own argument by indicating that there can be multiple pathways to
resistance, not a single preset, teleologically determined answer]
>
> http://www.dbbm.fiocruz.br/class/Lecture/d24/drug_resistance/mc4404.pdf
>
>> Your own example
>> of the evolution of lactase makes it clear that you cannot make ad hoc
>> calculations to tell you how long it will take for something to
>> evolve.
>
> What Hall's experiments with lactase evolution in E. coli tell us is
> that the lactase function is much harder to evolve than many types of
> bacterial antibiotic resistance. Certainly it is true that I do not
> know exactly how many potential lactase enzymes exist in the potential
> space of 10e1300 potential amino acid sequences of an equivalent size
> or less.
Nor in the genomes of all bacteria.
> However, Hall's experiment made it pretty clear that the
> ratio of lactase enzymes as compared with non-lactase sequences is not
> high enough to eliminate fairly significant neutral gaps.
What you apparantly mean is not "neutral gaps", but number of specific
changes needed before a selectable effect exists. I agree that if there
exist such gaps for a particular species, such gaps do provide a barrier to
evolution by natural selection to a particular end goal *in that species*.
That is why evolutionary biologists place so much weight on pathways in
which intermediate stages have functional utility (but not necessarily the
teleological end point's utility). Such intermediate states are a necessity
for evolution by selection (descent with modification) to work. [Horizontal
transfer, of course, does not require descent with modification in the
recipient species, but only in the donor species.]
> If the
> ratio of lactase enzymes to non-lactase sequences were as high as 1 in
> 10, then one would expect that the evolution of the lactase function
> would be easily demonstrable in just about any type of bacteria.
The relevant question is what sorts of enzymatic activities are close enough
to the sequences with lactase activity such that a change might give lactase
activity in that gene. If none exist in a particular organism, then,
indeed, that organism will be unlikely to evolve lactase from that
'intermediate' (its intermediacy would only be observable after the fact,
since it has independent activity in the present) precursor.
> In
> fact, just about 1 in 10 DNA sequences and/or genes in all bacteria
> would have some sort of lactase function. If this ratio were the real
> ratio, Hall would have discovered sequence after sequence with the
> lactase function. Every time he deleted another sequence with lactase
> function (as he did with the lacZ genes), a new one would quickly
> evolve (as happened with the ebg gene - but with no other gene after
> the ebg gene was deleted). The fact that no other lactase gene
> evolved after the ebg gene was deleted means that the ratio of
> sequences with the lactase function is low enough so that not very
> many lactase sequences can can be evolved by a fairly large population
> even with tens of thousands of generations of time.
Unless, for entirely unrelated reasons, one has a gene like ebg (dispensible
and close enough to lactase for the gap to selectable functionality to be
easily transited). If your view of evolution were true, then we would be
having hyperevolution, such as creationists often assume post-flood and
there would be no differentiation between bacteria due to descent. Any time
a bacteria came into an environment with lactose as the sole carbon source,
it could poof a lactase into existence in the next generation from some
unspecified random sequence of DNA. Instead, we see descent with
modification, whereby lactase activity does not appear to evolve from random
sequences of DNA, but only from enzymes which do not require extensive
remodeling to make into lactase. And why this is a problem for evolution?
I always thought that was how evolution was supposed to work. Rather than
poofing new activities into existence from random sequences of DNA.
> Based on this
> lack of evolution one can reasonable calculate the average neutral gap
> involved, at least to the extent that the gap is most likely *larger*
> than a particular ratio (Since any function with a higher ratio of
> representation in the total number of potential sequences should be
> realized after a given amount of time).
It also points out the high degree of variance, with some species (those
that by chance had a potentially evolveable precursor gene) easily evolving
lactase and others that lacked that precursor not being able to do so. That
variance is what would give a pattern of descent with modification for
lactases rather than a pattern of independent evolution of lactases from
random sequences in each bacteria that has lactase.
It has to exist somewhere. It need not be extremely high. Most evolution,
of course, involves only minor modification of pre-existing structures.
Such as the difference between humans and chimps.
> You yourself admit that the ratios do in fact go down as
> complexity increases. Well then, please explain to me where this
> ratio levels off so that evolution can keep up with these
> exponentially expanding neutral gaps.
>
>> Multiplying the number of genetic differences between two sequences in
>> related organisms by the estimated population size, mutation rate, and
>> generation time, is pretty irrelevant. No one thinks that evolution
>> works entirely by neutral mutation and random walks.
>
> Oh really? Evolution works by other mechanisms than random mutation
> and natural selection?
Neutral mutation and random walk is not random mutation and natural
selection. Those are two entirely different mechanisms. The first is what
is called neutral drift. Darwin did not propose it. Darwin proposed not a
random walk, but natural selection, which is most decidely non-random --
natural selection is the mechanism by which the environment imparts
information about itself into the organisms that live there.
> If there is a neutral gap, clear this gap
> destroys the power of natural selection. So, how is this gap crossed?
> What other evolutionary mechanisms do you know of that are capable of
> crossing such gaps?
Let's examine the consequences of your false idea about what evolution
claims to accomplish with the consequences of my much less false idea about
what evolution claims to accomplish. Specifically, let's address your false
assertion that evolution claims (or, in your view, should claim) to be
'all-powerful' and able leap giant gaps of sequence change in short periods
of time to achieve a currently perceived 'need' of an organism. If that
idea of evolution were true, then we would expect to see many independent
'novel inventions' that serve the same functional utility. This is because
any bacteria that initially lacked an enzyme, say lactase, should be able to
quickly invent one from scratch using a random walk across any sized gap of
no selection for lactase activity. In a sense, the only way that an
organism can cross such a gap is by Lamarckian inheritance, or a mechanism
by which it can 'will' the end teleologically required result. If evolution
actually worked this way, then we would expect to see many independent
inventions of, say, lactase, in nature rather than a pattern of common
descent (the twin nested hierarchy). And, to give the devil its due, one
does *on rare occassion* see evidence of the independent invention of a
biochemical activity. But only rarely. Most of the time, biochemical
activities show the twin nested hierarchy. OTOH, one does see multiple
independent inventions of traits that can vary continuously (or essentially
continuously) like aerodynamics in fish or the 'eye' (but not the
biochemistry of vision) and where there is a clear selective advantage for
each continuous pathway in certain environments.
In my much less false idea, evolution is constrained not just by the
environment (with the genome being infinitely plastic in a local situation),
but also is constrained by the genome of the organism the environment is
acting upon. Evolution is a consequence of an *interaction* between the
two. If this is true, then most 'novel' enzymatic activities will be
relatively rare events, requiring the combination of both a selective
environment *and* a genome with a sequence exaptated to be able to cross a
relatively short gap (or no gap, but only a single mutation) into a
selectable level of the new function. The expectation from this model is
that *most* 'novel' functions happen only rarely and then are retained (and
optimized) by selection and descent with modification (and horizontal
transfer in bacteria), leading to a twin nested hierarchy between the
sequences for that function and lineage as determined by other independent
means. I.e., *most* novelties occur only once and are retained by descent.
This model absolutely requires that the process of inventing the novelty
involves exaptation of function from pre-existing functional elements or
selectability at intermediate states. It eschews the (false) idea that
evolution involves the random walk of a random functionless sequence until
all the components are in place (it rejects the idea that evolution involves
the magical invention of IC systems) and points to the independent
functionality of simpler sub-systems and sequence similarity of such systems
and systems performing the other functionality as *evidence* that there is
the requisite *selectable* pathway from one state to the next.
Note that we are talking about quantity here. There are some types of
systems that can easily be modified (usually morphological, not requiring
new functions or proteins, such as the known differences between Pan and
Homo) continuously under the appropriate selective pressures. Others may be
an inadvertant consequence of selection for other purposes. Other types of
change tend to be fortuitous (and not necessarily of selective utility) and
historically are either sporadic or unique. These latter tend to be the
types of changes that define lineages.
>
>>>> So... Both resistances evolved in nature in years to decades;
>>>> evolution of mefloquine resistance has been reproduced in the lab;
>>>> evolution of chloroquine resistance has not. Does this mean that the
>>>> "Designer" let P. falciparum handle mefloquine on its own, but
>>>> intervened to help P. falciparum deal with chloroquine?
>>>
>>> You don't seem to understand the statistics involved here. Obviously,
>>> a neutral gap in function of 6 or 7 base pairs can easily be crossed
>>> by random walk alone given the much larger population sizes of the
>>> malaria parasites (P. falciparum) that exist in the wild as compared
>>> to the relatively limited population size that was most likely used in
>>> the laboratory experiments. No ID is needed to explain the evolution
>>> of chloroquine resistance in either case. The average time required
>>> is well within reason.
>>
>> We know what the "average time" is, not because of your post hoc
>> statistics, but because we observed the evolution of chloroquine
>> resistance in nature.
>
> Yes, we have observed the average time required and the mutations that
> are required first, before any calculations. However, based on the
> required mutations we can figure out how long these required mutations
> would take to evolve if they were in fact neutral mutations.
Please define what you mean by neutral mutations. You keep using this term
in ways that differ from the normal meaning.
> We can
> then see if these calculations are consistent with what we actually
> saw in nature. If the calculations are consistent, then we can know
> that the evolution that we saw take place in nature was in fact the
> result of random walk across a certain number of neutral steps. We
> can also know what would be required to evolve this function in the
> lab. Much better estimates on the needed population size could be
> pre-determined in order to achieve success in a given span of time.
>
> The reason why this example of CQR is helpful to me is because it
> shows that wider neutral gaps in function do in fact translate into
> longer spans of time due to the fact that random walk was involved in
> the process. There is no way around this conclusion that I can see.
> Why else would the evolution of the few steps involved in CXR have
> taken so long and why else is CXR not easily demonstrated in vitro?
And I have no problem with that. Only if you hold the false view that
evolution to a particular 'novel' function is a *necessity* that occurs by
the will of the organism (or the will of a designer) rather than being an
occasional consequence of the interaction between an organism and its
environment, does this somehow cause a problem for evolution. In fact, the
evidence is quite clear that new functionalities for individual genes are
relatively rare, *but not impossible*, and are contingent upon both the
environment and the genome of the organism. That is why most enzymes
exhibit one (or more rarely, two) only a single line of descent (sequence
parsimony) consistent with the lines of descent obtained from other methods
(e.g., fossil record) rather than multiple independent lines of descent.
Similarly, complexity, as in flagella, is viewed not as a *single* event,
but as a *series* or *pathway* of events, each of which had selective value
independent of an 'end result' we can only discern from the position of
hindsight.
>
>>>>> These very same bacteria would quickly evolve resistance to penicillin
>>>>> if it were added to their environment. No more than a handful of
>>>>> generations would be required. Why then is antibiotic resistance so
>>>>> much easier for them to evolve than the lactase function? What is it
>>>>> about the evolution of relatively simple enzymes that is so much more
>>>>> difficult than the evolution of antibiotic resistance?
>>>>
>>>> Enzymes are really complicated. You are right. It almost certainly
>>>> takes more time than you have to watch to evolve a new enzyme from
>>>> scratch (or even from an unrelated enzyme).
>>>
>>> I'm glad that you realize this because many people think that the
>>> evolution of antibiotic resistance is something very significant
>>> and/or complex. What many do not realize or admit is that even the
>>> relatively simple function of a single protein based enzyme, is far
>>> more complex than the function of antibiotic resistance.
>>>
>>> Obviously more time is required to evolve the enzymatic functions than
>>> the functions of antibiotic resistance. That question is, "Why?" Why
>>> is more time required to evolve functions of increasing complexity? I
>>> am proposing that neutral gaps are the reason for this observed
>>> phenomenon. What is your explanation?
Antibiotic resistance and enzyme evolution are both dependent upon the
pre-existence (or easy evolution) of a protein which can affect the
antibiotic (or new substrate). The differences you see are usually based on
the intensity of selection rather than a different mechanism. The only usual
difference is the intensity of selection and the necessity or dispensibility
of the process. In an environment with an antibiotic, evolving a resistance
of some sort is usually a *necessity* because the antibiotic directly
affects survival of the organism; evolving a new enzymatic function, OTOH,
is often a matter of being able to exploit a resource currently unavailable
to you, which only affects you if that is the only relavant resource
available (a bacteria without lactase can survive in a lactose-rich media
that also has enough glucose). That is, evolution of a new enzymatic
activity is not always a *necessity*; it is often *dispensible* (nice to
have under certain circumstance, but not usually a matter of necessity).
The usual mechanisms by which resistance (or new enzymatic activity) is
obtained falls into one of the following categories: 1) Resistance
(sufficient activity) by amplification. In this case, an antibiotic binds a
protein either much more strongly than the native substrate or strongly
enough to affect the amount of substrate conversion (the enzymatic activity)
below the level of survival. Resistance is obtained by simple amplification
of the target protein to either bind up enough of the antibiotic so that
enough enzyme activity remains to permit survival. This is how DDT and
other resistances like methotrexate resistance work. In the enzyme world,
this would involve amplification of an enzyme that has a primary function
different from the new one, but has some new activity. [Again, enzymes are
not all-or-nothing specified, but usually are *optimized* for one function,
while *suboptimally* using other substrates and thus creating other
products. Indeed, some enzymes may actually better utilize substrates that
are not the 'normal' one.] This both increases the amount of original
activity (which may not be harmful) *and* permit sufficient utilization of
the novel substrate so as to have a selective advantage. 2) Modification by
mutation and selection of a protein. In resistance, the usual protein
modified is the target of the antibiotic. Usually the modification must
cause a great enough decrease in binding affinity for the antibiotic while
retaining sufficient binding affinity for the original substrate to allow
survival. Because of the greater stringency of antibiotic selection, even a
very low level of original activity can be selected for. In producing 'new'
enzyme activity the problem is that most loss of specificity for the
original substrate produce sub-optimal levels of both activities. This can
only proceed up to a point, and that point may not produce sufficient
amounts of the new activity to make it selectable in its own right. Thus
this usually only happens when the original activity is both dispensible and
rarely used. 3) A combination of 1) and 2). This allows a way around the
difficulty of enzyme suboptimality and also provides a mechanism for
generating isozymes (enzymes that perform the same function but have
different properties, like temperature optimi) and families of genes
(enzymes that perform related, but not identical functions, like the globin
family of myoglobin and hemoglobins and all the different transmembrane
receptors). This is a *very* common feature of the evolution of new
functions in cells. 4) Modification of a non-target protein that
inactivates the antibiotic. This, of course, *is* the invention of a new
enzyme. The evolution of penicillinase and/or vancomycin resistance *is*
the invention of a new enzyme activity to the point where it has a
functionally important effect. It occurs by the modification of an existing
protein whose original function is dispensible.
>>>
>>>> We all agree that
>>>> evolution takes a long time. Building enzymes from scratch is actually
>>>> more a part of abiogenesis than evolution, but most scientists would
>>>> agree, I think, that abiogenesis took a billion years or so, not a few
>>>> months, even with artificially boosted mutation rates.
>>>
>>> Oh, so the evolution of even one little protein sequence is based on
>>> "abiogenesis" not on evolution? Really?! This is *most* interesting.
>>> This is exactly my whole point.
>>
>>> Abiogenesis is based on neutral
>>> drift/random walk. Natural selection really is limited when it comes
>>> to ideas on abiogenesis since by far most of the changes in
>>> abiogenesis are functionally neutral as far as a mindless nature is
>>> concerned.
>>
>> I have no idea why you think this. Most ideas about abiogenesis (apart
>> from creationist, junkyard to B727, strawmen) are based on selection.
>> We all agree that a random walk through all possible chemical
>> structures to cytochrome c is not what happened.
Rather, abiogenesis *initially* required the most primitive basic
'reproductive genetic system' (of which we do not know the minimum
requirements, but proteins were probably not required -- RNA or PNA may be),
which originially involves sequences generated randomly (a significant
number of the relevant enzymatic activities can be generated randomly in
50-mer RNAs in less than a millimole of material). At that point selection
will kick into action to optimize those functions that assist in
reproductive success.
>
> Oh really? What happened then? Specifically? Detail a scenario for
> the evolution of cytochrome c where each mutation is selectively
> advantageous. You even get to use an already established life form
> capable of self-replication. Getting this life form to begin with
> (via abiogenesis) is a whole different ball game. In fact, this is
> whole idea that abiogenesis could have given rise to the first living
> cell is what drove many like Sir Frederick Hoyle to other theories of
> living coming from outer space.
That merely changes "where", not "how".
> Then, once you have the first living
> cell, using the idea of random mutation and mindless selection
Mindless selection specifically tries to optimize your genome for
reproductive success in the environment that your parents faced. Do you
agree that that is precisely what selection does?
> to get
> other functions of increasing complexity is still an astronomical task
> that really is no easier than explaining the origin of the first life
> form to begin with.
Selection only leads to increased complexity to the extent that that
increased complexity leads to greater reproductive success in the
environment that your parents faced. It will clearly lead to an increase in
the frequency of those variants that are more complex under conditions in
which that is favored. Unless you are saying that mutation cannot increase
complexity, say by amplifying a gene and modifying it into an isozyme or
related gene in the same family. That would be a hard position to maintain
in the face of evidence that both amplification and modification are known
to occur.
>
>>> This is why scientists think that abiogenesis took
>>> billions of years to produce the first self-replicating cell.
>
> Actually you and I stand corrected on this point. Somehow scientists
> think that abiogenesis happened relatively quickly in a few millions,
> not billions, of years.
Scientist can point to clear evidence that procaryotic organisms existed on
the earth for at least 3.5 billion years or so. And for the first
half-billion years, the earth was probably pretty inhospitible to
carbon-based life forms. But that still leaves several *hundred million
years*, not a *few* million, *within which* abiogenesis must have occurred
(even if you think the abiogenesis event were supernatural in origin). How
long it actually took is not clear. But remember that most of the necessary
enzymatic (actually ribozyme) activities needed for nucleotide reproduction
(polynucleotide kinase, ligase) can be generated in random 50-mers in less
than a micromole of material.
>
>>> But
>>> why? Why does abiogenesis take so long? Because of the neutral gaps.
>>> When you actually start plugging in the numbers and doing some real
>>> estimates based on the idea of neutral gaps, you quickly find that the
>>> abiogenesis of much of anything would take far longer than a few
>>> billion or even many trillions or zillions or googols of years.
>>
>> Please, show your model. But it isn't a random walk.
>
> My model is based on random walk. What is your model? If random walk
> is not involved, then even millions of years are not required.
Millions of years may still be required *if* the process were not
teleologically determined, depending upon local selective pressures. If the
present state is not a predetermined end 'goal', there can be millions of
years of quite happy intermediate status. Indeed, the evidence shows
several billion years of single-cell (mostly procaryotic) status for the
entire biosphere. Even multicellularity does not even look like an
'inevitability'.
> Without random walk to slow things down, evolution would happen right
> before your very eyes. It would be a snap. Without random walk, the
> first cell would self-assemble in a matter of seconds in the right
> environment (one with all the required parts). Then, without random
> walk, this first cell would quickly go multi-cellular in just a few
> generations. A few years down the road and fish would be crawling out
> onto the land. A few thousand years later and Survivor would be a hit
> television show.
Only if you are thinking that the environment tends inexorably to increase
complexity and that evolution works by taking random sequences and poofing
new functional sequences into existence because of the 'will' of the
organism to gain a function. Selection is conservative more often than it
is creative.
>
> Random walk slows things down.
In the less false view of evolution, it is the necessity for the many stages
of intermediacy in the pathway to the current function being examined to
have *some* utility (but not necessarily *final* utility) that slows things
down. Random walks of truly significant lengths would tend to abort the
process.
> Without random walk, evolution would
> be very fast.
Only if both the rate of variation production and the rate of environmental
change were to speed up significantly.
> The fact that evolution seems to be very slow must mean
> that random walk is a real limiting force of nature. The problem is
> that random walk limits things too much for evolution to produce much
> of anything in the blink of an eye that is 4 or 5 billion years.
I do not regard 4-5 billion years as a blink of an eye, even in evolutionary
terms. You seem to be substituting random walks for the more usual
retarding principles, namely the need for intermediate utility (of *some*
kind) in the pathways of evolutionary change (some of which have few and
short random walks as part of the process and others having longer ones or
requiring fortuitous one-time events) *and* the absence of teleological end
goals for evolution (which leads to random walks of completely functional
intermediate states) *and* the need for the new functionality to be of
selective benefit in a local environment.
>
[snip]
John Wilkins
raised by the Pitmans of this group.
Howard Hershey <hers...@indiana.edu> wrote:
--
John Wilkins
"And this is a damnable doctrine" - Charles Darwin, Autobiography
catshark
Wilkins) wrote:
>I nominate this. Clear, informative and on matters that get repeatedly
>raised by the Pitmans of this group.
Seconded.
---------------
J. Pieret
---------------
Cogito sum, ergo sum, cogito.
- Robert Carroll -
Lilith
> Lilith wrote in message news:<75200cbc.03060...@posting.google.com>...
>
> snip
> > ID'ers must show that biological systems are perfect machines that
> > cannot move from one context to another context simply by adapting --
> > by evolutionary process as outlined -- their existing systems to other
> > contexts. Arguing that yeast cannot adapt to space conditions (as an
> > hypothetical example) is no argument, however, since evolution does
> > not require such great leaps. Evolution only requires reasonable
> > context jumps -- nylon instead of granite. The largest problem for ID
> > is, however, that they'd be arguing against observation.
>
> Nylon instead of granite? Granite? Do you know of anything that can
> eat granite? I was not aware that granite was such a potential energy
> source for biological organisms. But hey, that isn't really the point
> now is it?
No, it isn't. The point is that a reasonable context jump (nylon) is
available to the bacteria, not an unreasonable context jump (granite).
> I offered a simple example where certain E. coli colonies (lacking the
> lacZ and ebgA genes) had been grown on a lactose rich
> media/environment. They failed to evolve the lactase function despite
> the obvious benefit to them if they ever did evolve this relatively
> simple single protein based enzyme. These particular bacteria were
> grown on this lactose rich media for tens of thousands of generations
> with high mutation rates and large population sizes, and they still
> never evolved this relatively simple lactase function. Really, we are
> not talking about a dramatic shift in environment here. We aren't
> talking about a lethal "outer space" environment either. The E. coli
> bacteria grew just fine without the lactase function, but they would
> have done much better in the lactose rich environment if they did have
> this function. So, why didn't they evolve this function?
If they were growing just fine without the lactase function, why would
they need it? If they evolved a lactase gene, it would have to arise
out of either 2 copies of an extant enzyme with functions within reach
(whole gene duplications) or would have to disable working copies of
extant enzymes to change over into lactase utilization. The bacteria
would have had to decrease the existing abilities to process the
useful and optimized metabolic pathways to produce a new one out of
existing parts. There's nothing we've seen thus far that suggests that
organisms will always evolve that kind of function in ten generations,
ten thousand, or ten million. If all available lac-type enzymes are
knocked out, what's the chance that they'll evolve a new one?
Clue: Evolution within the context of the history of the organism is
as important as the context in which the organism finds itself.
In fact, why don't we grow e.coli on a bed of polyester? What's the
chance, in 10,000 generations, that they'll evolve a gene to eat
polyester? If the organism does not have a context in which it can
evolve by sequential steps, a function that will utilize existing
pieces to build a polyester-processing system, then it's unlikely to
evolve one.
In other words, you're expecting a gap to be crossed. But before you
use that as your "AHA" stage, let me tell you this: evolution has its
limits. Certain gaps cannot be crossed. The organisms that still live
today have been able to leap across reasonable gaps, one small step at
a time. THAT is what evolution describes. Your complaint about large
gaps not needing to be crossed is NOT what molecular evolution
requires. There is no large, "And here a miracle occurs" that is
required by evolutionary theory.
> These very same bacteria would quickly evolve resistance to penicillin
> if it were added to their environment. No more than a handful of
> generations would be required.
There's a difference. Evolution of lactase function requires a gene
duplication of a reasonably closely-related enzyme on demand (which
you have noted was certainly not within easy reach anymore as both
related enzymes were deleted) and subsequent mutations of several
residues within an existing enzyme to acquire lactase function.
As evolution is NOT DIRECTIONAL if it is not directly selected on,
Sean, as is certainly known to you, there is a very large "search
space" for this kind of evolutionary innovation. Are 10,000
generations of millions of e.coli enough to generate that kind of
innovation, enough to give a high probability that the search space
would be adequately covered? Obviously not.
If there is no selected pathway TO lactase evolution, then it's not
gonna happen except by hit or miss. And that's not what evolution's
about. Hit or miss is not what evolutionary theory supposes.
Heterogeneity and selection is what evolution supposes. If there is no
pathway selecting towards lactase evolution, then tell us, Sean, why
it would happen? Why would evolutionary theory say it must happen
without directed selection (evolutionary pathway) toward development
of lactase function?
> Why then is antibiotic resistance so
> much easier for them to evolve than the lactase function?
Because antibiotic resistance is based on mutation and selection on
existing enzymes. That's directed selection, right there.
> What is it
> about the evolution of relatively simple enzymes that is so much more
> difficult than the evolution of antibiotic resistance?
Because there's no direction that would be given by selection towards
lactase function? That's like growing E.coli on a rock and expecting
it to start spontaneously eating rock. While the chance of that
occuring is not zero, it's certainly not something within reach of
ordinary E.coli.
And in the case of the missing lactase enzyme itself, full lactase
function would take more than a few changes. It would require the
creation of a new enzyme by gene duplication and then evolution.
But antibiotic resistance only requires a few changes to adequately
process the antibiotics. Beta-lactamases, for example, break down
penicillin. Hall's shown a few changes is all that's needed in his
papers on evolving antibiotic resistence. See for example:
Barlow M, Hall BG. Experimental prediction of the natural evolution of
antibiotic resistance. Genetics. 2003 Apr;163(4):1237-41.
The TEM family of beta-lactamases has evolved to confer resistance to
most of the beta-lactam antibiotics, but not to cefepime. To determine
whether the TEM beta-lactamases have the potential to evolve cefepime
resistance, we evolved the ancestral TEM allele, TEM-1, in vitro and
selected for cefepime resistance. After four rounds of mutagenesis and
selection for increased cefepime resistance each of eight independent
populations reached a level equivalent to clinical resistance. All
eight evolved alleles increased the level of cefepime resistance by a
factor of at least 32, and the best allele improved by a factor of
512. Sequencing showed that alleles contained from two to six amino
acid substitutions, many of which were shared among alleles, and that
the best allele contained only three substitutions.
> Also, we have actually seen a few relatively rare real time
> demonstrations of enzyme evolution, to include the evolution of the
> lactase function in some types of E. coli, but never in other types of
> mutant E. coli and never in many other types of bacteria over the
> course of 50+ years.
Sean, antibiotic resistance IS real-time ENZYME evolution. Do you even
know what a beta lactamase (for instance) is? Don't you think you
better find out? It's an enzyme. It evolves.
So, yes, antibiotic resistence is enzyme evolution. The fact that
we've seen real-time evolution of anything is clue one: evolution
occurs. Under selection, the system is perfectly able to move towards
the desired, selected state: survival in the presence of an
antibiotic. That's a basis of Hall's research, up to the present day.
He's been able to recently "predict" some aspects of in-the-wild
antibiotic resistance by evolving the resistance in the laboratory.
> However, we have never seen a bacterial function
> evolve that requires multiple proteins working together at the same
> time, such as would be required for the function of bacterial
> motility.
I don't know of any experiment that's tried to direct that kind of
pathway, yet.
I maintain that there are no barriers to coupled evolution within a
complex system given gene duplication and mutation, among other
processes. That is the simplest answer: no restriction on evolution at
any level. I have seen no evidence that there is any barrier to
evolution as evolutionary theory currently presents itself.
I have only seen that a couple of knocked-out genes do not poof into
appearance out of nothing within ten thousand generations under
limited laboratory conditions with no selection along a pathway of
intermediate states...an experiment that would certainly take longer
than 10,000 generations of E. coli to generate results.
> Why is this type of multi-protein function so difficult to
> evolve in real time? Hmmmmm?
I don't understand your complaint. Evolution suggests many changes are
evolved within "reach", as in, step-by-step, by action on existing
genetic material or mechanisms. I don't see your problem with this.
Step-by-step evolution, even in coupled-systems, is perfectly
reasonable.
> I look forward to finally hearing from someone in the know as to why
> antibiotic resistance evolves so much faster than the functions of
> enzymes and why enzymes evolve at least on some rare occasions, but
> functions with multiple proteins working together at the same time,
> never seem to evolve in real time.
Um, Sean, antibiotic resistance IS evolution within enzymes. The
enzymes are themselves evolving better function in respect to new
antibiotics. The enzymes are in some cases changing their function to
adjust to the presence of a new antibiotic. Therefore, new antibiotic
resistance IS the change of an enzyme's function.
For instance, from Hall's recent paper: "The TEM family of
beta-lactamases has evolved to confer resistance to most of the
beta-lactam antibiotics, but not to cefepime"
A refresher from your biochemistry class, the "-ase" at the end of
that word means it's an enzyme. If you still don't believe me, go
here:
http://us.expasy.org/cgi-bin/nicezyme.pl?3.5.2.6
That's the page for beta-lactamases in the ENZYME nomenclature
database. Yea, they're enzymes.
And as to why we don't "see" multiple protein evolution, show me a
study where someone has done work on multiple-protein evolution
(coupled evolution). I can't seem to find studies like that. Maybe you
know of some. Until someone digs deeply into that kind of study, I'd
say that your complaint is premature.
>I mean, if it is so easy, as you
> seem to be saying, then evolution should proceed rapidly, should it
> not?
No. Evolutionary theory does not say that genes should poof out of
nothing without known processes. If there was no replacement for the
lacZ gene, or any gene within evolutionary "reach" even with gene
duplication, then why would we expect it to evolve lacZ function?
Do you have evidence that there are any enzymes less than a few
handfuls of mutations away from lacZ that the bacteria could have
evolved but didn't?
> If there were no neutral gaps to slow the process of evolution
> down, then given the proper environment, the evolution of beneficial
> functions, such as the lactase function in a lactose rich environment,
> should proceed very quickly.
Just like nylonase seemed to just spring out of nowhere but it was
really a selected copy of a differently-expressed, already-existing
gene.
How do you know that the knock-out E.coli had all the right conditions
to evolve a lactase function out of existing parts? If it had no
"within reach" enzyme to utilize as a weak lactase it could get a
foothold with, and then select for lactase function, then it wouldn't
be any more able to generate that lactase function than it could eat
rock. Frankly, to demand anything like that is silly.
> This lactose environment ain't outer
> space and it ain't granite you know.
It might as well be if there's no enzyme that has significant lactase
activity. It makes the enzyme effectively "blind" to evolutionary
change in that direction. What's your evidence that it had any kind of
weak lactase function at the end of the experiment? Did it?
> One little enzyme is all that is
> needed to use this new environment in a more advantageous way. And
> yet, many different types of bacteria seem unable to evolve the
> lactase enzyme despite hundreds of thousands and even millions of
> generations of time. What then, exactly, is slowing this process
> down? Please, you seem so knowledgeable . . . what is the answer?
The answer is that 10,000 generations of e.coli in a laboratory under
fixed experimental conditions were not enough to evolve, through
selection, a weak lactase activity.
I hope that helps.
Deanne
Von Smith
>
> > > > You are contrasting the ease with which a single mutation can lead to
> > > > gain of function (starting on the right background) with the problem
> > > > of evolving a new enzyme from scratch (or from an enzyme with
> > > > unrelated function). Yes. It is much faster if there is a gene
> > > > already there which needs just a single mutation to develop a new,
> > > > useful activity.
> > >
> > > Finally, someone who actually seems to understand what I am talking
> > > about. There are clearly different levels of functional complexity.
> >
> > Really? How is it clear that mefloquine resistance is less complex
> > than chloroquine resistance?
>
> Why do you think? More neutral mutations are needed to produce
> chloroquine resistance.
>
others.
What would the number of neutral mutations needed to achieve a
function have to do with its complexity?
Is this some sort of *definition* of complexity? If not, what is your
definition of "functional complexity", and why do you think the number
of neutral mutations needed is an appropriate metric of it?
Also, "neutral mutation" is often context-dependent. In an
environment with no chloroquine, probably just about all the steps
needed to evolve resistance to it would be neutral. By your metric,
the complexity of chloroquine would skyrocket, even though nothing had
changed except the selective pressures in the environment. Does that
sound right to you? Could a function be highly complex in one
environment, but less so in another, with different selective
pressures and a different fitness landscape?
Nonetheless they do differ in complexity, and as you admit, you cannot
tell which will be greater or less. So apparently the answer to my
question is: no, you cannot predict which one will be more complex
without already knowing the evolutionary path, even though you
consider the difference here to be "negligible", and that may satisfy
you. I, however, am not sure that I would consider the difference
between 1 mutation (0 neutral) and 6 (possibly at least 2 or 3
neutral) to be negligible.
>
> > Can you say
> > anything meaningful about their respective complexities without
> > peeking?
>
> Yes. I can say that both of them have a very low level of complexity
> since their actions are both very specific and would most likely be
> easily disrupted by one or two point mutations. . . perhaps a few more
> point mutations might be needed, but I wouldn't have predicted that
> more than a handful of mutations would be needed to produce a
> selectable advantageous disruption of their specified functions. This
> prediction continues to hold true, even for chloroquine resistance.
OK, so 4 or 5 additional mutations are a negligible difference in
complexity in your book. I'll keep note of that.
>
> > > The function of bacterial antibiotic resistance is extremely simple,
> > > even in comparison to the most simple enzymatic functions.
> >
> > Except of course for the cases in which antibiotic resistance *is* an
> > enzyme function, as in the case of, say vancomycin or cefotaxime
> > resistance.
>
<snip discussion of vancomycin resistance which, though informative,
doesn't really bear on the argument>
>
> So you see, the ability to produce the comparably complex
> penicillinase enzyme is by no means the only way for bacteria to gain
> resistance to beta-lactam antibiotics such as vancomycin and
> cefotaxime. And in fact, if these bacteria did not have ancestral
> access to a pre-formed code for such enzymes as penicillinase, they
> never do evolve it as a means of achieving antibiotic resistance.
> Instead, they rely on some of the other methods of interfering
> mutations described briefly here. In comparison, it is far more
> difficult or complex to evolve entire enzymes from scratch, like the
> penicillinase enzyme, as compared to one or two interfering point
> mutations that do give basically the same result without the cost of
> having to maintain a gene for an enzyme in the genetic real estate.
> Such maintenance costs extra energy, but it doesn't cost any extra
> energy to maintain one or two interfering mutations in a target
> sequence.
I think you missed my point. You referred to antibiotic resistance in
general as a "function", and claim that it is a relatively simple one
which you then tried to contrast to enzyme functions. I took this to
refer indifferently to all forms of antibiotic resistance, whether
they involve changes to enzyme activities or not. We both agree that
some do and some don't. But this means that "enzyme functions" and
"antibiotic resistance functions" aren't really different in kind;
they overlap, so any comparison of their respective complexities is
meaningless unless you are more precise in describing functions in
terms of the actual mechanisms they involve.
And the other point, of course, is that in spite of the apparently
great difference in complexity, both kinds of antibiotic resistance
are seen to evolve.
So how does this square with the fact that chloroquine resistance
takes at least 2 and possibly as many as 6 or 7 mutations, whereas
some enzyme functions take only require a single mutation to appear?-
>
> Take for example the human genome of around 6 or 7 billion base pairs
> (diploid). There is still some argument, but lets say that there are
> around 40,000 genes. How many of these genes or genetic sequences are
> capable of producing a protein with the lactase function? Not too
> many. You see, if the lactase function were really common, just about
> any protein, regardless of its usual job, could produce the lactase
> function as well. The fact is that only a tiny fraction of all the
> known proteins out there are capable of hydrolyzing lactose. This
> means that the lactose function is relatively rare. This relatively
> rarity means that there is a sizable gap that exists between sequences
> with the lactase function. Odds are that a sequence chosen at random
> will be a fair distance from the closest sequence with the lactase
> function.
But why would we choose a sequence at random, if we are discussing
possible evolutionary pathways? Shouldn't we be looking for homologs?
Most enzyme functions probably didn't evolve from scratch, any more
than most gross anatomical features did; they would have been produced
by gradual modifications of already-existing proteins, possibly
produced by duplicate copies of the genes that code for them. I
haven't looked yet at any literature dealing with the question of
evolution of mammal lactase, but it seems this would be a more useful
approach to the question than sitting in our armchairs calculating the
prior odds of its evolving from scratch.
>
> This seems to be a well-supported observation, even without Hall's
> experiments to back it up. I mean, before Hall did his experiments I
> would have bet a lot of money on the prediction that his E. coli would
> not be able to evolve more than a handful of different lactase enzymes
> even over the course of tens of thousands of generations per try. It
> turns out that this is exactly what happened. The E. coli bacteria
> were only capable of evolving one lactase enzyme. And, without this
> ebg gene, they weren't capable of evolving any more of them.
Actually, I was under the impression that Matsumura et al. got the
same function from a completely different gene.
Matsumura I, Ellington AD. In vitro evolution of
beta-glucuronidase into a beta-galactosidase proceeds through
non-specific intermediates. J Mol Biol. 2001 Jan 12;305(2):331-9
I have seen this article cited at you a couple of times, and I haven't
seen you address it. I have not read it myself, so I can only judge
from hearsay, but apparently the ebg gene is *not* the only E. coli
gene that can evolve a novel lactase function, nor even the only one
that has been observed to.
>
> I would bet the same way for many other enzymes, like the
> penicillinase enzyme. If one were to completely delete the
> penicillinase gene in a colony of bacteria, I would bet that this
> colony would not have too much genetic real estate close enough to any
> other penicillinase sequence that could be reached in hundreds of
> thousands of generations. Perhaps a rare colony would come up with at
> least one penicillinase enzyme, but if this were taken away, I am
> betting that the odds of it happening a second time would be much
> worse than the odds of lightening hitting the same place twice or the
> same person winning the California lottery twice in a lifetime. Why?
> Because enzymes of such complexity seem rather widely separated in the
> potential space of the junk-pile. Hall's E. coli experiments only
> highlighted this obvious conclusion.
What good are your guesses and assertions? I hope you can forgive me
for being unconvinced. Besides, if Matsumura et al. *did* get
beta-galactosidase a second time from a completely different gene,
what obvious conclusion does that highlight? Perhaps I should start
playing California lotto, after all.
Probably even less complexity than that, I would think.
> I would say that this
> original life form was quite limited in genetic real estate and
> function. And yet, your theory claims that in just a few billion
> years this life form, with its apparently limited and humble
> resources, was capable of giving rise to all that we see around us.
>
> How then are you trying to support this claim of yours that
> evolutionists do not "suggest" that anything can evolve from anything?
> I mean, it seems like, given the proper shifts in environment, a cow
> could evolve into a bat or a chicken could evolve into an elephant.
> Certainly this is what you believe.
I believe in your non-sequiturs and strawmen? I don't think so. Just
because you react to two propositions with equal incredulity does not
make them logically equivalent or even comparable. Certainly the
evolutionary and developmental constraints faced by early prokaryotes
over a period of 2 billion years are not equivalent to those faced by
an organ-grade chicken or elephant over a period of a few tens of
millions.
> If you truly think that some
> starting points do in fact have significant limits, how on earth do
> you explain evolution? And, what is it exactly that creates these
> supposed limits for the process of evolution? I mean, starting with
> the very first cell, what were its limits? Was it impossible for that
> cell to evolve a flagellar apparatus? Certainly not since it is here.
> Was it impossible for that cell to evolve a camera type eye? Nope.
> How about a bat or a pigeon or a pine tree? Nope. So then, where are
> the limits?
Again, your incredulity does not make all evolutionary scenarios
logically equivalent. In fact, your incredulity is pretty much
irrelevant.
Was it impossible fo a cell to evolve a flagellar apparatus? No, not
if it already had some form of secretory system, the ability to
produce tubulin filaments, and many if not most of the other
components that go into making a flagellum. If there were no basis
for suspecting it actually had any of those things, or any selective
pressure favorable to their appearance, we might worry.
Was it impossible for a cell to evolve a camera type eye? Well, I
think camera type eyes are pretty much a property of multicellular
creatures so I'm not sure what you mean by that. But there has
already been work done on how it could have evolved by a series of
selected-for intermediates, and there will almost certainly be more
research done in the future. Evolutionary biologists aren't just
waving their hands and saying anything is possible. They leave that
to ID advocates.
>
> You just don't like the fact that these limits do in fact seem to
> exist and so you try to claim that your theory has already taken all
> this into account. . . when it really hasn't. These limits really
> are significant enough to destroy your theory. That is the problem
> and that is why you are trying to blow smoke over this whole mess.
I did not make up the notion of evolutionary constraints. It exists.
It is part of the theory. That evolutionary theory takes them into
account is not something I "try to claim". It is a fact.
As for problems significant enough to destroy "my" theory: you have
not demonstrated that any such problem exists. Apart from incredulity
and some armchair calculations whose accuracy you cannot possibly
know, your only argument is a claim based on an irrelevant conclusion
from one of Hall's experiments, a claim which may already have been
falsified by other research.
As for evolutionary constraints, I personally like them very much. It
would be very bad for all of us if there were no such constraints, and
if the nastertiums my mother plants in her garden could sprout funnel
spiders. Fortunately, that doesn't happen, except in Dr. Pitman's
absurd version of evolutionary theory.
More later.
RobinGoodfellow
[snip]
You beat me to the nomination! Thirded.
Von Smith
> > But your theory isn't simply that "neutral gaps" exist. That would be
> > fairly uninteresting, and of no real importance to the theory of
> > common descent at all. Your theory is that they are so pervasive as
> > to preclude evolution of life as we see it today in the available
> > history of the world. The fact that chloroquine resistance may take a
> > large population several years to evolve hardly supports such a
> > generalization.
>
> There is plenty of evidence to support the idea that neutral gaps are
> extremely pervasive. The experiments of Hall and the evidence
> supplied by chloroquine resistance are only parts of the puzzle. They
> support this position very well.
I fail to see how evidence of the evolution of novel functions is
evidence against the evolution of novel functions, but OK, if you say
so.
> It is actually you and your position
> who have very little evidence to suggest that these gaps are not very
> pervasive or that they do not really interfere too much with the
> evolution of new and increasingly complex functions. What evidence do
> you have to counter my position? What examples of evolution can you
> point out to prove me wrong?
First of all, it doesn't work that way. Your entire ID argument
relies upon an eliminative inference: you have no *positive* evidence
for your designer, so you go about making your case by trying to
eliminate competing possibilities, and declaring victory for your own
hypothesis by default. That means, among other things, that you bear
the burden of demonstrating that evolution is not a practical
possibility. You don't get to take the position that it is wrong by
default. If you had simply taken the skeptical position that you
didn't buy common descent based on the evidence you'd seen, things
would be different. You would be well within your rights to demand
whatever evidence could reasonably be expected to satisfy you. But
since you have gone beyond mere skepticism and made the positive claim
that evolution is impossible, that becomes the point that needs to be
proven. I don't see that you have done that, so basically, there is
no argument for me to refute.
If you feel that this burden is unfair, then don't make the claim.
>
> As far as I can tell, the best you have is antibiotic resistance,
> chloroquine resistance and other types of drug resistance, and the
> occasional new single protein enzyme. Is that it? What kind of
> evidence is that? All it is based on is the idea that it is easier to
> break something that it is to create something from scratch and
> occasionally, one might actually make something that does not really
> on breaking something else, as long as this new function is extremely
> simple and relatively common. You call that evidence?
Since most of evolution proceeds precisely by "breaking" something
that was there before, rather than creating from scratch, yes, I call
that evidence. The central idea of common descent is that it is
descent with gradual modification. "Modification" means that just
about everything we see in life is a modification of some earlier
structure, often at the expense of its original function. Because any
lineage must maintain a certain level of fitness to survive at any
stage in its history, and because few individual mutations lead to
dramatic beneficial changes in morphology, this modification is
necessarily "gradual". That is far more similar to breaking something
than it is to creating from scratch.
You are not a created-from-scratch being. You are a developmentally
retarded proto-chordate that never outgrew its brain and notochord
(something that urochordates and sea urchins have only in their
immature stages of life). You are a broken fish that would no longer
last a day in your ancestral aquatic environment. You are a broken
amniote whose quadrate and angular bones now rattle around loosely in
your middle ear, and who can't replace your teeth more than once in
your whole life. You are a broken mammal with no claws with which to
combat predators, who can't produce your own ascorbic acid, and who
doesn't have enough hair to keep your body warm on a cold day. You
are a broken ape who can barely brachiate at all, or grasp anything
with your toes; you have a grossly deformed cranium that makes
childbirth extremely painful and hazardous for the whole species (or
at least for about half the species). Your ancestors had to leave the
jungle and forage in the savannah because even the bonobos could kick
your ancestors' sorry australopithicene butts.
You are as much a broken Humpty-Dumpty as you are a put-together one.
Which is exactly how evolution works.
Except of course that it isn't quite as simple as you make out.
Chloroquine resistance seems to be acquired by changing the transport
proteins on the membrane of a particular vacuole in such a way that it
retains its original function while excluding chloroquine. This would
be a subset of all sequences that can produce a transport protein at
all. Is the sequence density going to be larger or smaller than the
sequence density for evolving some sort of transport protein? Are
there more sequences with high transport activity but little or no
chloroquine resistance, or with suboptimal transport activity and
substantial chloroquine resistance? I don't know, and I don't think
the answer is as self-evident as you make out. Fortunately, the
question is probably irrelevant. What matters is the evolutionary
distance between the precursor and the derivative, and whether
selective pressures will facilitate bridging this distance in a
reasonable amount of time. In this particular case, the environment
selects for any resistance to chloroquine at all, even if it is
purchased at the cost of considerable transport efficiency.
>
> > So obviously you have no idea what the sequence density for any given
> > function is ahead of time,
>
> Actually I do have a very good idea about sequence densities ahead of
> time. You tell me the type of function and I can predict for you,
> with a fair degree of accuracy, how easy that function will be to
> evolve.
OK. What is the sequence density for lactase activity?
What is the sequence density for beta-lactamase activity?
What is the sequence density for ESBL activity?
What is the sequence density for electron transport?
> Functions that are based on the interference of
> pre-established interactions will take a lot longer to evolve than
> those functions that are not based on the interference of other
> functions. Some enzymes are more simple than others. More or less
> densities might be involved. However, as a rule, the functions of
> enzymes are far less dense than the functions of various types of
> antibiotic resistance described above (the ones that do not involve
> enzymes obviously).
Can you provide (and justify) actual estimates for the sequences
densities I asked you for?
>
> > Although you are good at saying: "See, I
> > knew that!" after the fact.
>
> Not after the fact at all. You come up with a new antibiotic, I will
> predict right now that resistance to that antibiotic will happen real
> quick like. You come up with a new enzymatic function, and I am
> betting right now that this new enzymatic function will not be
> realized by very many life forms if any. You come up with a new
> function that requires a dozen or so proteins all working together at
> the same time and I am betting right now that no life form will evolve
> this function or anything equivalent in your lifetime or by the time
> your offspring have reached a billion generations.
Fine. Calculate the sequence densities I asked you for above, and
justify them. Give me a 50% and a 90% confidence interval.
>
> > Nor do you know what the available
> > evolutionary pathways were, nor what sort of fitness landscapes they
> > traversed.
>
> Certainly not, and neither do you. I don't believe that these
> pathways exist, so why would I even hope to know what they were? I
> think the evidence clearly supports this position. You have no
> evidence about how your supposed fitness landscapes did change or
> could have changed in a way that could have even theoretically produce
> the variety that we see in the world today.
> You have faith that such
> pathways and landscape changes did exist and did in fact give rise to
> what we find today, but you really have no clue as to how it worked or
> could have worked. You have a bunch of just so stories, but no real
> evidence to back your stories up.
Not at all. That such pathways and landscapes exist is not so much an
article of faith as a prediction. A prediction that could be
falsified by the data, and would be continuously if the theory were
false. Paleoanthropologists didn't just take it on faith that there
might be viable human ancestors out there somewhere, or that the
fitness landscape would be just right; they figured out what those
ancestors were likely to be, and where on earth they were likely to be
found. They went to Africa and started digging. They might have
found nothing. Certainly they've found precious few fossils of
chimpanzees. But they didn't find nothing. In addition to the
fossils, they studied the other life-forms in the area and the
paleosols for clues of environment and climate.
Microbiologists didn't take it on faith that the flagellum must just
have evolved somehow. They reasoned that if they had, there would be
clues that might be found in comparisons with structures in other
microorganisms. That is a testable predictions: if the flagellum
evolved, there ought to be homologs in non-flagellate microbes as
well. There ought to proteins with substantial sequence-similarity
serving other functions. These functional homologs should suggest an
evolutionary pathway that could preserve fitness.
They looked, and they found what they predicted. Most if not all the
major sub-components of the flagellum can be shown to contribute
individually to the fitness of various other microorganisms, and it is
fairly easy to demonstrate how the components can be added one at a
time in ways that contribute to fitness. There is no "keystone".
Many of the proteins can be shown to share substantial sequence
similarity with one another, exactly what one would expect from a
process that would be expected to involve gene duplications, probably
multiple ones. The flagellum could have looked exactly like Behe
describes: an IC machine with unique components. It doesn't.
I do not consider the ubiquity of homologies at both a morphological
and molecular level that is implied by common descent to be an article
of faith; it is a very strong pattern in what we actually observe, and
it is a prediction about what we will continue to observe. On the
level of gross anatomy, this is trivial; there are no new structures
that set us apart from other primates; we have a bigger brain, but it
is basically just a souped-up primate brain, not something sui
generis. Apart from that, there is no difference between us and
chimpanzees that you probably wouldn't dismiss as trivial if they
appeared in other creatures. There aren't really any truly novel
structures that distinguish us from more typical mammals, either. All
of our anatomical differences are, to use your phrase, "variations on
a theme" that present nothing unique.
And that is what we see on the molecular level as well. We don't see
unique proprietary designer molecules that don't look like anything
else but themselves. By and large we see "variations on a theme",
exactly what evolution would produce. We find enzyme cascades built
largely out of multiple copies of the same enzymes, subsequently
modified. We find that these proteins, in turn, share substantial
sequence similarity with other proteins that serve completely
different functions, ones that would have existed in ancestors before
the appearance of the cascade. Five of the enzymes in the
blood-clotting cascades are all homologous to trypsin, a protein that
has nothing to do with blood clotting at all.
Looking for the sort of precursors you are so confident don't exist is
as vibrant a research program as any in science today. It wouldn't
still exist if it didn't produce results. It wouldn't have any
structure or coherence if it routinely failed to even generate leads.
Your contempt of evolutionary biology seems to stem from ignorance,
not knowledge, and your rhetoric in this post bears this out.
> All you have is a bunch of hopeful
> people on your side with a very great faith and an overactive
> imagination. You expect me to give you far more evidence than you are
> willing to produce yourself.
What is the point of giving evidence if all you will do is sneer at
it? AFAIAC, you have not earned the right to sneer at evolutionary
biology because you don't even understand the theory (indicated by the
fact that you cannot correctly describe its predictions) let alone the
evidence that supports it.
> You have nothing to support these
> imagined evolutionary pathways and tree of yours. Truly, the
> important missing links are not those missing from the fossil record,
> they are the missing genetic links from the imagined phylogenetic
> trees of life.
And what missing links are those? I haven't heard of any. Name one
functioning molecular sequences that you can demonstrate to be
separated from any avaiable precursor by 30 neutral gaps. Or 20, or
10. How is that asking for too much evidence for your claim? How
much less evidence do you think you ought to have to provide? Your
own assertions and incredulity?
Phylogenetic analyses are not imagined; they are based on actual data,
and on mathematical analyses of that data. They are based on exactly
the same sort of methods used to identify and trace strains of
illnesses and viruses, and on the same methods that established the
illegitimate heirs of Larry Hillbloom in the absence of DNA from him
or any of his acknowledged family members. They are based on methods
that have been tested blind in the lab on mutated populations of
viruses, and found to work. They have also been found to agree to a
significant degree to phylogenies already constructed based on other
lines of evidence. I think phylogenies are far more real than your
neutral gaps. They certainly have more data and sounder methods to
support them.
>
> > Nonetheless, you are sure that there are enough neutral
> > gaps around to prevent evolution of many of the functions we observe
> > in life today; you base your confidence on the "statistics involved",
> > which enable you to predict with confidence that the density for
> > functional sequences in a sequence space is somewhere between 1 in 3
> > and 1 in 1e106 (or perhaps even as low as 1e1277).
>
> Depending on the type of function in question, this range is quite
> easily supported. But this is not the worst of it. The range gets
> far worse when you start including those functions that are based on
> multiple proteins all working together at the same time. For such
> levels of complexity, the "density" might be as low as 10e1000e1000.
> And then, it gets worse. . .
And this number comes from where?
>
> > > Obviously,
> > > a neutral gap in function of 6 or 7 base pairs can easily be crossed
> > > by random walk alone given the much larger population sizes of the
> > > malaria parasites (P. falciparum) that exist in the wild as compared
> > > to the relatively limited population size that was most likely used in
> > > the laboratory experiments. No ID is needed to explain the evolution
> > > of chloroquine resistance in either case. The average time required
> > > is well within reason.
> >
> > OK, so at least you are smart enough not to deny the evolvability of
> > something that has been observed to evolve.
>
> If the numbers make sense, and they do, then such an observation is
> not a mystery at all.
Which numbers? The ones you guess? You have never explained your
method for estimating sequence density. Since you throw out actual
numbers, it is certainly reasonable to justify them. I have seem Ian
Musgrave and others cite figures that actually *have* appeared in the
literature. They seem to range from 1e12 to 1e20, not for some
arbitrarily specified function, but for *a* function that would
potentially be of use to an organism, which is all that is required.
<snip>
> >
> > Right, and the history of life is certainly replete with such losses
> > of function. The loss of fins in early amphibians was certainly a
> > loss of function; critters like ichthyostega were no longer as
> > efficient swimmers as their fish counterparts, because their fins had
> > been replaced by deformed protrusions that were fit for little more
> > than scudding along the bottom of shallow waters. Mammals have
> > "broken" reptilian jaw hinges which have lost their function; now they
> > do nothing more than rattle around in our middle ear, creating these
> > annoying vibrations inside our heads. Humans and other apes have
> > "broken" claws that are useless for fighting. All we have are these
> > stupid flat cuticled fingernails. If we want to scare off a lion, we
> > have to resort to something like a rock or a pointed stick.
>
> LOL - too funny. This is classic. Often when I ask for examples of
> evolution in action, all I get are a bunch of examples detailing the
> loss of previous functions. Certainly this is a type of evolution,
> but you must admit that breaking Humpty Dumpty is a far cry from
> explaining how Humpty Dumpty got put together to begin with! ; )
Don't be obtuse. The optimization of any new function very often
entails the loss of a previous one. That is exactly what
"evolutionary constraints" are all about; the plasticity of life forms
is constrained by the need to maintain a level of fitness throughout
any changes that occur, and by the fact that those changes are
generally gradual. I'm sure that you understand full well what my
examples above are referring to, and that this is exactly how
evolution is supposed to work. But just to make it more explicit:
The evolution of terrestrial vertebrates involved a loss not only of
fins, but also of every other function that enabled their ancestors to
live in the water. The evolution of the mammalian middle ear, with
our corresponding hearing acuity, only evolved at the cost of losing
the reptilian quadrate-angular jaw joint, and was only able to happen
after another solution to the jaw problem was available. And our
ability to grasp and manipulate objects with dexterity, which stems in
part from our not having long, sharp claws in the way, was purchased
at the expense of losing a major natural weapon. I assume you can
appreciate the irony of insisting that the development of improved
hearing, the ability to live on land, and the ability to manipulate
objects were all simply "losses of function", and yet that is exactly
what you have done.
I'm not sure exactly what you mean by "how Humpty Dumpty got together
to begin with". Perhaps you mean abiogenesis or the first
multicellular life or what not. Assuming their was some sort of
content behind that particular sneer, I would appreciate it if you
would make your argument a bit clearer.
<snip rest>
Howard Hershey
hers...@indiana.edu wrote on 6/14/03 7:12 PM:
[snip]
I forgot, although I actually had thought of it at the time, to add 5) Loss
of function. One mechanism by which resistance to a toxin can occur is loss
of function (because many toxins must be biochemically converted in the cell
to the terminal toxin, and knocking out a gene that converts the non-toxic
precursor to the toxin, if the gene is not necessary most of the time, is an
easy evolutionary solution). This often has 'unintended consequences', such
as the build-up of intermediate chemicals that ordinarily are present in
only small amounts. This can lead to secondary pathways when these
intermediates get shunted off by enzymes for which they are secondary
substrates. Whether the 'unintended consequences' is good or ill is
measured by natural selection and can lead to subsequent modification of
other genes to adapt to this change, producing IC adaptation.
Loss of function is a pretty common evolutionary tool (often accompanied
with a modification of other parts). For example, amphibians can extract
oxygen from gills, skin, and lungs (as can lungfish). The reptiles that
evolved from amphibians (and the birds and mammals from them) have *lost*
the ability to extract oxygen from gills and skin (secondary to selection
for ability to live in less aqueous environments) and concentrated on
modifying lungs as a source of oxygen.
No guarantee, of course, that I haven't still missed some other mechanism.
>
[snip]
Howard Hershey
significant or profound.
The human genome has about 30,000 genes.
The first ur-organism appeared 30,000,000,000 years ago.
So how often does a 'new' gene need to appear within the evolutionary
lineage from ur-organism (with, say, 300 genes) to human genome with 30,000
genes? Keep in mind that many of the 30,000 genes are members of gene
families that can rather easily be accomplished by simple duplication and
divergence, so we are probably overestimating the difficulty.
We would need an average of one 'new' gene each 3,000,000 years, by my
calculations. Actual numbers, of course, are slightly different (3.5
billion years and 29,700 new genes), but the above is a back of the envelope
calculation of what would be needed.
Von Smith
<snip>
>
> > > Obviously more time is required to evolve the enzymatic functions than
> > > the functions of antibiotic resistance. That question is, "Why?" Why
> > > is more time required to evolve functions of increasing complexity? I
> > > am proposing that neutral gaps are the reason for this observed
> > > phenomenon. What is your explanation?
> >
> > My explanation is that you claim with hindsight a level of complexity
> > based on what you already know about the evolutionary pathway, so that
> > your "theory" is basically a circular argument that lacks the
> > predictive value you need for it to be pose much of a challenge to
> > evolution.
>
> All hypotheses are based on "hindsight". All observations happened in
> the past. Based on these "hindsight" observations one makes
> hypothesis or predictions about the future. I predict that enzymes
> have been and will always be harder to evolve than antibiotic
> resistance functions.
Again, some enzyme functions *are* antibiotic resistance functions.
They aren't distinct categories. If you're going to refer to them as
distinct categories, you need a better term, I think.
> This is not a circular argument at all. It is
> hypothesis that is based on past experience and past evidence that
> makes a prediction based on this evidence that can be tested in a way
> that will give it predictive power.
>
I notice that Howard Hershey has done an excellent job of explaining
how evolutionary theory explains the difference between enzymes and
antibiotic functions (for lack of a clearer label right now), so I
will not expand on that. I would just note that parsing the problem
in terms of "complexity" isn't really helpful. How is an enzyme
function any more complex than antibiotic resistance, except for the
fact that I am pretty much guaranteed to have functional precursors
for the latter (which is what the antibiotic was targeting in the
first place), but not for the former? Is the exact same lactase
function more "complex" for an E. coli without an ebg gene than it is
for one that has it? But that isn't a meaningful definition of
complexity, since it depends as much on the current genome of the
organism, as well as the shape of the fitness landscape as it does on
anything else.
If, on the other hand, an organism *does* happen to have a viable
precursor to an enzyme function, as in the case of the ebg gene in
Hall's experiment, then this will proceed fairly quickly. It doesn't
matter what the prior odds are that an organism will just happen to
have such a precursor; we are looking at functions that have already
evolved, so the probabilities need to be conditioned on what we know.
If evolutionary theory is correct, then when we look at the evidence
we will find that organisms almost always "just happen to have" other
genes with near sequence-similarity as precursors to their current
functions. And that is exactly what we see.
A good half of our genes appear to be copies of other genes, many of
which we share with other organisms serving different functions. Our
blood-clotting cascade evolved the way it did because early chordates
just "happened to have" proteins like trypsin and fibrinogen already.
The eubacterial flagellum evolved the way it did because its ancestor
just "happened to have" tubulin structures, protein transport
mechanisms, and chemosensing abilities already. This is exactly the
sort of pattern of homology that motivated the proposal of common
descent in the first place.
> > > > We all agree that
> > > > evolution takes a long time. Building enzymes from scratch is actually
> > > > more a part of abiogenesis than evolution, but most scientists would
> > > > agree, I think, that abiogenesis took a billion years or so, not a few
> > > > months, even with artificially boosted mutation rates.
> > >
> > > Oh, so the evolution of even one little protein sequence is based on
> > > "abiogenesis" not on evolution? Really?! This is *most* interesting.
> > > This is exactly my whole point. Abiogenesis is based on neutral
> > > drift/random walk. Natural selection really is limited when it comes
> > > to ideas on abiogenesis since by far most of the changes in
> > > abiogenesis are functionally neutral as far as a mindless nature is
> > > concerned. This is why scientists think that abiogenesis took
> > > billions of years to produce the first self-replicating cell. But
> > > why? Why does abiogenesis take so long? Because of the neutral gaps.
> > > When you actually start plugging in the numbers and doing some real
> > > estimates based on the idea of neutral gaps, you quickly find that the
> > > abiogenesis of much of anything would take far longer than a few
> > > billion or even many trillions or zillions or googols of years.
> >
> > Actually, the oldest accepted unicellular fossils are about 3.6 Gya,
> > indicating that life arose within no more than a couple hundred
> > million years after conditions on earth made it possible.
>
> That is the theory anyway . . . which is quite amazing indeed.
Fossils are not theories. They are physical evidence. And yes, it is
amazing. Did you expect life to be otherwise?
> A few
> million years is all that is needed to get random molecules to self
> assemble themselves into a living organism. Amazing speed isn't it?
I don't know if this time frame is amazing or not. Depends on what
the actual mechanisms involved are. At least a few of the processes
that may have been involved seem to happen fairly readily, such as the
spontaneous evolution from a simple replicator into one that expresses
a catalytic cycle, or the self-assemby of monomers and oligomers on a
suitable surface, or the appearance of enzyme-like activities in
random sequences of RNA, even the formation of proteinaceous spheres
that may give some indications as to how cells might have come about.
> In any case, I only used the "billion years" figure because Bill used
> it. It wasn't an important point to challenge him on.
>
> > And I would
> > love to see you "start plugging in the numbers and doing some real
> > estimates". All you need is a detailed model of what the likely
> > precursor molecules were, what their population size and composition
> > was like, what their mutation and replication rate was like (both
> > probably much faster initially than that we typically see in life
> > forms today), what the environment was, what the fitness landscape
> > looked like over the sequence space and what evolutionary constraints
> > there were (since the earliest replicators would have had few
> > functions, there was almost no place to go but up, as someone quoted
> > Maynard Smith as saying elsewhere).
>
> Almost no place to go but up? Amazing! I thought you said that
> depending on your starting point there could be a lot of restrictions
> to evolution? In any case, I'll give you every benefit of the doubt.
Actually, you'd be better off not pretending to misunderstand my
argument. I would very much prefer that to a "benefit of the doubt".
The connection is obvious: an organism with fewer functions will have
fewer constraints, since just about any mutation that doesn't destroy
replication won't really hurt it, as well as more possibilities of
improve fitness, since it is starting out very low on just about any
fitness landscape, and will be under all sorts of selective pressures.
Does that mean that it's plasticity is infinite and that it can turn
into a bird at any time and fly away? Not at all. It took more than
two billion years for even the first multicellular life to evolve, and
that evolution appears to have evolved at least one major
endosymbiosis event, and probably quite a few horizontal transfers as
well. It didn't just happen with point mutations.
> Start with a relatively advanced E. coli bacterium as your first
> creature. E. coli have a relatively rapid generation time, as fast as
> 20 minutes or so. Give these E. coli all the food and building blocks
> they need to grow and massively reproduce to cover the entire globe
> and every available square millimeter of water on earth. They still
> would never get across a gap of just 30aa in 4 billion years.
Nor have you provided a shred of evidence that they would ever have
any need to. Can you name one function that you can demonstrate to be
separated from all others by a neutral gap of 30aa? Can you point to
a missing link of this magnitude anywhere? If not, why entertain such
a notion?
Also, why are gaps being defined in terms of individual residues?
Point mutations aren't the only kind. Insertions, deletions, exon
shuffling and frame-shifts can bridge such gaps in a single pop.
Consider nylon oligomerase: How many aa apart is the oligomerase from
its precursor. The mutations involved seem to have been a 93b
insertion plus a frameshift mutation to a previously non-functional
bit of DNA. I'm willing to bet that's a bit more than a 30aa gap, yet
it happened fairly readily. Perhaps it would be more accurate to
measure neutral gaps in terms of possible mutational steps rather than
in residues?
Also, why would I want to start out with a relatively advanced
organism? As has already been pointed out, an advanced organism has
more evolutionary constraints, not fewer. Using an advanced organism
potentially makes things harder, not easier.
>
> Now, you explain this same scenario and detail to me how these E. coli
> could evolve new functions of increasing complexity. Make your
> description a genetic description and not a morphologic description as
> is so often done. You must explain using genetics or even other coded
> systems like the letters of the alphabet and comparisons to the
> English language system as to how this evolution could have taken
> place.
Why not use a real-world example? Show me a naturally-occuring
protein sequence that you know for a fact is separated from all other
naturally-occuring protein sequences by 30 or more neutral mutations
(to include insertions, deletions, frameshifts, etc. not just point
mutations). Explain why you think that the gaps are all neutral, and
that none of them are likely to have been selected for during the
organism's evolutionary history. Tell me what the nearest known
sequence similarity to the protein actually is, and in what organisms
it is found. Do you have such an example? If not, then why should I
address a possibly irrelevant problem?
>
> > I'm sure you'll be able to
> > estimate the length of time it would take to within about, oh, 106
> > orders of magnitude (given that error, what you estimate to take
> > googles of years could actually have taken place within a few minutes
> > or even seconds)
>
> Oh really? A few seconds? How so? Explain your marvelous hypothesis
> to me. I'll even give you access to a ball of bacteria with a
> diameter the size of the galaxy. . . . and you still couldn't do much
> in just 4 billion years.
You don't know that because you're just making up numbers as you go
along. That was my point.
Perhaps you are taking "simple replicators" a bit too literally. The
earliest life forms would already have had some catalytic and
metabolic function, although not nearly as many as even the simplest
life-forms we see today. The work of Szostak and Ekland in RNA
sequences, and of the Ghadiri group in self-replicating ligases
suggests this.
You also seem to be confusing evolutionary constraints with selective
pressures, or lack thereof. Evolutionary constraints are
considerations that can keep an organism from evolving greater fitness
in *spite* of positive selection. Cytochrome c probably didn't evolve
until there was some selection for it; the point is that once there
was, there were probably very few functions that a relatively
primitive replicator couldn't have afforded to give up in exchange for
the benefits of improved electron transfer. Early life would have
little trouble evolving a lot of different proteins -not necessarily
all the ones we see today, but a broad base of precursors from which
later life could evolve.
>
> snip
> > > > Antiobiotic resistance is often easy because
> > > >
> > > > (1) The gene already exists on plasmids in wild populations of the
> > > > bacterium in question and the plasmid is exchanged in the bacterial
> > > > populations (that is the case for some forms of penicillin
> > > > resistance). Remember, we've only been using penicillin for 60 or 70
> > > > years, but fungi have been using it for millions, so the bacteria have
> > > > had plenty of time to develop a suite of resistance genes.
> > >
> > > That is a nice "just-so" story that many use to explain the origin of
> > > rather complex enzymes like the penicillinase enzyme.
> >
> > We already know that enzymes of comparable sequence lengths can evolve
> > in real time. Ian Musgrave pointed out to you elsewhere that many
> > different novel cefotaxime-resistant strains using extended spectrum
> > b-lactamases have evolved in just the last 20 years or so. I would
> > think that if beta-lactamase is a complex enzyme, then ESBLs are even
> > more complex, wouldn't you?
>
> When I started reading this paragraph I thought you claimed that you
> were going to point me to an example of an "enzyme of comparable
> sequence length" that could or did "evolve in real time." You did
> nothing of the sort. Your example is not a sequence of "comparable
> length" at all. Your example is an example of an alteration of an
> existing enzyme, not its original evolution. So, how do we know that
> such enzymes of comparable length and complexity "can evolve in real
> time"?
I find it difficult to believe that you were stupid enough to think
any such thing, but it's a nice rhetorical ploy anyway. Alteration of
an existing enzyme to serve a novel function *is* the evolution of a
novel enzyme. That is how evolution works.
>
> These bacteria did not evolve these enzymes from scratch. They were
> already making these beta-lactamases to begin with. When the new
> synthetic antibiotics came along, all that they did to combat the new
> antibiotics was to alter their pre-existing enzymes with one or two
> point mutations so that the interaction with the antibiotics would be
> enhanced. No beta-lactamases were evolved without a prior existence
> of the code for such enzymes. The ESBL's are hardly more complex than
> the original beta-lactamase enzyme. In fact, I would say that they
> are really no more complex. It would be just as hard to evolve the
> ESBL's as it would be to evolve the original beta-lactamase enzyme to
> begin with, starting from scratch.
You are absolutely correct. The enzymes didn't evolve from scratch.
They didn't have to. One prediction of evolutionary theory is that
the functions we see in life today evolved from pre-existing ones.
This means that, wherever we find an apparently unique activity, it
will in fact usually turn out to be a modification of an already
existing one that we "just happened to have". I say "usually" because
there are occasions, such as the case of nylon oligomerase, where a
new function arises from scratch. This would have been important in
early life as well. Evolution is descent with gradual modification,
not descent from scratch. That's what people have been trying to tell
you all along. That's why your neutral gap nonsense is a crock. You
want to refute the theory that any arbitrary genetic sequence can
evolve any pre-specified function in a very short time. You want to
call this theory "evolution" but it isn't. In fact, no such theory
exists except in creationist literature.
>
> Come on man . . . Don't you have anything better than this?
>
No, and until you can prove otherwise, I don't need anything better
than this. Neither does life.
> > I'm guessing that, no, *you* probably wouldn't think that, because you
> > would already have "peeked" at the evolutionary pathways from known
> > precursors and asserted that the evolution of ESBLs from an ancestor
> > was "trivial".
>
> It was trivial and that is only to be expected. A series of
> sequentially selectable variants is quite trivial. No neutral gaps
> need be involved or would be expected to be involved in such a
> scenario. Try getting an ESBL from scratch however, and we'll just
> see how easy it is. Delete the original beta-lactamase from the
> genome and then see if you can ever demonstrate the de novo evolution
> of an ESBL or even a regular beta-lactamase for that matter. You
> can't. That is certainly curious.
Not at all. It is exactly how evolution works. If you had deleted
primates from earth about 8 million years ago, humans would not have
evolved either. Fortunately, we don't find any structures in life
with all viable precursors "deleted". We don't find sui generis
functions. We almost invariably find homologs for them. We find
functions that are variations of other functions that the organism's
ancestors "just happened to have". It was this pattern that suggested
the theory of evolution in the first place.
>
> > Of course, if you didn't already know the pathway, you
> > would have no way of making such an argument.
>
> Certainly I would. There are many "generations" of beta-lactams now.
> I expect that there would be more "generations" coming along in the
> future. I predict that with just a few mutations the current
> beta-lactams will be able to adjust to these new antibiotics in short
> order. It isn't so complicated you know.
OK, so whats the problem? One implication of what you are saying is
that even apparently primitive beta-lactams are probably relatively
late generations of earlier proteins, whose activities would have been
different. At some point they were probably as poor at resisting
penicillin as classic beta-lactams are at resisting methicillin or
cefotaxime; they did something else instead. This isn't so
complicated either, it is exactly how evolution works, and it is
implied by what you yourself argue above.
>
> > In spite of this, it
> > doesn't seem to bother you in the least to make pronouncements about
> > the complexity of a function in the *absence* of such extrinsic
> > knowledge about the evolutionary history of penicillinase: you are
> > somehow convinced that it must be unevolvably complex by default until
> > it is proven otherwise.
>
> Can you demonstrate it or explain it? The best you can come up with
> are variations on a theme, but you can't come up with the theme
> itself? Please, what do you have that makes you so sure you are
> right?
How sure do I have to be? The observed ubiquity of homologies
indicate to me that all the functions we see in life today are simply
variations of themes that our precursors "just happened to have". Can
you name a single function or structure you can reasonably demonstrate
to be sui generis, that isn't just a variation of some theme found
elsewhere in life, exactly the sort of variation you have already
admitted can evolve? The flagellum isn't sui generis. Lactase
function isn't. Human morphology certainly isn't.
>
> > > It may be true,
> > > but until it can be demonstrated or until some real statistical
> > > calculations can be made to estimate the number of neutral gaps that
> > > would need to be crossed, it is just a story without any real backing
> > > in actual evidence.
> >
> > As is *any* talk about neutral gaps, including yours. Funny, when I
> > first pointed out that one needed such detailed knowledge of the
> > evolutionary pathways involved to meaningfully estimate neutral gaps,
> > you seemed to consider this an unreasonable burden of proof on you.
> > But here you lay down exactly the same requirement (for exactly the
> > same reason) without blinking when it suits your argument.
>
> The fact is that the current evidence for neutral gaps is
> overwhelming.
Then please present it. Find one function that is separated by at
least 30 neutral gaps from any possible precursor. Find one function
that appears to be sui generis, and not a possible homolog of some
other structure.
> In order to overcome this evidence, you must present
> something that at least explains how they really aren't all that
> significant. What have you done to do this? You have to have at
> least *some* evidence you know. You are the one claiming that
> bacteria turned into trees, bears, bugs, and humans.
That is an
> impressive, counterintuitive statement. What genetic evidence do you
> have for this?
There are molecular phylogenies that provide such evidence. They
correspond to a significant degree with the theory of common descent.
What sort of genetic evidence were you talking about?
> Where are your demonstrations? Where are your
> calculations of probability? Where are your predictions for the paths
> and time involved for the crossing of these imagined paths of yours?
Where are yours? I see a bunch of made up numbers whose values vary
from 10e12 to 10e1000e1000. Can you justify any of them?
>
> You want me to prove you wrong, but you don't really want to have to
> come up with any evidence to support yourself.
I don't have to prove anything. You are the one that has a problem
with a well-established scientific theory. You are the one who
proposes the paradigm shift. Evolutionary theory doesn't need me to
defend it. It has paid its dues and justified its existence, as much
as you might not like that. ID has nothing but hot air, made-up
calculations, and arguments from incredulity, or at least you don't.
> You make up stories
> that really cannot be falsified and then you say, "prove me wrong."
> You say, "You can't prove beyond all question that a path could have
> existed somewhere." Well no I can't, but neither can I prove beyond
> all question that there is no elevator to the moon.
Well then you have a problem, because such a claim is precisely what
eliminating evolution as an explanation entails, and your case for ID
rests almost entirely on the claim of such an eliminative inference.
If you want a different burden of proof, try a different line of
argument, may I suggest one that tries to make a positive case for a
positive claim.
> It is the weight
> of evidence, not the providing of absolute evidence, that is important
> here.
The weight of what evidence? Please explain to me again the evidence
for pervasive neutral gaps.
> You have yet to provide convincing evidence that an
> evolutionary path even possibly existed. The evidence is that such a
> path most likely did not exist.
That doesn't seem to be what any of the scientists working in the
field think. Why should I trust your incredulity over their work?
> There are no absolutes. What you
> have to do is to show that such a path *probably* did exist. Good
> luck.
>
Evolutionary path for what? What evolutionary path would you like to
discuss? The flagellum? Human anatomy? The blood-clotting cascade?
The evolution of molluscs? Of whales? Beta-lactamases?
<snip rest>
Howard Hershey
hers...@indiana.edu wrote on 6/15/03 3:55 PM:
Once every 1,000,000 years, not 3,000,000. I had the right number written
down, but somehow had a brain deletion event between that organ and my
fingers.
Note that I also forgot about polyploidy as a wholesale mechanism for
increasing the number of genes, some of which can, because they are
redundant, form 'new' genes with related or different functionalities.
And a million years implies about 5-6 different genes in the human lineage
after divergence with chimps. I suspect rather fewer actual new or novel
genes (as opposed to modified genes, aka alleles, present in common in both
chimps and humans or modified expression of such existing genes), however.
But I could be wrong.
Sean Pitman
> in article 80d0c26f.0306...@posting.google.com, Sean Pitman at
> seanpi...@naturalselection.0catch.com wrote on 6/13/03 7:23 PM:
> >> Some antibiotic resistance genes encode enzymes.
> >
> > Yes, penicillinase is an enzyme that destroys the antibiotic function
> > of penicillin. However, there are a lot of other ways to gain
> > penicillin resistance that are a lot less complex than the evolution
> > of a fairly complex enzyme like the penicillinase enzyme.
>
> Just as there are a lot of mutations that can interfere with and protect
> individuals from malaria as well. Sickle cell is merely one of these.
> There are thalassemias, and favism, and several other forms of Hb changes,
> including HbC. So, yes, there can be simple single mutations that can
> affect complex systems.
And, interfering with a function is far easier than creating a new
function from scratch. That is why it is far easier to interfere with
the antibiotic-target interaction than it is to evolve a new enzyme
like the penicillinase enzyme. The reason for this is that the ratio
of sequences that could produce some sort of interference with a given
function is significantly higher than the ratio sequences that would
create that function in the first place.
> But no one except you ever claimed that a complex enzyme, like
> penicillinase, evolved from *absolutely* random sequences with *no*
> intermediate steps having *any* selectable activity or function of *any*
> sort. Just the opposite. All the evolutionary claims are constrained to
> producing changes that have selectable function *of some sort* after each
> step or few steps.
Yes, this is the claim that is put forward by the theory of evolution,
but this is exactly what has not been demonstrated in a convincing
manner as one moves up the ladder of complexity. What if there are no
selectable functions that are beneficial over the course of several
steps of random walk? The suggestion is commonly made that the
penicillinase enzyme obviously evolved from intermediate sequences
with other types of functions. Certainly, if evolution were
responsible for the creation of the penicillinase enzyme, such
intermediate sequences would have to have existed. The problem is
explaining how this path could or did exist when it has not been
demonstrated experimentally or even theoretically. The neutral gap
problem, even in this case of penicillinase evolution (a single
protein based enzymatic function) has not been explained away.
> Evolution is *descent with modification*, not *invention
> of a needed product from nothing*.
Actually, evolution is supposed to explain how we got here from
nothing. But, even starting with something, the problem is that with
increasing complexity, the ratio of genetic modifications that
actually produce "something" as far as a functionally beneficial
change, becomes exponentially smaller and smaller.
> The latter process is called
> "creationism" of some sort.
Oh really? What then would you call the theory that mindless
processes produced not only the universe, but also life on this planet
. . . starting from nothing?
> That *necessarily* means that some organisms,
> those that lack the appropriate precursor capable of being modified to form
> a new functionality (or that lacks the redundancy to allow modification of a
> redundant copy without losing the original activity) *will not* evolve the
> end product. That is why there are bacteria today that cannot evolve
> "lactase" activity in the short time frame you allow. They lack the
> necessary precursor protein (which need not itself have lactase activity and
> may serve some related function in the cell) capable of being modified to
> "lactase" activity.
Yes, this is the problem for those E. coli and other bacteria that do
not seem to be able to evolve the relatively simple lactase function.
They simply do not have anything close enough to any one of the
potential lactase sequences. This creates a neutral gap between what
they have and the lactase function. This neutral gap is obviously of
such a magnitude that huge populations and tens of thousands of
generations simply cannot cross this gap using random walk alone.
Certainly, this is a problem.
> Of course evolution by natural selection will easily
> work only in those organism that, by the chance vagaries of their historical
> past, chance to have a 'precursor' capable of being modified to the new
> functionality.
Yes, this is what the theory proposes. But, given the size of the
neutral gaps involved, what are the odds that a specific environmental
change or a long span of time for random walks with huge population
sizes, will be able to come across more than a handful of such
functions? And, we are only talking about relatively simple functions
that are based on the potential of single proteins. What about those
functions that require multiple proteins working together at the same
time?
> Other organisms, that lack this exaptive 'precursor' will
> simply either die or not grow as well in media that has lactose as a major
> or sole ingredient.
The key phrase here is "a major or sole ingredient." The theory of
evolution proposes that with increasing competition for resources that
organisms take advantage of various aspects of their environment that
are not being used to their full potential by their peers. Such is
the case with Hall's E. coli experiments. The environment was one
that was lactose enriched, but also had other sugars and sources of
food. As the individuals in these colonies competed with each other
for survival in this environment, it would have been a great benefit
if just one of the bacteria evolved the lactase function and passed it
on to its subsequent offspring. The fact is, they simply seemed
incapable of doing this despite the advantages that would have been
gained.
> Evolution is constrained by the structure of the
> organism being put under selective pressure (or selective opportunity -- as
> in the opportunity to exploit a resource, like lactose, that your neighbors
> cannot).
Certainly this does seem to be the case. Evolution is greatly
constrained by not only the genetic real estate of a given population,
but also by the current environment that this population is living in.
Neither the population nor the environment have access to unlimited
options for evolution to work with. The limited nature of the genetic
real estate and the current environment puts significant limits upon
what evolution can do.
> No one but you claims that *any* organism, put in *any* new environment
> *somehow*, according to evolutionary (due to selection) ideas, *must* be
> able to evolve a function that allows it to survive.
Actually, this is very much what the theory of evolution is
suggesting. The very first organism was quite limited indeed and it
was in a limited environment as well. And yet, it supposedly evolved
many new functions in relatively short order. Really, given enough
time, any self-replicating organism should be able to morph itself
into just about any phenotypic shape and function imaginable, given
the proper environment. As long as the new environment is not
immediately lethal, and time is allowed for extended growth and
competition for survival, then yes, the theory of evolution suggests
strongly that new functions will evolve that allow some organisms to
survive better than their peers in this new environment.
> Nor has anyone but you
> ever claimed that selection is a teleological process which "knows" what
> specific end point must be reached.
I never claimed this either. I'm just saying that given a certain
level of complexity, all the endpoints are equally far apart in the
open sea of neutral sequences. Getting to any one of these rare
islands of function would be difficult and this difficulty increases
exponentially as the level of complexity increases. A given starting
sequence is surrounded on all sides by this sea of neutrality. Moving
in any direction requires the use of random walk. At this point,
natural selection is worthless.
> Evolution by natural selection is a
> blind process working to adapt organisms to local conditions.
Natural selection is not a blind process at all. Random walk is a
blind process but natural selection is not blind when it is actually
working. Natural selection is a real force of nature that works when
genotypic changes actually produce a change in phenotypic function.
The force of natural selection can see such functional changes
clearly. It is not "blind" to these changes. Nature can see and
preferentially select among such functional changes.
> There is no
> guarantee that *all* organisms will be able to evolve to *any* arbitrarily
> stated conditions.
Certainly not. However, what you are basically saying is that the
theory of evolution cannot be tested. Experiments cannot be set in a
falsifiable way because if they fail, all you have to say is, "Well, I
guess we just didn't use the right environment or the right organisms
to demonstrate evolution this time." This always leaves you an out.
Without the theory of evolution being falsifiable in such genetic
experiments, you can always believe in it no matter what the
experiments say. Tell me, what genetic experiments could be done that
would falsify the theory of evolution? Really, unless you can detail
such an experimental result that would counter the theory of
evolution, your theory really is not scientific. You must have a
genetic test that is testable and falsifiable. What is it?
> If there is no pathway from the current state of an
> organism to the end state that includes regular useful functionality at
> intermediate points, evolution by natural selection will not occur.
Agreed.
> If
> there are useful intermediates from which a single (or a few) changes can
> produce a new functionality, it can occur.
Agreed.
> All the "story-telling" pathways
> that we present wrt to flagella are pointing out just such pathways *and*
> the evidence to support those pathways.
Not so. All your story telling about how such pathways must exist
don't even work well on paper and they have never been demonstrated
experimentally in the case of flagellar evolution (or other bacterial
motility systems for that matter). Huge gaps are missing that aren't
really discussed beyond a bit of hand waving to cover them up.
> We fully *recognize* that bacterial flagella (or any complex function)
> cannot evolve by a mechanism in which you start with no useful function
> whatsoever, randomly produce products with no functional utility whatsoever,
> and only get functionality when the final chance step is complete.
Yes, you and most other do recognize this point, that is why you
hypothesize the crossing of such a gap with the proposed existence of
intermediate functional sequences. The only problem is, you don't
have enough of these intermediate sequences. Even on paper, large
neutral gaps remain. And, when it comes to real life experiments, you
haven't even demonstrated the real time crossing of even some of your
proposed steps between your proposed intermediates in the path to
flagellar evolution.
> That is
> precisely why it is necessary that the proteins involved in flagella
> formation must have other utilities or utility as subsets of the final
> flagella.
Yes, this would be necessary.
> They do.
Some of them do, but not all of them. And, even if all of them did
have other functions within other systems of function within the
bacterium, this would not explain how parts of other systems of
function simply came together to form a brand new system of function.
This is just like the problem with forming single protein enzymatic
functions to begin with. All the parts are there to produce the
lactase enzyme. All the amino acids are there, within the cell, as
parts of other proteins. All the DNA bases are there, as parts of
other genes. And yet, they do not self-assemble themselves to produce
the lactase function even in the proper environment. So, a simple
demonstration that all the parts for a required function already exist
within a cell, is not enough to explain the evolution of that
function. You must then explain how all these parts knew how to
self-assemble themselves in the proper way to produce the new
function. That is the trick that simply has not be demonstrated in
real life or even very well on paper.
> In short, evolution by natural selection specifically
> rejects your stated premise that systems evolve by a random walk through a
> sea of totally useless intermediate steps. You have yet to show that any
> biological system appeared by such a system.
LOL - When did I ever say that systems of increasing functional
complexity evolve by random walk? My whole point is that if
significant neutral gaps exist between functions of increasing
complexity, that random walk would prevent their evolution. My
argument is that functions of high complexity did not appear by random
walk, but by design. The theory of "natural selection" does not
reject this hypothesis at all since natural selection requires that
these gaps not exist. The existence of natural selection does not
automatically rule out the existence of neutral gaps or their
exponential growth with increasing functional complexity.
> >> How could you possibly know anything about a "dramatically higher
> >> ratio of functional mutations as compared to neutral mutations in
> >> the development of antibiotic resistance as compared to the evolution
> >> of a certain enzymatic activities" without specifying in a whole lot
> >> more detail what genes you are talking about and without doing
> >> experiments to determine which changes are or are not functional or
> >> neutral? Everything depends on the starting material and the "fitness
> >> landscape" around the point you start from. In some cases you pretty
> >> clearly even "cannot get there from here," e.g., not many feathered
> >> bats, or gilled whales, even though such creatures might be at finess
> >> optima if they existed.
> >
> > If cow-like creatures could turn into whales and reptiles into birds,
> > then why do you think it would be so hard to get bats to evolve
> > feathers or whales to evolve gills if they would in fact benefit from
> > such structures?
>
> Future evolution is constrained by past history.
Yes it is . . .
> It may be possible to
> evolve something functionally "similar" to feathers (in bats) or gills (in
> whales), but it is unlikely that it will occur by the same mechanism because
> of historical constraint.
I am arguing against anything even "similar" to these functional
structures evolving in such creatures even given trillions of years
and all the environmental shifts that you want.
> Evolution is not teleological, Sean. It cannot
> magically poof whatever an organism needs into existence like your
> "intelligent designer" could have done.
Certainly not! We are in total agreement here!
> It has to work via a chain of
> events constrained by history and by the necessity of intermediate
> functionality.
Right again, but what if this chain is broken? What if the links of
the chain are separated from each other in all directions by neutral
gaps that can only be crossed via random walk?
> > Really, the theory of evolution has proposed that
> > such dramatic changes have occurred that practically anything is
> > possible given enough time. The starting point really has little to
> > do with it. All that is needed is the right environment and enough
> > time.
>
> Evolutionary theory does not say this. You do.
The theory of evolution does say this, not me. I agree with you in
your understanding of the limits of evolution, but you evidently do
not understand that the modern theory of evolution is all about the
time involved. As long as the current environment is not lethal, the
theory proposes that organisms will evolve wondrous new functions if
only enough time is given.
> Evolution via variation and
> selection *also* needs for there to be a pathway of intermediate
> functionality working within the structural and functional constraints of
> the organism.
And, this is what you have to demonstrate - The missing genetic links
to your puzzle. I'm saying that these missing links simply do not
exist. You are saying that they do exist. I have show experiments
where they do not exist. What experiments do you have to show that
they do exist - beyond the evolution of the most simple functions of
antibiotic resistance, single protein based functions, or other
functions that are based on the interference with or loss of previous
functions?
> It needs what you assert (since you have presented no
> evidence) cannot ever exist, pathways of intermediacy with functional
> utility (not necessarily the end function, since that would be a
> teleological pathway, not an evolutionary one).
I have presented evidence for the existence of these gaps. It is you
who have presented nothing but paper theories and hand waving to
support your position. You call that evidence?
> > Knowledge of the starting point is only important if neutral gaps do
> > in fact exist and if random walk would in fact pose a problem for
> > evolution. An argument based on the idea of a starting point is
> > really one that is based on the validity of my position.
>
> Knowledge of the entire pathway by which a system arose is important if the
> evolutionary idea is valid, precisely because of the need for functional
> utility in intermediate states. This is why it is important that there be
> 'eyes' with intermediate ability of focusing images in the animal world --
> they demonstrate that the structural intermediate states in a pathway
> between a light sensitive spot and a camera eye (which is similar to what is
> seen during organogenesis) can have functional utility.
Oh . . . the common "intermediate eye" argument again. Don't you
realize that any morphologic collection of items can be categorized in
groups and that all of these groups will have some sort of morphologic
intermediate? I can do this with the books on my bookshelf or the
contents of my desk drawer. Arguments based on morphology are weak
and often contradictory or at best inconclusive. You must get out of
this morphologic appearance mode and start concentrating on finding
genetic intermediates that are functionally beneficial along this
evolutionary path. Arguing from morphology is easy to do, but it is
deceptive in that it covers up the complexity of the genetics
involved. A morphologic change may look really simple, but when you
check out the required changes in the underlying code, it can be very
complex indeed. And again, no one has ever demonstrated even one of
these evolutionary steps in the evolution of one type of eye into
another type of eye. It is all a paper theory, just like the supposed
steps in the evolution of the flagellum.
> That is why the fact that bacterial flagella also function as protein export
> machinery in ways that suggest utility of an incomplete subset of the enzyme
> complex involved in its formation (also shown in the organogenesis of the
> flagella) is important.
Again, a big paper theory with no experimental backing. Not even one
of these supposed steps in the evolution of the flagellum has been
demonstrated to evolve in real time.
> *You* are the one who has to demonstrate a *pathway* in which there is what
> you misleadingly call "neutral" steps (actually, what you are proposing is
> not 'neutral', but what I call 'keystone' or 'group' selection -- that a
> function does not appear until a final 'keystone' mutation plus a bunch of
> completely inutile changes have occurred) that lead to the formation of new
> functions that only appear at the end point.
Actually, if my theory is correct, it would be impossible to
demonstrate such evolution because my theory is one that proposes that
mindless evolution cannot happen beyond very limited levels of
complexity. You are the one who must demonstrate your supposed paths,
not I. I don't think they exist, you do. So, demonstrate them.
> > So anyway, you suggest that there is no way to know where the starting
> > point is, and this is true. However, one can get a pretty good idea
> > that a random starting point will be a certain distance away from a
> > given function in a particular creature like a bacterium. Certainly
> > it is true that when Hall deleted the lacZ genes in various colonies
> > of E. coli, these E. coli happened to be just one step away from a
> > different lactase sequence. What where the odds? How fortunate for
> > them!
>
> Yet that is precisely how evolution works. E. coli did "just happen" to
> have a protein, which served a different but dispensible function, which
> could be modified to serve a "lactase" functionality in one or a few
> mutational steps. If the function were not dispensible, then there would
> have to be two steps, one of which would truely be "neutral" -- namely
> generating redundancy.
And, how does this solve the problem of neutral gaps?
> > We know that this was quite a stroke of luck indeed when we
> > consider how very difficult it is for many other bacteria to evolve
> > the lactase function.
>
> That is, other bacteria did not have a gene serving this other process, or
> this other protein was not redundant or dispensible. SFW? How does this
> mean that the evolution of lactase activity is impossible? It merely means
> that evolution of lactase activity is contingent upon the existence of an
> evolvable step.
I never said that the evolution of the lactase function was
"impossible." I only said that the lactase function was more complex
than other types of functions and that there was a clear widening of
the neutral gaps between potential lactase sequences. As one moves up
the ladder of complexity, these gaps do indeed seem to grow at an
exponential rate. At the level of multi-protein functions, such as
bacterial motility, the gaps are truly enormous. If a colony does not
already have access to such a motility function, most likely, even
given zillions of years of time in the proper environment(s), it will
never evolve this ability.
> > Granted, on occasion some life forms might just
> > happen upon a particular complex sequence, like the lactase enzyme,
> > because of the luck of their starting point.
>
> So what? That merely means that, if the environment, which usually contains
> more than one bacterial species has lactose (not as the sole carbon source)
> and no bacteria which can use it, that the bacteria with the shortest
> pathway to generating a "lactase" function from one of its other current
> 'functional' enzymes -- some of which may have rudimentary b-galactosidase
> activity -- will be the probable winner in the race to utilize this
> previously unuseable resource.
It depends upon the average gaps involved between the two different
starting points. Let's put a colony of Proteus and a colony of Hall's
E. coli onto a lactose enriched environment. Neither one of them have
been able to evolve the lactase function in hundreds of thousands of
generations. Which one of them will win the race? Perhaps neither of
them will win even in if given a billion generations of time? And,
even if one of them does happen to win in this amount of time, that
does not mean that the other species of bacteria are not out of the
race. Still, if they happened to evolve the lactase function, they
would gain an advantage over their peers within their own population.
> At that point, however, since bacteria do
> have mechanisms for horizontal transfer, it is likely that this gene will
> spread horizontally from that point, with selection merely deciding which of
> the bacteria that get it will retain it for any length of time.
Yes, once the sequence is evolve initially, all further transfer and
proliferation of this code within the population or even between some
different populations is not a problem.
> How does
> this obviate evolution by natural selection?
Don't you see? It shows a trend that increasing complexity
exponentially decreases the ratio of functional sequences. This
creates neutral gaps that block the power of natural selection.
> It merely shows that descent
> with modification requires a pathway where there is no long chain of
> completely inutile, but absolutely necessary, random mutational events.
Yes, this is exactly what is shows. The problem is that your long
chain of "absolutely necessary" mutational events is not functionally
intact. There are wide neutral gaps all along your chain.
> On
> that both you and I agree. But, other than assertion, I have not seen you
> present any evidence other than your personal incredulity that such long
> chains of completely inutile, but absolutely necessary, random mutations are
> actually involved in the formation of complex structures. In every case
> where there *is* evidence, there are intermediate stages with utility.
Your examples of intermediates are still too wide for me to understand
in many cases. Your hypothetical paths don't even work on paper and
even small portions of them have yet to be demonstrated in real life.
Your theory is one big "just-so story" with little real experimental
evidence supporting it. There are no experiments that show the
stepwise crossing of progressive of intermediates that you propose
exist along the path too the flagellar function or even the far
simpler penicillinase function. Really, what do you have?
> > However, how long will
> > this luck hold out? What are the odds that they will not only just
> > happen to be close to one of the fairly rare lactase sequences out
> > there, but also close to one of the fairly rare penicillinase
> > sequences as well?
>
> Quite good, actually. Most enzymes have a range of substrates that they can
> use other than the one that is ordinarily considered to be the 'substrate'
> that the enzyme works on.
That is true, but many enzymes are quite limited. A given lactase
enzyme will most certainly not have the penicillinase function. Try
it and see. What are the odds that a lactase enzyme will also have
penicillinase activity or that a penicillinase enzyme will also have
lactase activity? Not so good considering the that ratio of function
compared to non-function sequences are very low in both cases.
> And there are a limited number of types of
> biochemical activities: hydrolases, dehydrogenases, hydrogenases, etc.
> That, in fact, is why one can find medicines and drugs and venoms and toxins
> that can be used by existing enzymes and why simple mutations can alter
> substrate specificities.
It depends on the enzyme and the type of substrate it is working on.
A simple mutation, I am betting, is not going to alter a lactase
enzyme to have act on a new penicillin substrate.
> Something that does not interact with some
> biochemical is unlikely to have any biological effect. If it does interact
> with some biochemical, then somewhere, somehow, a change in biochemistry can
> alter that effect. That does not mean that some *particular* arbitrarily
> chosen organism will *necessarily* be able to modify an effect or organ to a
> predetermined end point (for that would be teleological).
Yes, but you must at least consider the odds and averages involved.
Quickly, the odds outpace any potential "double effect" that your
sequences may have. The average distances between such enzymes make
it highly unlikely that very many of the potential benefits in a
particular environment of limited potential will be realized by even a
huge population over the course of thousands of generations. The is
in fact the rational for given multiple antibiotics to fight a given
bacterial infection in the hospital. The odds that the bacteria will
develop resistance to several types of antibiotics are reduced and the
time involved is expanded according to the number of neutral mutations
required to achieve resistance to multiple antibiotics. Since even
these gaps are relatively small, multiple drug resistance does evolve
quite rapidly, but the point remains the same. The wider the gaps,
the more time is required.
> > I mean, look at how many different complex enzymes
> > and other functional proteins that an E. coli bacterium can produce.
> > What are the odds that its original ancestral genetic real estate was
> > that close to all of these various functional sequences? And we are
> > only talking about the function of single proteins here. We haven't
> > even started talking about the relative rarity of more complex
> > multi-protein systems of function as are required for bacterial
> > motility and the like.
>
> The above is a hand-waving argument of no utility or evidence at all, other
> than personal incredulity.
Not at all. The odds involved in evolving even one of the enzymes
used by an E. coli bacterium are quite low. What then are the odds
that this same pool of genomes would be also be just as close to
another or several other equally rare sequences?
> *Most* proteins, even in E. coli, are not
> *necessary*, they are *dispensible* (and are dispensed with in other
> organisms).
Actually, most genes in E. coli are beneficial. If they were not,
they would be quickly eliminated by natural selection. Just because a
bacterium may survive without a particular gene does not mean that
this gene was not beneficial. I can survive without my right arm, but
that does not make it any less beneficial to me.
> There are only a few *necessary* genes and enzymatic functions,
> and one can even dispense with many of these if you posit RNA-based genomes.
> Modification of duplications (redundancy) of *necessary* genes seem to be
> the source of many *dispensible* genes, whose functions are, in fact, often
> related to that of the *necessary* genes.
Again, just because some gene is not vital for life does not lessen
its benefits to the organism that has it.
> >> Your own example
> >> of the evolution of lactase makes it clear that you cannot make ad hoc
> >> calculations to tell you how long it will take for something to
> >> evolve.
> >
> > What Hall's experiments with lactase evolution in E. coli tell us is
> > that the lactase function is much harder to evolve than many types of
> > bacterial antibiotic resistance. Certainly it is true that I do not
> > know exactly how many potential lactase enzymes exist in the potential
> > space of 10e1300 potential amino acid sequences of an equivalent size
> > or less.
>
> Not in the genomes of all bacteria.
Yes. All bacteria can evolve antibiotic resistance to all antibiotics
much easier than they can evolve enzymes of the level of the lactase
or penicillinase enzymes from scratch.
> > However, Hall's experiment made it pretty clear that the
> > ratio of lactase enzymes as compared with non-lactase sequences is not
> > high enough to eliminate fairly significant neutral gaps.
>
> What you apparantly mean is not "neutral gaps", but number of specific
> changes needed before a selectable effect exists.
That is the definition of a neutral gap.
> I agree that if there
> exist such gaps for a particular species, such gaps do provide a barrier to
> evolution by natural selection to a particular end goal *in that species*.
Yes - But what other species do you know of that can evolve the
lactase function or the bacterial motility function easily?
> That is why evolutionary biologists place so much weight on pathways in
> which intermediate stages have functional utility (but not necessarily the
> teleological end point's utility). Such intermediate states are a necessity
> for evolution by selection (descent with modification) to work. [Horizontal
> transfer, of course, does not require descent with modification in the
> recipient species, but only in the donor species.]
Yes, these intermediates are required, but you have yet to demonstrate
that they exist beyond your "just-so stories" and hand waving. The
odds are clearly against you. You think that a few islands here and
there will explain how to cross from the continent of one function to
another. You seem not to understand that the gaps between your
intermediate islands are still huge.
> > If the
> > ratio of lactase enzymes to non-lactase sequences were as high as 1 in
> > 10, then one would expect that the evolution of the lactase function
> > would be easily demonstrable in just about any type of bacteria. In
> > fact, just about 1 in 10 DNA sequences and/or genes in all bacteria
> > would have some sort of lactase function. If this ratio were the real
> > ratio, Hall would have discovered sequence after sequence with the
> > lactase function. Every time he deleted another sequence with lactase
> > function (as he did with the lacZ genes), a new one would quickly
> > evolve (as happened with the ebg gene - but with no other gene after
> > the ebg gene was deleted). The fact that no other lactase gene
> > evolved after the ebg gene was deleted means that the ratio of
> > sequences with the lactase function is low enough so that not very
> > many lactase sequences can can be evolved by a fairly large population
> > even with tens of thousands of generations of time.
>
> Unless, for entirely unrelated reasons, one has a gene like ebg (dispensible
> and close enough to lactase for the gap to selectable functionality to be
> easily transited). If your view of evolution were true, then we would be
> having hyperevolution, such as creationists often assume post-flood and
> there would be no differentiation between bacteria due to descent.
That's right. . .
> Any time
> a bacteria came into an environment with lactose as the sole carbon source,
> it could poof a lactase into existence in the next generation from some
> unspecified random sequence of DNA.
Yes, this would be the case if there were no neutral gaps to slow this
process down. In fact, this is what happens with antibiotic
resistance. Many different species of bacteria are capable of
evolving resistance to a particular type of antibiotic equally
rapidly. Given an environment with a particular antibiotic in it,
many different type of bacteria would evolve resistance in short
order. Why? Because the neutral gaps are short between the various
sequences that have the resistance function in many different
bacteria.
> Instead, we see descent with
> modification, whereby lactase activity does not appear to evolve from random
> sequences of DNA, but only from enzymes which do not require extensive
> remodeling to make into lactase.
Yes. With just one point mutation the ebg was able to produce a
lactase enzyme. But, what are the odds that a particular group of
individuals would be so close to one of the lactase sequences? Not
very good. The odds get much much lower as one moves up the ladder of
complexity. That is the whole point here. The "intermediates" that
are required for your theory of evolution to work simply become
unbelievably rare.
> And why this is a problem for evolution?
> I always thought that was how evolution was supposed to work. Rather than
> poofing new activities into existence from random sequences of DNA.
Again, the problem is that these "rare events" become more and more
rare as you move up the ladder of complexity. As rare as lactase
evolution is, it is far more common than the evolution of functions of
higher complexity, like the bacterial motility function.
> > Based on this
> > lack of evolution one can reasonable calculate the average neutral gap
> > involved, at least to the extent that the gap is most likely *larger*
> > than a particular ratio (Since any function with a higher ratio of
> > representation in the total number of potential sequences should be
> > realized after a given amount of time).
>
> It also points out the high degree of variance, with some species (those
> that by chance had a potentially evolveable precursor gene) easily evolving
> lactase and others that lacked that precursor not being able to do so. That
> variance is what would give a pattern of descent with modification for
> lactases rather than a pattern of independent evolution of lactases from
> random sequences in each bacteria that has lactase.
What are the odds that by chance a particular species would be close
to such a rare lactase sequence as well as to many other equally rare
sequences with other functions in a given environment?
Yes it does and it has to be very common indeed in order for your
theory to be true.
> It need not be extremely high.
Yes, it does.
> Most evolution,
> of course, involves only minor modification of pre-existing structures.
> Such as the difference between humans and chimps.
You cannot say this since you have no idea what the required genetic
differences are that produce the phenotypic differences between humans
and chimps.
> > You yourself admit that the ratios do in fact go down as
> > complexity increases. Well then, please explain to me where this
> > ratio levels off so that evolution can keep up with these
> > exponentially expanding neutral gaps.
> >
> >> Multiplying the number of genetic differences between two sequences in
> >> related organisms by the estimated population size, mutation rate, and
> >> generation time, is pretty irrelevant. No one thinks that evolution
> >> works entirely by neutral mutation and random walks.
> >
> > Oh really? Evolution works by other mechanisms than random mutation
> > and natural selection?
>
> Neutral mutation and random walk is not random mutation and natural
> selection. Those are two entirely different mechanisms.
Yes there are these two different mechanisms and one of them cannot
work if neutral gaps are present.
> The first is what
> is called neutral drift. Darwin did not propose it.
That's because Darwin didn't know about genetics or the possibility of
neutral genetic changes.
> Darwin proposed not a
> random walk, but natural selection, which is most decidedly non-random --
Again, natural selection only works if there are no gaps. Clearly, if
there are no neutral gaps, then there are no problems for Darwinian
evolution.
> natural selection is the mechanism by which the environment imparts
> information about itself into the organisms that live there.
This can only happen if there are no neutral gaps. Without neutral
gaps, this process is extremely fast. The very fact that evolution is
supposed to require millions and billions of years of time supports
the idea of neutral gaps. The only way to cross neutral gaps is with
random walk. Natural selection cannot work during the process of
random walk - Period. That is the problem. If natural selection were
capable of always working, then this method would be a perfect
evolutionary mechanism. The problem is that it does not work when
there are neutral gaps that need to be crossed. The only mechanism
left at this point is random walk.
> > If there is a neutral gap, clearly this gap
We disagree on what is "clear" as far as a pathway is concerned. You
again appeal to supposed *morphologic* intermediates. You need to
work on your examples of genetic intermediates and come up with some
actual experiments were at least some of the steps that you propose as
intermediate steps can be crossed in real time.
> In my much less false idea, evolution is constrained not just by the
> environment (with the genome being infinitely plastic in a local situation),
> but also is constrained by the genome of the organism the environment is
> acting upon.
LOL - This is not just your idea, this is a big part of my argument
as well. Evolution is constrained by both the limits of the genetic
real estate as well as the limits of the current environment. Neither
one is infinite as some would like to believe. I'm very glad you
brought up this point yourself because it is quite significant.
> Evolution is a consequence of an *interaction* between the
> two.
Yes.
> If this is true, then most 'novel' enzymatic activities will be
> relatively rare events, requiring the combination of both a selective
> environment *and* a genome with a sequence exaptated to be able to cross a
> relatively short gap (or no gap, but only a single mutation) into a
> selectable level of the new function.
Certainly true.
> The expectation from this model is
> that *most* 'novel' functions happen only rarely and then are retained (and
> optimized) by selection and descent with modification (and horizontal
> transfer in bacteria), leading to a twin nested hierarchy between the
> sequences for that function and lineage as determined by other independent
> means. I.e., *most* novelties occur only once and are retained by descent.
Yes - If a beneficial novel function does happen to evolve, it would
be maintained by natural selection after that if the environment is
stable. However, I wouldn't say that "most" novelties evolve only
once. I would say that most novelties were intelligently designed.
Those novel functions that can and have evolved are of such a
relatively simple level of complexity that they have the capability of
evolving relatively commonly. For example, the evolution of
antibiotic resistance is not exactly rare. This function is commonly
and quickly evolved in many different species of bacteria. It is not
rare and does not evolve just once. If a particular antibiotic is
removed from the environment of a particular colony of bacteria, that
colony will quickly revert back to its wild-type target sequence.
After some time, if the antibiotic is added to the environment again,
many members of that colony will in fact be susceptible to that
antibiotic again. This would require another round of evolution,
which would again produce this function in sort order.
> This model absolutely requires that the process of inventing the novelty
> involves exaptation of function from pre-existing functional elements or
> selectability at intermediate states.
Yes it does. . .
> It eschews the (false) idea that
> evolution involves the random walk of a random functionless sequence until
> all the components are in place (it rejects the idea that evolution involves
> the magical invention of IC systems) and points to the independent
> functionality of simpler sub-systems and sequence similarity of such systems
> and systems performing the other functionality as *evidence* that there is
> the requisite *selectable* pathway from one state to the next.
Now, all you have to do is explain how this path could have existed
between any starting sequence that did not have something like
bacterial motility, and the existence of the function of bacterial
motility in many different species of bacteria. Your problem is that
you have no such experimentally supported paths to support your
theory. Your theory is one big just-so story. Where is your
experimental demonstration? Where is your falsifiable hypothesis?
Your arguments are largely based on morphology, not on genetics. What
looks like a short step morphologically is not necessarily so short
when you look at the underlying code. Please, we know more than
Darwin knew and so your arguments need to be based on the
demonstration of genetic pathways, not on widely spaced morphologic
intermediates.
> Note that we are talking about quantity here. There are some types of
> systems that can easily be modified (usually morphological, not requiring
> new functions or proteins, such as the known differences between Pan and
> Homo) continuously under the appropriate selective pressures.
Another just-so statement. This conclusion of yours is not as clear
as you make it out to be. What are the morphologic differences based
on? What are the genetic changes involved? You cannot simple say
that these changes can be "easily" achieved without any new genetic
functions. You really cannot change morphology without changing
genetics. You must therefore explain the genetics and not just assume
that they are as "simple" as the morphology appears to be.
> Others may be
> an inadvertant consequence of selection for other purposes. Other types of
> change tend to be fortuitous (and not necessarily of selective utility) and
> historically are either sporadic or unique. These latter tend to be the
> types of changes that define lineages.
Any genetic examples or is all you have morphologic just-so stories
like I see on public television all the time? The Devil is in the
genetic details you know, and you really seem to be avoiding him ; )
> >> We know what the "average time" is, not because of your post hoc
> >> statistics, but because we observed the evolution of chloroquine
> >> resistance in nature.
> >
> > Yes, we have observed the average time required and the mutations that
> > are required first, before any calculations. However, based on the
> > required mutations we can figure out how long these required mutations
> > would take to evolve if they were in fact neutral mutations.
>
> Please define what you mean by neutral mutations. You keep using this term
> in ways that differ from the normal meaning.
Please, I use the term exactly according to its normal meaning. A
neutral genetic mutation is one that does not change phenotypic
function.
> > We can
> > then see if these calculations are consistent with what we actually
> > saw in nature. If the calculations are consistent, then we can know
> > that the evolution that we saw take place in nature was in fact the
> > result of random walk across a certain number of neutral steps. We
> > can also know what would be required to evolve this function in the
> > lab. Much better estimates on the needed population size could be
> > pre-determined in order to achieve success in a given span of time.
> >
> > The reason why this example of CQR is helpful to me is because it
> > shows that wider neutral gaps in function do in fact translate into
> > longer spans of time due to the fact that random walk was involved in
> > the process. There is no way around this conclusion that I can see.
> > Why else would the evolution of the few steps involved in CXR have
> > taken so long and why else is CXR not easily demonstrated in vitro?
>
> And I have no problem with that. Only if you hold the false view that
> evolution to a particular 'novel' function is a *necessity* that occurs by
> the will of the organism (or the will of a designer) rather than being an
> occasional consequence of the interaction between an organism and its
> environment, does this somehow cause a problem for evolution.
Wrong. The problem for evolution is that the neutral gaps become so
prevalent with increasing complexity of function that the existence of
functions of higher and higher complexity becomes harder and harder
for the mindless process of evolution to just "occasionally" come
upon. These "occasions" turn into trillions upon trillions upon
zillions of years. That is the problem.
> In fact, the
> evidence is quite clear that new functionalities for individual genes are
> relatively rare, *but not impossible*, and are contingent upon both the
> environment and the genome of the organism.
What makes them "possible" in light of what makes them "relatively
rare"? If the neutral gaps make them relatively rare and these gaps
grow exponentially with increasing complexity, wouldn't the evolution
of functions of increasing complexity also require exponentially
greater amounts of time?
> That is why most enzymes
> exhibit one (or more rarely, two) only a single line of descent (sequence
> parsimony) consistent with the lines of descent obtained from other methods
> (e.g., fossil record) rather than multiple independent lines of descent.
Or, more likely, such similar enzymes that do a similar job in
different creatures (like the cytochrome c protein) are evidence of
conservation of design. If you designed many different types of cars,
would you redesign each individual part in each car, or, would you
conserve some of your designs and use the same water hoses, bolts, and
break pads, sheet metal, and paint in some of them?
> Similarly, complexity, as in flagella, is viewed not as a *single* event,
> but as a *series* or *pathway* of events, each of which had selective value
> independent of an 'end result' we can only discern from the position of
> hindsight.
Which you cannot demonstrate, even on paper, without leaving many
large gaps unexplained.
snip
> >>> Obviously more time is required to evolve the enzymatic functions than
> >>> the functions of antibiotic resistance. That question is, "Why?" Why
> >>> is more time required to evolve functions of increasing complexity? I
> >>> am proposing that neutral gaps are the reason for this observed
> >>> phenomenon. What is your explanation?
>
> Antibiotic resistance and enzyme evolution are both dependent upon the
> pre-existence (or easy evolution) of a protein which can affect the
> antibiotic (or new substrate). The differences you see are usually based on
> the intensity of selection rather than a different mechanism.
This is clearly mistaken. The difference in evolvability between
antibiotic resistance and an enzyme activity like lactase is not based
on the intensity of selection at all. First off, antibiotic
resistance that arises via the production of an enzyme, like the
penicillinase enzyme, has never been shown to evolve de novo. The
code for the penicillinase enzyme was always there. However, this is
not the only way bacteria become resistant to antibiotics such as
penicillin. The de novo evolution of penicillin resistance involves
the blocking of the interaction of penicillin with its target. Many
different mutations can interfere with this antibiotic-target
interaction to produce resistance to penicillin. The same holds true
for the evolution of resistance to other types of antibiotics. It is
therefore the commonality of the interfering sequences that gives rise
to the rapid evolution of antibiotic resistance, not so much the
intensity of the selection method. This is not true for the evolution
of enzymes like the lactase enzyme. Despite high selection pressures,
the E. coli (lacZ and ebgA negative) that could quickly evolve
resistance to many different types of antibiotics could not evolve the
lactase function even under similar levels of selection pressure.
>The only usual
> difference is the intensity of selection and the necessity or dispensibility
> of the process.
Not so. Intensity of selection is not nearly as important as the
ratio or availability of functional sequences.
> In an environment with an antibiotic, evolving a resistance
> of some sort is usually a *necessity* because the antibiotic directly
> affects survival of the organism;
Not so. Antibiotic resistance actually arises very rapidly in
sublethal levels of antibiotic exposure.
> evolving a new enzymatic function, OTOH,
> is often a matter of being able to exploit a resource currently unavailable
> to you, which only affects you if that is the only relavant resource
> available (a bacteria without lactase can survive in a lactose-rich media
> that also has enough glucose).
Just as a bacterium in a penicillin environment can survive just fine
if the level of penicillin is below lethal limits.
> That is, evolution of a new enzymatic
> activity is not always a *necessity*; it is often *dispensible* (nice to
> have under certain circumstance, but not usually a matter of necessity).
Just as the evolution of penicillin resistance is not "necessary" for
survival but it is beneficial even in environments that have
sub-lethal levels of the antibiotic. The problem is, when comparing
such equivalent environments, antibiotic resistance arises extremely
fast. The lactase function does not. In both cases, the selection
pressure can be set up to be very much the same.
> The usual mechanisms by which resistance (or new enzymatic activity) is
> obtained falls into one of the following categories: 1) Resistance
> (sufficient activity) by amplification. In this case, an antibiotic binds a
> protein either much more strongly than the native substrate or strongly
> enough to affect the amount of substrate conversion (the enzymatic activity)
> below the level of survival. Resistance is obtained by simple amplification
> of the target protein to either bind up enough of the antibiotic so that
> enough enzyme activity remains to permit survival. This is how DDT and
> other resistances like methotrexate resistance work. In the enzyme world,
> this would involve amplification of an enzyme that has a primary function
> different from the new one, but has some new activity. [Again, enzymes are
> not all-or-nothing specified, but usually are *optimized* for one function,
> while *suboptimally* using other substrates and thus creating other
> products. Indeed, some enzymes may actually better utilize substrates that
> are not the 'normal' one.] This both increases the amount of original
> activity (which may not be harmful) *and* permit sufficient utilization of
> the novel substrate so as to have a selective advantage.
Such upregulation or amplification occurs easily with just one or two
mutations (more may be realized, but each one is selectable
advantageous). Often amplification is the result of a loss of control
over the gene in question. Again, this loss of control is based on an
interference mutation to the gene/protein that normally suppresses the
production of the controlled gene. Loss of control and overproduction
is really easy to achieve. Not a problem at all.
> 2) Modification by
> mutation and selection of a protein. In resistance, the usual protein
> modified is the target of the antibiotic. Usually the modification must
> cause a great enough decrease in binding affinity for the antibiotic while
> retaining sufficient binding affinity for the original substrate to allow
> survival. Because of the greater stringency of antibiotic selection, even a
> very low level of original activity can be selected for. In producing 'new'
> enzyme activity the problem is that most loss of specificity for the
> original substrate produce sub-optimal levels of both activities. This can
> only proceed up to a point, and that point may not produce sufficient
> amounts of the new activity to make it selectable in its own right. Thus
> this usually only happens when the original activity is both dispensible and
> rarely used.
It actually happens more commonly than indicated here, but in any
case, this method is also based on the interference of a
pre-established interaction or function that is very specific.
Breaking or interfering with such a function is not a problem. The
ratio of mutations or sequences that could do this is relatively high.
> 3) A combination of 1) and 2). This allows a way around the
> difficulty of enzyme suboptimality and also provides a mechanism for
> generating isozymes (enzymes that perform the same function but have
> different properties, like temperature optimi) and families of genes
> (enzymes that perform related, but not identical functions, like the globin
> family of myoglobin and hemoglobins and all the different transmembrane
> receptors). This is a *very* common feature of the evolution of new
> functions in cells.
Again, a combination of methods 1 and 2 is still easy to achieve as
described above. The neutral gaps involved are extremely short.
>4) Modification of a non-target protein that
> inactivates the antibiotic. This, of course, *is* the invention of a new
> enzyme. The evolution of penicillinase and/or vancomycin resistance *is*
> the invention of a new enzyme activity to the point where it has a
> functionally important effect. It occurs by the modification of an existing
> protein whose original function is dispensible.
The only problem with this statement is that penicillinase has never
been demonstrated to evolve in real time. It is a just-so statement
of belief that it ever did evolve. Again, another paper theory. And,
even if it did evolve as you say it did, this level of enzymatic
function is obviously much much harder to evolve than the 1 through 3
types of functional evolution you detailed above. The evolution of an
enzyme, like the penicillinase enzyme, is much harder than the
evolution of other types of antibiotic resistance functions which are
by far the most common methods of *de novo* antibiotic resistance in
bacteria.
snip
> >> I have no idea why you think this. Most ideas about abiogenesis (apart
> >> from creationist, junkyard to B727, strawmen) are based on selection.
> >> We all agree that a random walk through all possible chemical
> >> structures to cytochrome c is not what happened.
> >
> > Oh really? What happened then? Specifically? Detail a scenario for
> > the evolution of cytochrome c where each mutation is selectively
> > advantageous. You even get to use an already established life form
> > capable of self-replication. Getting this life form to begin with
> > (via abiogenesis) is a whole different ball game. In fact, this is
> > whole idea that abiogenesis could have given rise to the first living
> > cell is what drove many like Sir Frederick Hoyle to other theories of
> > living coming from outer space.
>
> That merely changes "where", not "how".
The "how" is the important question you need to answer. To say that
they simply "where" is just another "trust me" statement.
> > Then, once you have the first living
> > cell, using the idea of random mutation and mindless selection
>
> Mindless selection specifically tries to optimize your genome for
> reproductive success in the environment that your parents faced. Do you
> agree that that is precisely what selection does?
Yes, when selection is capable of working. Again, the problem is that
selection does work when all the options have the same function or
nonfunction (i.e., The differences are functionally neutral).
> > to get
> > other functions of increasing complexity is still an astronomical task
> > that really is no easier than explaining the origin of the first life
> > form to begin with.
>
> Selection only leads to increased complexity to the extent that that
> increased complexity leads to greater reproductive success in the
> environment that your parents faced. It will clearly lead to an increase in
> the frequency of those variants that are more complex under conditions in
> which that is favored. Unless you are saying that mutation cannot increase
> complexity, say by amplifying a gene and modifying it into an isozyme or
> related gene in the same family. That would be a hard position to maintain
> in the face of evidence that both amplification and modification are known
> to occur.
Amplification and modification cannot explain the rise of new
functions of higher and higher complexity since amplification doesn't
really produce anything new and modification is soon limited by
neutral gaps in function.
> >>> This is why scientists think that abiogenesis took
> >>> billions of years to produce the first self-replicating cell.
> >
> > Actually you and I stand corrected on this point. Somehow scientists
> > think that abiogenesis happened relatively quickly in a few millions,
> > not billions, of years.
>
> Scientist can point to clear evidence that procaryotic organisms existed on
> the earth for at least 3.5 billion years or so.
I disagree. The fossil record is far from conclusive on this point.
And, the genetic evidence is non-existent.
> And for the first
> half-billion years, the earth was probably pretty inhospitible to
> carbon-based life forms. But that still leaves several *hundred million
> years*, not a *few* million, *within which* abiogenesis must have occurred
> (even if you think the abiogenesis event were supernatural in origin).
I don't care if you had several hundred billion years or several
hundred trillion years to work with. The time needed for abiogenesis
is on the order of googols and googols to the power of googols of
years.
> How
> long it actually took is not clear. But remember that most of the necessary
> enzymatic (actually ribozyme) activities needed for nucleotide reproduction
> (polynucleotide kinase, ligase) can be generated in random 50-mers in less
> than a micromole of material.
Complete BS. You just don't get it do you? Try taking your micromole
of material and putting a stretch of DNA into it and see if it gets
replicated. Then, see if it survives very long much less evolves into
anything but a homogenous ooze. Entropy tends toward homogeny. That
is the problem for the mindless processes of nature.
> >> Please, show your model. But it isn't a random walk.
> >
> > My model is based on random walk. What is your model? If random walk
> > is not involved, then even millions of years are not required.
>
> Millions of years may still be required *if* the process were not
> teleologically determined, depending upon local selective pressures.
Not without random walk being involved. Without random walk, nothing
stops the evolution of new functions. As long as the genetic real
estate is within striking distance (a few steps or so) of a particular
beneficial function via a short stretch of random walk, that sequence
will evolve rapidly.
> If the
> present state is not a predetermined end 'goal', there can be millions of
> years of quite happy intermediate status.
Not so. Not if the distance to a new function is within the reach of
random walk. If the random walk is only one or two steps wide, the
new beneficial function will be realized in short order.
> Indeed, the evidence shows
> several billion years of single-cell (mostly procaryotic) status for the
> entire biosphere. Even multicellularity does not even look like an
> 'inevitability'.
Yes, it does if random walk is not required.
> > Without random walk to slow things down, evolution would happen right
> > before your very eyes. It would be a snap. Without random walk, the
> > first cell would self-assemble in a matter of seconds in the right
> > environment (one with all the required parts). Then, without random
> > walk, this first cell would quickly go multi-cellular in just a few
> > generations. A few years down the road and fish would be crawling out
> > onto the land. A few thousand years later and Survivor would be a hit
> > television show.
>
> Only if you are thinking that the environment tends inexorably to increase
> complexity and that evolution works by taking random sequences and poofing
> new functional sequences into existence because of the 'will' of the
> organism to gain a function. Selection is conservative more often than it
> is creative.
You don't understand. Without random walk to slow things down, new
functions would "poof" into existence just like antibiotic resistance
"poofs" into existence all the time for many different kinds of
bacteria.
> > Random walk slows things down.
>
> In the less false view of evolution, it is the necessity for the many stages
> of intermediacy in the pathway to the current function being examined to
> have *some* utility (but not necessarily *final* utility) that slows things
> down. Random walks of truly significant lengths would tend to abort the
> process.
Yes, it would. But, without random walk of at least some distance,
there would be no slowing of the process at all. Things would poof
into existence all over the place. If your intermediate steps were as
close as you say they are, they would be crossed in very short order.
Nothing would slow the process down.
> > Without random walk, evolution would
> > be very fast.
>
> Only if both the rate of variation production and the rate of environmental
> change were to speed up significantly.
Not so. If there is a required change in environment, then this
required change creates a random walk between what is and what might
be beneficial. If one of your intermediate steps would only be
beneficial in a particular type of environment, then it would cease to
be an intermediate step in the current environment. Getting beyond
this intermediate position would therefore require the random walk.
This would slow things down.
> > The fact that evolution seems to be very slow must mean
> > that random walk is a real limiting force of nature. The problem is
> > that random walk limits things too much for evolution to produce much
> > of anything in the blink of an eye that is 4 or 5 billion years.
>
> I do not regard 4-5 billion years as a blink of an eye, even in evolutionary
> terms.
You would if you realized that the neutral gaps involved expand the
required time into the trillions upon trillions upon zillions of
years. Your few billion years of time becomes nothing in comparison.
>You seem to be substituting random walks for the more usual
> retarding principles, namely the need for intermediate utility (of *some*
> kind) in the pathways of evolutionary change
This need for the intermediate utility of some kind of intermediate
sequence is what creates the random walk. If that utility is not
there right now, then random walk is the only way to get across it.
If a particular environment is needed to make this intermediate
sequence useful, then that is also a type of random environmental
walk. Many different environments could come around, but what are the
odds that the "right" environment will come around out of all the
potential environments that could come around? There are a lot of
potential "junk environments" just like there are a lot of potential
junk amino acid sequences. The organism must also walk randomly
through changing environments before the "right" environment comes
along. You see, random walk is not limited to randomly changing
genetic sequences in a stable environment, but also to randomly
changing environments.
> (some of which have few and
> short random walks as part of the process and others having longer ones or
> requiring fortuitous one-time events) *and* the absence of teleological end
> goals for evolution (which leads to random walks of completely functional
> intermediate states) *and* the need for the new functionality to be of
> selective benefit in a local environment.
All these "ands" - What are the odds? This is needed and that is
needed for evolution to work. That is the problem. The poor odds of
everything coming together just right start really becoming a problem
for evolution to explain. But hey, since evolution has no goals and
needs not be able to explain anything or be testable in any
falsifiable way, it certainly could be true . . . and someday cows
may just jump over the moon.
Sean
Adam Marczyk
[...]
>> But no one except you ever claimed that a complex enzyme, like
>> penicillinase, evolved from *absolutely* random sequences with *no*
>> intermediate steps having *any* selectable activity or function of *any*
>> sort. Just the opposite. All the evolutionary claims are constrained
>> to producing changes that have selectable function *of some sort* after
>> each step or few steps.
>
> Yes, this is the claim that is put forward by the theory of evolution,
> but this is exactly what has not been demonstrated in a convincing
> manner as one moves up the ladder of complexity. What if there are no
> selectable functions that are beneficial over the course of several
> steps of random walk?
Yes, and what if the sky turned green and the sun rose in the west
tomorrow? You can speculate and hypothesize all you want about selective
gaps, but in the end it's just handwaving.
[...]
>> Of course evolution by natural selection will easily
>> work only in those organism that, by the chance vagaries of their
>> historical past, chance to have a 'precursor' capable of being modified
>> to the new functionality.
>
> Yes, this is what the theory proposes. But, given the size of the
> neutral gaps involved, what are the odds that a specific environmental
> change or a long span of time for random walks with huge population
> sizes, will be able to come across more than a handful of such
> functions? And, we are only talking about relatively simple functions
> that are based on the potential of single proteins. What about those
> functions that require multiple proteins working together at the same
> time?
Experiments have been done to answer just this question. I can give you two
answers - one relating to the artificial evolution of complex functions in
a computer simulation, and one relating to the natural evolution of complex
functions in the wild. The two papers are:
Lenski, Richard, Ofria, Charles, Pennock, Robert and Adami, Christoph. "The
evolutionary origin of complex features." Nature, 8 May 2003, vol. 423,
p.130.
and
Hastings, I.M., Bray, P.G. and Ward, S.A. "A Requiem for Chloroquine."
Science, 4 October 2002, vol. 298, p. 74.
The first paper concerns an experiment with simulated evolution. An
evolving program was provided with the ability to perform only one logic
function, NAND (compares two bits and returns a 1 if either bit is 0, 0
otherwise), and was given the task of creating all other possible binary
logic functions (in level of increasing difficulty: NOT, AND, OR, NOR, XOR
and EQU) by randomly mutating and recombining instructions. Programs that
could successfully perform one or more of these functions were rewarded
with "energy units" that enabled them to execute their instructions and
thus reproduce more quickly; the more difficult the function, the more
energy units a program received for performing it. (Reproduction did not
come for free - a successful program had to be able to copy *itself* as
well as be able to perform the logic functions). An exhaustive search
proved that the shortest possible program that performed EQU, the most
complex and difficult logic function, required a minimum of five NAND
operations executed on the correct registers in the correct sequence (i.e.,
the code for this operation is "irreducibly complex"). In 344 generations,
a program evolved that could not only perform EQU, but all the other logic
functions as well. (IIRC, AND had to be lost to produce EQU - an apparently
deleterious mutation one step before that knocked out AND turned out to be
vital for creating EQU. The experiment continued to run after that point,
though, and subsequent mutations restored AND while preserving EQU.)
The second paper concerns the emergence of immunity to chloroquine, the
drug used to kill the parasite that causes malaria. Molecular studies show
that nine sequential mutations, in a gene which encodes a complex transport
protein called PfCRT, must accumulate for chloroquine immunity to develop;
each of these mutations provides gradually increasing resistance, although
only once the eighth has arisen is the parasite resistant to clinical doses
of the drug, and only once all nine are in place is there total immunity.
It took almost 20 years, but that is precisely what has happened. In fact,
this appears to have happened independently at least four times in
different geographical locations. You will notice that at no point did this
step-by-step evolution encounter an uncrossable barrier or have to leap a
gap of no selective utility.
[...]
>> No one but you claims that *any* organism, put in *any* new environment
>> *somehow*, according to evolutionary (due to selection) ideas, *must* be
>> able to evolve a function that allows it to survive.
>
> Actually, this is very much what the theory of evolution is
> suggesting.
Absolutely not. Nothing about evolution ever said that the first cell was
required to survive; in fact it's been proposed that life arose more than
once on the early Earth, but all but one (obviously) of those attempts
ended in extinction. And the first living things were, so to speak,
building themselves from the ground up. This is a significant difference
from an experiment where a well-established species that had grown
dependent on a particular source of energy suddenly had the rug pulled out
from under it.
> The very first organism was quite limited indeed and it
> was in a limited environment as well. And yet, it supposedly evolved
> many new functions in relatively short order.
Who says? As far as we know the first eukaryotic cell, incorporating many
new cell structures that do not exist in prokaryotes, did not arise until
only about 1.5 billion years ago.
> Really, given enough
> time, any self-replicating organism should be able to morph itself
> into just about any phenotypic shape and function imaginable, given
> the proper environment. As long as the new environment is not
> immediately lethal, and time is allowed for extended growth and
> competition for survival, then yes, the theory of evolution suggests
> strongly that new functions will evolve that allow some organisms to
> survive better than their peers in this new environment.
New functions will evolve, yes. No one ever said (except perhaps
creationists pushing strawmen) that organisms should be able to evolve into
"just about any" imaginable configuration. Doubtless there are many
configurations that no living thing will ever reach precisely because there
is no selectable path leading to them. But that is as far as we're
justified in going, that is the farthest such a line of argument can be
supported. We, at this moment with our present state of knowledge, are by
no means justified in saying what specific configurations those might be.
Whenever we say something is impossible, life tends to surprise us. (Who
would ever imagine something like a spider, or a firefly, or a bombardier
beetle, without first seeing one?)
[...]
>> There is no
>> guarantee that *all* organisms will be able to evolve to *any*
>> arbitrarily stated conditions.
>
> Certainly not. However, what you are basically saying is that the
> theory of evolution cannot be tested. Experiments cannot be set in a
> falsifiable way because if they fail, all you have to say is, "Well, I
> guess we just didn't use the right environment or the right organisms
> to demonstrate evolution this time." This always leaves you an out.
Yes, and? This is *life* we're dealing with here. It's a complex, messy,
chance-dependent, sloppy, unpredictable thing. A mutation that could make
all the difference could be caused by the unintended presence of a
mutagenic pollutant in extremely small quantities impinging on a cell; it
could be caused by a cosmic ray arriving from the explosive death of a star
halfway across the cosmos billions of years ago; it could be caused by a
background quantum fluctuation, the most intrinsically unpredictable
phenomenon in existence. This isn't like simple Newtonian physics where you
can throw a ball up into the air, and given the same initial conditions, it
will always land in exactly the same spot.
> Without the theory of evolution being falsifiable in such genetic
> experiments, you can always believe in it no matter what the
> experiments say. Tell me, what genetic experiments could be done that
> would falsify the theory of evolution? Really, unless you can detail
> such an experimental result that would counter the theory of
> evolution, your theory really is not scientific. You must have a
> genetic test that is testable and falsifiable. What is it?
Easy: You could test to see if organisms ever undergo beneficial genetic
changes that can be inherited by their descendants. Sorry if you wanted
something more specific, but evolution is by its very nature a process that
is partially dependent on chance. Sometimes the right mutations that would
enable an organism to survive in a given situation just don't come up
(which is why a rather overwhelming majority of all the species that have
ever lived are now extinct). It would be absurd to put an organism in a
situation and demand it evolve in a specific way, and conclude evolution is
falsified if it doesn't.
[...]
>> All the "story-telling" pathways
>> that we present wrt to flagella are pointing out just such pathways
>> *and* the evidence to support those pathways.
>
> Not so. All your story telling about how such pathways must exist
> don't even work well on paper and they have never been demonstrated
> experimentally in the case of flagellar evolution (or other bacterial
> motility systems for that matter). Huge gaps are missing that aren't
> really discussed beyond a bit of hand waving to cover them up.
This argument cuts both ways. Given our extremely incomplete knowledge of
the possible configuration space of genes, given our still painfully
limited ability to calculate how proteins fold and interact, and given the
immense, incalculable complexity of the system as a whole, why do you feel
yourself justified in proposing that *no* selective path exists? In what
substantive way does your argument differ from an argument from ignorance?
[...]
>> It has to work via a chain of
>> events constrained by history and by the necessity of intermediate
>> functionality.
>
> Right again, but what if this chain is broken? What if the links of
> the chain are separated from each other in all directions by neutral
> gaps that can only be crossed via random walk?
What if, what if, what if! That does not constitute a scientific argument;
it is merely handwaving. It is an argument from ignorance and incredulity.
[...]
>> *You* are the one who has to demonstrate a *pathway* in which there is
>> what you misleadingly call "neutral" steps (actually, what you are
>> proposing is not 'neutral', but what I call 'keystone' or 'group'
>> selection -- that a function does not appear until a final 'keystone'
>> mutation plus a bunch of completely inutile changes have occurred) that
>> lead to the formation of new functions that only appear at the end
>> point.
>
> Actually, if my theory is correct, it would be impossible to
> demonstrate such evolution because my theory is one that proposes that
> mindless evolution cannot happen beyond very limited levels of
> complexity. You are the one who must demonstrate your supposed paths,
> not I. I don't think they exist, you do. So, demonstrate them.
You said earlier that evolutionary experiments of this sort were
unfalsifiable. I would now like to turn that argument back on you. If such
a pathway could be experimentally shown to exist for, say, the bacterial
flagellum, would you abandon your skepticism, or would you simply move to
the next gap over and conclude, "Yes, well, I guess that could have evolved
after all, but *this* one you'll never explain, for sure!" What would you
accept as falsifying your argument?
[...]
--
"We have loved the stars too fondly | a.a. #2001
to be fearful of the night." | http://www.ebonmusings.org
--Tombstone epitaph of | e-mail: ebonmuse!hotmail.com
two amateur astronomers, | ICQ: 8777843
quoted in Carl Sagan's _Cosmos_ | PGP Key ID: 0x5C66F737
----------------------------------------------------------------------
Morbert
> systems are more simple than other systems of function. There is a
> spectrum of complexity, but all systems along this spectrum from
> simple to more and more complex are all IC. In other words, not all
> setups of a given number of parts or part types will be able to
> perform a given function. The parts in any system of function can in
> fact be altered, removed, or ordered in a different manner so that the
> function of the system is completely destroyed. In fact, there are
> vastly more non-functional potential arrangements of parts than there
> are beneficially functional arrangements of parts in a particular
> scenario.
No no no...
Many functions we see today that appear to be irreducible are actually
very reducible.
Through gene duplication, seemingly irreducibly complex systems can be
formed.
Take "blood clotting" for example. Our blood contains several
clotting factors, each essential to the Blood clotting mechanism we
know and love. Take even one of these factors out, and the entire
system disoolves and breaks down. Also, the chances of our genes
being able to mutate such complex structures is practically
impossible. Similar to the ecoli you mentioned. Yet, by studying
early vertebrates it is possible to solve the mystery.
Imagine an animal that lacted any clotting features (ie. starfish).
Now imagine a gene for slicing enzymes was duplicated (gene
duplication happens at almost the same rate as base gene mutation.)
This gene would form a single clotting factor was very crude, but
superior to the origional methods of healing wounds. Now imagine if
that gene was duplicated again, making the clotting gene more
sensitive, Now imagine this happening several times, natural
selection ensuring that such genes were emphasisised. Over time, we
would eventually get the clotting system we get today. But when we
take a gene away, the chances of it "remutating are impossible.
Its like building a house from the foundation up, and then taking away
the bottom bricks. The entire house collapses, and replacing the
bottom bricks will not repair the entire house.
All our genes evolve this way, and the strange thing is, Behe
recognises this. When he finds a system supposedly irreducibly
complex, but then discoveres a simpler structure in another cell, he
writes it off as evolution and moves to the next cell.
He even toys with bringing back life to the an origional cell, and
saying that this cell contained ALL the genes necessary. Some genes
were merely "silenced" as time went on.
This leaves so much of biochemistry unexplained. It is true that we
do have silenced genes, but according to Behe, we should have silenced
genes found in other species. This is not the case. Where in our
DNAis the gene for producing rattlesnake venom for instance?
The whole Idea of DNA "realestate" a misconception as well, as
Evolution does not need to "create new DNA" but only tinker with
existing configurations. To put a limit on what DNA can become is to
misunderstand the concept of evolution.
Michael Behe also Accepts Microevolution. He claims that species can
diversify into subspecies. HIV can adapt, birds can grow longer beaks
etc. What he doesnt realise is that MIcroevolution and Macroevolution
use the same principles. If species can diversify into subspecies,
what is stopping a common ancestor "diversifying" into the life on
earth today?
Ron Okimoto
> Howard Hershey <hers...@indiana.edu> wrote in message news:<BB10DB71.B02B%hers...@indiana.edu>...
> > in article 80d0c26f.0306...@posting.google.com, Sean Pitman at
> > seanpi...@naturalselection.0catch.com wrote on 6/13/03 7:23 PM:
>
I'll just point out a few really dumb things because it really isn't
worth responding to most of this post until you respond to what has
already been presented to you in other posts.
Snip:
> Yes, this is the problem for those E. coli and other bacteria that do
> not seem to be able to evolve the relatively simple lactase function.
How can this possibly be true when E. coli did evolve this function
using the ebg gene and Hall got it to work in at least two other
species, and I bet other researchers got lactase function in more
species. How many species were tested? You keep harping about how
rare lactase evolution is, but your definition of rare seems to be a
little off. How many species did Hall test. Did he get it to work in
3 out of 3? 5 tries? You're the expert, tell us how rare this is.
You also keep mentioning that things had to evolve in short order, but
you never define what short order is and what time scale that you are
talking about. For things like the flagellum there are probably a
billion or more years to evolve it. This is nearly 5 orders of
magnitude different from your estimate of how long there has been
since the creation. It is a mind boggling quirk you have in
considering such a long period of time short.
Snip:
Tell me, what genetic experiments could be done that
> would falsify the theory of evolution? Really, unless you can detail
> such an experimental result that would counter the theory of
> evolution, your theory really is not scientific.
Just because there are no experiments that we can now do to disprove
evolution only reflect the fact that the experiments that we did do
supported the theory. Darwin didn't know about genetics, but he knew
enough to know that his traits had to be heritable. If we found that
some designer was involved in the creation of every new born baby and
that there was no genetic basis of heredity that would have disproved
Darwinian evolution (What is the difference between the ID assertion
that some god makes babies from the ID assertion that some god made
flagellum?). The designer could have still changed lifeforms over the
eons and accounted for the fossil record, but naturalistic processes
would have been pretty much out the window.
We could have found that each "kind" had their own biochemistry or
genetic code, but that is not what we found. You are full of baloney.
The theory of evolution is a testable scientific theory. Your
problem is that it has been tested and it has been verified. Just
because it would be impossible to redo the tests and come up with the
answers you need to disprove the theory, doesn't make the theory
untestable or untested. I have news for you, biological evolution
would not be a scientific theory if it had not been thoroughly tested
by now. It would be the evolution hypothesis. What gets to me is
that your version of what happened hasn't even gotten to the
hypothesis testing stage and where it has (age of the earth, one world
wide flood etc.) it has failed testing and has been scientifically
falsified. Point out a similar failure for biological evolution.
Before Darwin creationists had already falsified the one world wide
flood hypothesis. They did it by hard work and starting from the
false premise.
Demonstrate the existence of one neutral gap in the evolution of the
flagellum.
You keep harping on the exponential increase in "neutral gaps" but you
never get around to demonstrating that gaps of the size that you need
actually existed. Your lactase example demonstrated that Hall found
that the gaps did not exist in at least three species tested. Your
own example indicates that these gaps do not have to exist, so where
is your evidence that they did exist when the flagellum was evolving?
Your penicillinase example is wrong. Enzymatic degredation of
antibiotics has been observed to evolve. You mean that penicillinase
activity has not been observed to evolve in the lab. Even that may
not be true, but I don't know the antibiotic literature that well.
What protein did the penicillinase enzyme evolve from and what was the
sequence of the gene at that time. How many hundreds of millions or
even over a billion years ago did penicillinase evolve and is the
protein it evolved from even still in the genomes of extant bacteria?
It only had to evolve once and then it gets horizontally transferred
from species to species. Why did your designer create such an enzyme
if it didn't evolve? Just think for a moment. Why would your
designer produce fungi that make antibiotics to defend themselves if
he was going to give bacteria the means to thwart that defense. Why
waste the time? Why screw us in the process?
Where are the clothes on your emperor? The story you start off your
web page with is as bogus as your interpretation of the rest of the
material at that site.
The rest of your antics just tell people that we have real clothes on
our emperor, but you still have none on yours. Why do you think that
it is that science has real evidence and you have none? If our
emperor is naked, your emperor doesn't even have a reasonable
expectation of existing.
The rest of the blather sniped:
Ron Okimoto
Sean Pitman
snip
> > I offered a simple example where certain E. coli colonies (lacking the
> > lacZ and ebgA genes) had been grown on a lactose rich
> > media/environment. They failed to evolve the lactase function despite
> > the obvious benefit to them if they ever did evolve this relatively
> > simple single protein based enzyme. These particular bacteria were
> > grown on this lactose rich media for tens of thousands of generations
> > with high mutation rates and large population sizes, and they still
> > never evolved this relatively simple lactase function. Really, we are
> > not talking about a dramatic shift in environment here. We aren't
> > talking about a lethal "outer space" environment either. The E. coli
> > bacteria grew just fine without the lactase function, but they would
> > have done much better in the lactose rich environment if they did have
> > this function. So, why didn't they evolve this function?
>
> If they were growing just fine without the lactase function, why would
> they need it?
Because, they could survive better than their peers with the lactase
enzyme. They would become more "fit" in their competition for
survival.
> If they evolved a lactase gene, it would have to arise
> out of either 2 copies of an extant enzyme with functions within reach
> (whole gene duplications) or would have to disable working copies of
> extant enzymes to change over into lactase utilization.
Not exactly true. Some proteins can do multiple functions in
different systems of function. But, you do have a point here. Too
many mutations would in fact disable what is already working. This
limits the genetic real estate that a given bacterium can allow to
undergo very much random walk, placing yet another limit on the powers
of evolution. Also, gene duplication doesn't help much since
maintaining a duplicated gene is expensive. It costs energy. Unless
the mutations to this gene happen fast enough to give it some sort of
advantage really quick like, natural selection will get rid of that
gene in short order. The gene duplication hypothesis is also quite
limited.
> The bacteria
> would have had to decrease the existing abilities to process the
> useful and optimized metabolic pathways to produce a new one out of
> existing parts. There's nothing we've seen thus far that suggests that
> organisms will always evolve that kind of function in ten generations,
> ten thousand, or ten million. If all available lac-type enzymes are
> knocked out, what's the chance that they'll evolve a new one?
Not very good at all - Just like it is not very likely that such
bacteria who don't already have systems of motility would ever evolve
them. The same holds true about eye spots, abilities to utilize
radiation energy from the sun, or many other such functions.
> Clue: Evolution within the context of the history of the organism is
> as important as the context in which the organism finds itself.
Certainly this would have to be the case, if it were true.
> In fact, why don't we grow e.coli on a bed of polyester? What's the
> chance, in 10,000 generations, that they'll evolve a gene to eat
> polyester? If the organism does not have a context in which it can
> evolve by sequential steps, a function that will utilize existing
> pieces to build a polyester-processing system, then it's unlikely to
> evolve one.
Very true. However, the likelihood that this ability or function
would be evolved is proportional to the ratio of potential polyester
enzymes as compared to the total number of potential sequences in
potential protein space. If the ratio is high, then the likelihood
that random walk will happen to come upon one of the winning sequences
is correspondingly high. If the ratio is low, the likelihood that
random walk will happen to come upon one of the winning sequences is
correspondingly low. Of course, as you already noted, the likelihood
that random walk will succeed is also greatly influenced by the amount
of genetic real estate that can actually be spared by a particular
organism to undergo random walk in the first place.
> In other words, you're expecting a gap to be crossed. But before you
> use that as your "AHA" stage, let me tell you this: evolution has its
> limits. Certain gaps cannot be crossed.
Well, we both certainly agree on this point. But this begs the
question, if evolution has its limits, then how exactly did we get all
this variety of fantastically complex functions? I suppose that there
were no gaps to cross? Really? Can you provide evidence for this
beyond examples of the evolution of the most simple antibiotic type
functions and single protein enzymatic type functions?
I'll ask you the same thing I asked some others in this forum - Can
you suggest a genetic experiment that would falsify the theory of
evolution if it failed? In other words, is the genetic theory of
evolution falsifiable? I ask this because I can present evidence for
vast neutral gaps until the cows come home and all you have to do is
say, "Well, I guess that the path must have existed somewhere else."
You see, you really don't ever have to demonstrate this evolutionary
path that you are talking about because you can always fall back on
the idea that evolution does not have to do anything. If something
doesn't evolve in one way, that doesn't mean that it couldn't have
evolved some other way given some other type of experiment or
environment or starting sequence. The problem with this is that your
little "scientific" theory cannot be falsified.
My theory, on the other hand, can be tested in a falsifiable manner.
All you have to do is show that functions of increasing complexity do
not create larger and larger neutral gaps or that such functions can
be evolved if given the proper environment with the use of beneficial
intermediate sequences that I hear so much about. For example, if the
bacterial motility function is so obviously evolvable, then all one
would have to do to falsify my theory is demonstrate the evolution of
such functions starting with a colony of bacteria that never had such
functions.
> The organisms that still live
> today have been able to leap across reasonable gaps, one small step at
> a time. THAT is what evolution describes.
Yes, that is what the theory of evolution suggests happened. What you
have to do is to demonstrate that these intermediate sequences of
beneficial function actually exist in such common numbers so as to
make easy stepping-stones for evolution to walk over without falling
into the vast sea of neutral function.
> Your complaint about large
> gaps not needing to be crossed is NOT what molecular evolution
> requires. There is no large, "And here a miracle occurs" that is
> required by evolutionary theory.
You don't call going from a bacterial-like creature to a human being a
fantastic transformation? The gaps do obviously exist. What is not
so obvious, at least when you stop arguing from morphology and start
trying to argue from genetics, is how such gaps are crossed. You
suggest that there are intermediate stepping-stones that allow
evolution to traverse these gaps quite easily. Well then, it should
be a piece of cake for you to demonstrate these stepping-stones
experimentally. If you cannot demonstrate them, then the neutral gaps
really are a problem for you because there is no known mechanism,
outside of ID, that can explain how such neutral gaps could be
crossed.
> > These very same bacteria would quickly evolve resistance to penicillin
> > if it were added to their environment. No more than a handful of
> > generations would be required.
>
> There's a difference. Evolution of lactase function requires a gene
> duplication of a reasonably closely-related enzyme on demand (which
> you have noted was certainly not within easy reach anymore as both
> related enzymes were deleted) and subsequent mutations of several
> residues within an existing enzyme to acquire lactase function.
You don't seem to have a very good grasp of the experiment in question
here. Evolution of the lactase function would not or at least did not
require a gene duplication of a "closely related" enzyme at all.
Also, the ebgA gene (produced a hexamer lactase enzyme) that was able
to evolve the lactase function was neither closely related to the
original lacZ gene sequence (produced a tetramer lactase enzyme that
had very low sequence homology with the protein produced by the ebgA
gene) nor did it require several mutations to achieve the lactase
function. A single point mutation was all that was needed to turn the
ebgA gene into one that produced a functional lactase enzyme.
However, the relatively low ratio of potential lactase sequences was
soon demonstrated quite nicely when Hall deleted both the lacZ and
ebgA gene sequences. Without these sequences, no other proteins
produced by the E. coli bacteria were close enough to any one of the
potential lactase enzymes to evolve this function back again.
> As evolution is NOT DIRECTIONAL if it is not directly selected on,
> Sean, as is certainly known to you, there is a very large "search
> space" for this kind of evolutionary innovation. Are 10,000
> generations of millions of e.coli enough to generate that kind of
> innovation, enough to give a high probability that the search space
> would be adequately covered? Obviously not.
Obviously not. Again, we agree. So, how are such functions evolved?
Did the original bacterium have enough genetic real estate to be close
enough to several much less all of the functions that we see around us
today? Oh, I know, you will say that the environment changed over
time in different areas so that stepping stone functions arose to
supply the needed paths to create these functions. Hmmm . . . What
are the odds that the proper sequence of environmental changes would
come along at just the right times to give rise to such things as
bacterial motility systems, multi-cell groups and creatures, eye
spots, and a host of other functions that require the simultaneous
function of hundreds or even thousands of parts? A change in the
environment might make new islands of beneficial function rise out of
the sea of neutrality, but it would also make form islands of function
sink.
For example, try to evolve the phrase, "Methinks it is like a weasel",
one letter change at a time, into any other phrase that makes sense in
English *and* is beneficial in a particular situation. You can change
the situation/environment at will to help you out if you start getting
stuck . . . but I really don't think this will help you much because
the nonfunctional gaps are too large.
You see, I know that this is how the paper theory is suppose to work,
but in light of the neutral gaps involved, I don't see how evolution
can really get across the gaps.
> If there is no selected pathway TO lactase evolution, then it's not
> gonna happen except by hit or miss. And that's not what evolution's
> about.
Oh really? So then how does evolution do it? I mean, functions of
increasing complexity are here. How did they get here? Explain to me
the genetic changes in light of these exponentially expanding neutral
gaps in function.
> Hit or miss is not what evolutionary theory supposes.
> Heterogeneity and selection is what evolution supposes.
Heterogeneity? Hmmm, now that's a fancy word. How the heck does that
word help you? How is it different from "homogeny"? How is
heterogeneity, as far as differences in functions and levels of
functional complexity, achieved?
> If there is no
> pathway selecting towards lactase evolution, then tell us, Sean, why
> it would happen?
Yes, why would it happen? That is my whole point. I wouldn't happen
without either a functional path or an intelligent designer.
> Why would evolutionary theory say it must happen
> without directed selection (evolutionary pathway) toward development
> of lactase function?
The theory of evolution doesn't say it happens without a path, it just
can't detail the path is all. Evolutionary theory suggests that the
paths are there, but they can't be pointed out. We are simply told
that they do exist but upon what basis? Where is the evidence for
them? Where have they ever been demonstrated beyond the shortest
paths around (i.e., simple functions like antibiotic resistance and
single protein enzymes)? Oh, it is fine to SAY that they exist, but
it is another thing entirely to actually test this theory in a
falsifiable way.
> > Why then is antibiotic resistance so
> > much easier for them to evolve than the lactase function?
>
> Because antibiotic resistance is based on mutation and selection on
> existing enzymes. That's directed selection, right there.
Actually you are mistaken here. Antibiotic resistance that is based
on enzymes, such as the penicillinase enzyme, does not evolve de novo.
The code for the penicillinase enzyme has never been shown to evolve
de novo in real time experiments. This code was always there whenever
it is detected as a cause for penicillin resistance. It was either
inherited vertically or transferred horizontally, but it did not
evolve de novo.
But, there are several other ways to achieve antibiotic resistance
besides having access to a preformed enzyme or code. Many such
methods of antibiotic resistance are based on the specificity of the
antibiotic and its interaction with a target sequence. Many different
mutations can interfere with this antibiotic-target interaction. The
ratio of interfering sequences as compared to non-interfering
sequences is very high. This makes the neutral gap very small between
such sequences. The reason for this is that it is far easier to break
or interfere with a pre-established function or interaction than it is
to create a brand new function from scratch. As a result, resistance
to antibiotics like penicillin can be and are achieved in short order
even without preformed antibiotic enzymes like penicillinase. The
very same E. coli bacteria that could not evolve the lactase function
in tens of thousands of generations would quickly evolve resistance to
penicillin in a handful of generations using the same level of
selection pressure.
> > What is it
> > about the evolution of relatively simple enzymes that is so much more
> > difficult than the evolution of antibiotic resistance?
>
> Because there's no direction that would be given by selection towards
> lactase function? That's like growing E.coli on a rock and expecting
> it to start spontaneously eating rock. While the chance of that
> occuring is not zero, it's certainly not something within reach of
> ordinary E.coli.
Actually, if the rock was made out of granite, as you suggested
previously, the chances of E. coli being able to get energy out of it
are pretty much zero no matter what enzymes were evolved. The lactase
function is no like this. Any E. coli bacterium that evolved the
lactase function in a lactose rich environment would instantly gain a
significant survival advantage for itself. Also, the lactase function
is not all that complex, relatively speaking. It is based on the
functional potential of a single protein. This is not some
multi-protein function we're talkin here, like bacterial motility.
This is just one single protein.
> And in the case of the missing lactase enzyme itself, full lactase
> function would take more than a few changes. It would require the
> creation of a new enzyme by gene duplication and then evolution.
If gene duplication occurred, the "evolution" would have to happen
extremely fast and by random walk before nature selected to get rid of
the non-beneficial duplicated gene that was costing the organism
energy to maintain. Yes, evolution does have its significant limits
doesn't it?
> But antibiotic resistance only requires a few changes to adequately
> process the antibiotics. Beta-lactamases, for example, break down
> penicillin. Hall's shown a few changes is all that's needed in his
> papers on evolving antibiotic resistence. See for example:
>
> Barlow M, Hall BG. Experimental prediction of the natural evolution of
> antibiotic resistance. Genetics. 2003 Apr;163(4):1237-41.
>
> The TEM family of beta-lactamases has evolved to confer resistance to
> most of the beta-lactam antibiotics, but not to cefepime. To determine
> whether the TEM beta-lactamases have the potential to evolve cefepime
> resistance, we evolved the ancestral TEM allele, TEM-1, in vitro and
> selected for cefepime resistance. After four rounds of mutagenesis and
> selection for increased cefepime resistance each of eight independent
> populations reached a level equivalent to clinical resistance. All
> eight evolved alleles increased the level of cefepime resistance by a
> factor of at least 32, and the best allele improved by a factor of
> 512. Sequencing showed that alleles contained from two to six amino
> acid substitutions, many of which were shared among alleles, and that
> the best allele contained only three substitutions.
Very interesting, but not any news. There were no gaps involved here.
The evolution of cefepime resistance required at most a neutral gap
of two mutations to the pre-existing beta-lactam enzyme. A gap of 3
or even 6 neutral mutations would not be a problem for random walk to
overcome in an average sized bacterial population. However, try
evolving the beta-lactamase enzyme de novo, from scratch, and see how
fast this happens.
Examples of "evolution" like this are all over the place. While they
are real examples of evolution in action, they really don't explain
the evolution of much of anything beyond the most simple of functions
that have very limited neutral gaps and very high ratios of beneficial
sequences as compared to the total number of potential sequences.
Hall demonstrated this same sort of thing in his lactase evolution
experiments. He showed how the lactase gene (ebgA) could get mutated
to produce enzymatic activities on several different types of sugars.
Of course, each of these new functions was achieved with just one
mutation. One of the enzyme function required two mutations, but this
is not statistically significant. Likewise, new lactam antibiotics
will most certainly be within the reach of existing lactamases. The
target is so specific that any changes to the antibiotics cannot be
too major. Because of this problem of required specificity, limited
changes to the antibiotic can be overcome by equally limited changes
to the antibiotic enzymes.
Also, even if the bacteria didn't have access to the pre-formed
beta-lactamase enzyme, they would still evolve resistance to cefepime
in relatively short order via mutations to target sequences.
> > Also, we have actually seen a few relatively rare real time
> > demonstrations of enzyme evolution, to include the evolution of the
> > lactase function in some types of E. coli, but never in other types of
> > mutant E. coli and never in many other types of bacteria over the
> > course of 50+ years.
>
> Sean, antibiotic resistance IS real-time ENZYME evolution. Do you even
> know what a beta lactamase (for instance) is? Don't you think you
> better find out? It's an enzyme. It evolves.
Again, you didn't get this lactamase enzyme de novo. Just because it
can change slightly to accommodate slight changes in various new
antibiotics that come out does not mean that this enzyme evolved from
scratch. Delete the lactamase enzyme and see how quickly you can get
it back. Then, after that, you can claim that de novo enzyme
evolution produces antibiotic resistance. For now, this doesn't
happen. If the preformed enzyme is not already there, it does not
evolve de novo - period. However, antibiotic resistance still evolves
de novo. How? Because of mutations to target sequences and the like.
> So, yes, antibiotic resistence is enzyme evolution.
No, it is not. You have to have the enzyme there already preformed to
a significant degree. Even your example of the evolution of cefepime
resistance started with a preformed enzyme that was 99.9% identical to
the "new" enzyme that attacked cefepime. This really isn't what I'm
talking about here, and you know it. You are trying to blow a smoke
screen over the main point. The point is that evolving enzymes from
scratch is much much harder than evolving functions like antibiotic
resistance that arises de novo, without any preformed enzymes.
> The fact that
> we've seen real-time evolution of anything is clue one: evolution
> occurs.
Certainly mindless processes of evolution do occur, but they are very
very limited in what they can do and explain. The de novo evolution
of antibiotic resistance in bacteria without preformed enzymes is very
easy to explain since it involves interference with or the breaking of
a preformed interaction or function. Again, the principle that it is
far easier to destroy than to create holds true here. De novo
antibiotic resistance is really based on the destruction of a function
and not the creation of a new function from scratch.
> Under selection, the system is perfectly able to move towards
> the desired, selected state: survival in the presence of an
> antibiotic.
Yes, even if that bacterial colony does not have access to a
pre-formed antibiotic enzyme. Again, this is because of the
specificity of the antibiotic for a particular target. Get rid of the
target or change it in some way so that the antibiotic cannot bind
well with it, and resistance is gained - simple. Moving up the ladder
of complexity though, to the evolution of just one simple enzyme from
scratch, is a lot more challenging however since the neutral gaps have
just expanded exponentially.
> That's a basis of Hall's research, up to the present day.
> He's been able to recently "predict" some aspects of in-the-wild
> antibiotic resistance by evolving the resistance in the laboratory.
You don't need to evolve anything in the laboratory to successfully
predict the evolution of antibiotic resistance. I predict that no
matter which new antibiotic is put on the market that bacteria will
quickly develop resistance to it. I also predict that if that
antibiotic is pulled off the shelf for a while, that the bacteria will
revert back to their wild-type nonresistant state and the antibiotic,
if used again, will be as effective as it was initially. I suggest
then, based on this hypothesis of mine, that it would be wise for
hospitals to get together to start a antibiotic rotation. Use one
type of antibiotic for a given span of time, and then stop using it
altogether and start using another type of antibiotic with a different
target for a while, and then stop using that one and move on to
another type. Then, after moving on to several different antibiotics,
start the rotation over again. I am betting that the bacterial
population will be susceptible to the original antibiotic once again.
> > However, we have never seen a bacterial function
> > evolve that requires multiple proteins working together at the same
> > time, such as would be required for the function of bacterial
> > motility.
>
> I don't know of any experiment that's tried to direct that kind of
> pathway, yet.
Yeah, me either! Perhaps you should suggest this to some of your
evolutionist buddies? I'm betting that many have thought of doing
something like this and perhaps they have tried, but I am betting that
it just won't work. But, knock yourself out trying - go for it! ; )
> I maintain that there are no barriers to coupled evolution within a
> complex system given gene duplication and mutation, among other
> processes.
Yes, you and all other evolutionists "maintain" this position, but
where is your evidence? If your gene duplication is not immediately
advantageous, nature will select to get rid of the duplicated gene.
If the neutral gaps between what is and what is needed are too large,
your duplicated gene will get eliminated before it can undergo very
much random walk toward much of anything. Then, where are you? - Back
to square one? Your mutations need to follow a path of beneficial
functions. But, what if this path comes to sequences that offer no
beneficial changes in any direction? What if your island is
surrounded on all sides by a huge sea of non-function/neutral
function/detrimental function? What are these "other processes" that
you would need to save you from this predicament?
> That is the simplest answer: no restriction on evolution at
> any level. I have seen no evidence that there is any barrier to
> evolution as evolutionary theory currently presents itself.
Oh really? How do you get across the gaps of nonfunction to produce
such multi-protein functions as bacterial motility? Please, how,
exactly, does your current theory of evolution explain this? What
falsifiable experiments can you put forward in support of this
statement?
> I have only seen that a couple of knocked-out genes do not poof into
> appearance out of nothing within ten thousand generations under
> limited laboratory conditions with no selection along a pathway of
> intermediate states...an experiment that would certainly take longer
> than 10,000 generations of E. coli to generate results.
Yes, and you don't find this significant? How so? How do you explain
the crossing of such gaps that are obviously increasing exponentially
with each step of increasing complexity? Some functions, such as de
novo antibiotic resistance, arise rapidly and commonly, while others
that are only slightly more complex, such as single protein enzymes,
arise so much less commonly and others, such as multi-protein systems
of function (i.e., bacterial motility) have never been shown to arise
de novo. How is this explained? Please, you do seem quite informed.
I'm curious to hear your answer to why some functions are so easy to
evolve while others are so much harder to evolve. Also, I would be
curious to hear your predictions on how you would calculate the
average time needed to evolve such functions as bacterial motility
starting with a non-motile bacterium. I don't think you can be all
that specific. I think that you are going to try and be as vague as
possible by saying that various environmental changes must have come
along, but you aren't going to even try to detail these changes or the
average time involved for such changes to produce such levels of
function.
> > Why is this type of multi-protein function so difficult to
> > evolve in real time? Hmmmmm?
>
> I don't understand your complaint. Evolution suggests many changes are
> evolved within "reach", as in, step-by-step, by action on existing
> genetic material or mechanisms. I don't see your problem with this.
> Step-by-step evolution, even in coupled-systems, is perfectly
> reasonable.
Oh yeah - detail this reasonable explanation for such genetic changes
in function.
> > I look forward to finally hearing from someone in the know as to why
> > antibiotic resistance evolves so much faster than the functions of
> > enzymes and why enzymes evolve at least on some rare occasions, but
> > functions with multiple proteins working together at the same time,
> > never seem to evolve in real time.
>
> Um, Sean, antibiotic resistance IS evolution within enzymes.
Not really - see above
> The
> enzymes are themselves evolving better function in respect to new
> antibiotics.
Um, Deanne, this is not the de novo evolution of an enzyme. Such
enzyme changes always start with a pre-existing enzyme that is very
similar. Beta-lactamases have never been shown to evolve de novo
(i.e., in a population that didn't have some pre-formed beta-lactamase
to begin with).
> The enzymes are in some cases changing their function to
> adjust to the presence of a new antibiotic. Therefore, new antibiotic
> resistance IS the change of an enzyme's function.
See above - You are trying to dodge the issue.
> For instance, from Hall's recent paper: "The TEM family of
> beta-lactamases has evolved to confer resistance to most of the
> beta-lactam antibiotics, but not to cefepime"
>
> A refresher from your biochemistry class, the "-ase" at the end of
> that word means it's an enzyme. If you still don't believe me, go
> here:
>
> http://us.expasy.org/cgi-bin/nicezyme.pl?3.5.2.6
>
> That's the page for beta-lactamases in the ENZYME nomenclature
> database. Yea, they're enzymes.
LOL - Oh really? I didn't know!? Shocker! Please Deanne - get with
the program and stop trying to blow smoke.
> And as to why we don't "see" multiple protein evolution, show me a
> study where someone has done work on multiple-protein evolution
> (coupled evolution). I can't seem to find studies like that. Maybe you
> know of some. Until someone digs deeply into that kind of study, I'd
> say that your complaint is premature.
Fine - But until such studies and successes can be demonstrated by
you, I'm saying that your belief in evolution is a poorly supported
belief that is based on a whole lot of faith a not much else. But, I
do admire great faith in a person. Hang in there . . . Perhaps the
experiments you need will come along just before cows start hopping
over the moon.
> >I mean, if it is so easy, as you
> > seem to be saying, then evolution should proceed rapidly, should it
> > not?
>
> No. Evolutionary theory does not say that genes should poof out of
> nothing without known processes. If there was no replacement for the
> lacZ gene, or any gene within evolutionary "reach" even with gene
> duplication, then why would we expect it to evolve lacZ function?
Evolution claims that a lot of new functions did arise via purely
mindless natural processes. If there were no neutral gaps to slow
this process of evolution down, these functions that did arise would
have arisen far faster than they did. Millions and billions of years
would not have been required. Without neutral gaps, the evolutionary
forces would "poof" a great many things into existence.
> Do you have evidence that there are any enzymes less than a few
> handfuls of mutations away from lacZ that the bacteria could have
> evolved but didn't?
LOL - No!!!! That is the whole point. There is a average gap
between functional lactase sequences that is apparently quite large
given the potential sequence space of 10e1300. The ratio of lactase
sequences in this space seems to be fairly small indeed.
> > If there were no neutral gaps to slow the process of evolution
> > down, then given the proper environment, the evolution of beneficial
> > functions, such as the lactase function in a lactose rich environment,
> > should proceed very quickly.
>
> Just like nylonase seemed to just spring out of nowhere but it was
> really a selected copy of a differently-expressed, already-existing
> gene.
Yes - The nylonase function arose via frame-shift mutation. I
wouldn't call this anything like the previous gene. The coding
sequence was entirely new. Of course, there may be a higher ratio of
nylonases out there as compared to lactases, but the point is the
same. The ratio of even nylonase sequences is far lower than the
ratio of antibiotic resistance target sequences in E. coli. The gap
is wider. And, this gap increases in size as one moves up the ladder
of functional complexity.
> How do you know that the knock-out E.coli had all the right conditions
> to evolve a lactase function out of existing parts? If it had no
> "within reach" enzyme to utilize as a weak lactase it could get a
> foothold with, and then select for lactase function, then it wouldn't
> be any more able to generate that lactase function than it could eat
> rock. Frankly, to demand anything like that is silly.
You are on the verge of understanding the problem I think, but you do
not yet understand that the limits to evolution are more widespread.
Increasing gaps with increasing complexity means that if evolving a
relatively simple lactase function is as hard as eating rock for some
creatures, that evolving anything more complex than this would be all
that much harder. The genetic real estate of a given creature is
severally limited, as no is its environment. The odds that it is
close to ANY enzyme of the complexity of lactase or nylonase or
penicillinase is pretty low. Occasionally though, the odds are still
within range so that one or two of such enzymes may come around at
just the right time. But, this is quite rare. Given the rarity of
such events, consider how rare it would be for such creatures to
evolve anything more complex, like a motility function or other such
multi-protein functions where all the proteins work together at the
same time. Remember, just because all the needed parts are being made
by the same creature as parts of other systems of function does not
mean that they will spontaneously self-assemble to produce a new
function. For example, all the amino acids are present in a cell
doing many different functions. They could make many new functions as
well, but they just don't know how to self-assemble themselves. All
the parts are there, but ordering them is important. How is this
done?
> > This lactose environment ain't outer
> > space and it ain't granite you know.
>
> It might as well be if there's no enzyme that has significant lactase
> activity. It makes the enzyme effectively "blind" to evolutionary
> change in that direction.
Yes! I'm so glad that you recognize this point.
> What's your evidence that it had any kind of
> weak lactase function at the end of the experiment? Did it?
What? I don't exactly understand your question here. The ebgA gene
produced a protein with beneficial lactase function. But, no other
gene was able to produce such an enzyme with a beneficial level of
lactase activity.
> > One little enzyme is all that is
> > needed to use this new environment in a more advantageous way. And
> > yet, many different types of bacteria seem unable to evolve the
> > lactase enzyme despite hundreds of thousands and even millions of
> > generations of time. What then, exactly, is slowing this process
> > down? Please, you seem so knowledgeable . . . what is the answer?
>
> The answer is that 10,000 generations of e.coli in a laboratory under
> fixed experimental conditions were not enough to evolve, through
> selection, a weak lactase activity.
Yes, that is the conclusion that I came to as well.
> I hope that helps.
Oh, it does. . .
> Deanne
Sean
Dunk
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
<snip, as if you couldn't tell>
>I'll ask you the same thing I asked some others in this forum - Can
>you suggest a genetic experiment that would falsify the theory of
>evolution if it failed? In other words, is the genetic theory of
>evolution falsifiable?
An observation, not an experiment since it depends on how the
experiment comes out. One observation would be the spontaneous
generation of rats and mice all over the world well adapted to local
conditions. Another would be a much higher rate of
occurrence of beneficial mutations than is expected by chance.
Dunk
Dunk
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
<snip>
>Evolution claims that a lot of new functions did arise via purely
>mindless natural processes. If there were no neutral gaps to slow
>this process of evolution down, these functions that did arise would
>have arisen far faster than they did. Millions and billions of years
>would not have been required. Without neutral gaps, the evolutionary
>forces would "poof" a great many things into existence.
It's your theory that doesn't require billions of years. What is your
explanation of why the Designer took so long?
Dunk
Dunk
> Gaps gaps neutral gaps gaps gaps gaps neutral gaps gaps ....
A word of duplications and neutral gaps.
Mutations including gene duplications are frequent. The fate of most
new mutations including duplications is to disappear via neutral or
nearly neutral drift. Of the remainder the majority are eliminated by
negative selection. Many of those that remain and become widespread
are in the nearly neutral zone, and may be slightly harmful. Some are
distinctly beneficial. Some genes including some duplications are not
expressed, and undergo a good many neutral mutations.
But of those duplications that become fixed or become established
polymorphisms very few spend much time wandering around neutrally.
Checking recent & moderately recent papers I think you will find that
duplications that are going to 'succeed' are duplications of a gene
that was already doing two things, or duplications that soon come
under selection for a new function.
Note that what we call 'gene duplication' is better called short
segment duplication. When there is some 'extra' DNA between a gene
and its duplicate, especially unexpressed DNA, it is quite possible
that the two copies will be differently regulated. One copy may be
unexpressed or always (constituatively) expressed or expressed at a
bad time. Or a good time. Gene regulation is also based on certain
parts of the DNA (and usually subject to external influence).
Mutations that change one amino acid in a protein are the most
predictable in their effect, while mutations in regulation are rather
unpredictable.
A case has been made that there are lots of neutral paths that a
protein might take, especially one based on a duplicate gene.
However, they don't. Just because a path exists does not mean it is
taken. Duplicates that acquire new functions very typically follow
selective paths from here to there, with few or no neutral steps.
> Why didn't certain bacteria acquire a lactase function in the lab
> (even though others with a different starting point did)?
> Why oh why?
This question has been repeated for months. The answer has been
expressed differently at different times but is essentially this:
You can't get desired mutations on cue just because you want them.
You can't.
> The likelihood that a function
> would be evolved is proportional to the ratio of
> enzymes that do it as compared to the total number of potential sequences in
> potential protein space.
No. As has been mentioned before, proteins do not 'explore' this
conceptual space. First, most are members of sizable families related
by duplication. This alone tells you they haven't explored very much
of the mathematical sequence space. That they do all that they do
anyway tells you that functional proteins are not that rare. Frame
shift mutations and other multiple amino acid changes may create novel
proteins and sometimes start new families, but functional proteins do
not spend much time wandering around lost in space. Selection makes
them follow functional paths.
> If evolution isn't held up by the necessity of crossing vast neutral gaps then it should be much quicker.
No. It takes as long as it does because beneficial mutations do not
happen on cue.
Because of all the ways that genetic change may occur, care must be
taken in concluding that any 'gap' is unbreachable. There are low pH
bacteria that eat rocks.
Dunk
Sean Pitman
> Sean Pitman <seanpi...@naturalselection.0catch.com> wrote in message
> news:80d0c26f.03062...@posting.google.com...
> > But, given the size of the
The "breeding" or evolving a "bit string" in the Alife program is not
based on "randomly swapping bits" but on the "Standard Genetic
Algorithm." In this algorithm, a crossover point is selected
randomly, then the left portion of one string is "mated" or
"recombined" with the right portion of another string (and vice
versa). This allows chunks of circuitry, which work well together, to
have some chance of not being disrupted. Some random flipping of
single bits is also used, but this is relatively rare.
In this particular Lenski experiment the researchers studied 50
different populations, or genomes, of 3,600 individuals. Each
individual began with 50 lines of code and no ability to perform
"logic operations". Those that evolved the ability to perform logic
operations were rewarded, and the rewards were larger for operations
that were "more complex". After 15,873 generations, 23 of the genomes
yielded descendants capable of carrying out the most complex logic
operation: taking two inputs and determining if they are equivalent.
The lines of code that made up these individuals ranged from 49 to 356
instructions long. The ultimately dominant type of individual
contained 83 instructions and the ability to perform all nine logic
functions that allowed it to gain more computer time.
In principle, 16 mutations (recombinations) coupled with the three
instructions that were present in the original digital ancestor could
have combined to produce an organism that was able to perform the
complex equivalence operation. What actually happened was a bit more
complicated. The equivalence operation function evolved after 51 to
721 steps along the evolutionary path, and the "organisms" used
anywhere from 17 to 43 instructions to carry it out. The most
efficient of the evolved equivalence functions was just 17 lines of
code - two fewer than the most efficient code the researchers had come
up with beforehand. Evolving even as few as 17 lines required a few
more than 16 recombination/mutation events (but not that many really,
considering that the majority of these "mutations" were functional).
In one case, 27 of the 35 instructions that an organism used to
perform the logic operation were derived through recombination, and
all but one of them had appeared in the line of descent before the
complex function was performed.
The researchers' model involved 103 single mutations/recombinations,
six double mutations, and a pair of triple mutations. In the
short-term 45 of those were good, 48 neutral, and 18 detrimental.
Thirteen of the 45 beneficial steps gave rise to logic functions not
expressed by the immediate parent. Fifteen of the 18 detrimental
mutations made the offspring slightly less fit, or likely to
propagate, than the parent. Two of the detrimental mutations cut in
half the offspring's fitness. One of these very detrimental mutations,
however, did produce offspring that one step later produced a mutation
that in turn gave rise to the complex logic operation.
So, there are several interesting constraints to this experiment. For
one thing, the ultimate functional goal was predetermined as with
Dawkins's "Methinks it is like a weasel" computer evolution
experiment. However, there was a difference here in that each of the
steps involved with Lenski's experiment were actually functionally
unique. The problem is that these functions were predetermined by the
scientists to be functionally beneficial. Basically, the proper
environment was a set-up for the success of a particular evolutionary
scenario, which was already pre-determined via intelligent design.
Also, the types of mutations that were used were not point mutations,
but were based on swapping large sections of pre-programmed meaningful
bit code around. The researchers knew that with a relatively few
recombinations of code such a logic function of "increasing
complexity" would be realized. After all, the environment was set up
to produce changes were the ratio of beneficial changes as compared to
all other potential changes was very high. Like the evolution of
antibiotic resistance this function was easy to evolve given the
restraints used by the scientists because the neutral gaps were set up
to be so small. Also, the success of the experiment was dependent on
pre-established lines of code that were set up to work together to
solve logical problems of a specific type. I suggest however that
this particular setup would not be able to evolve other types of
functions, like the ability to open the CD-drive or the ability to
cause the monitor to blink off and on. The gaps involved would
require different types of starting code sequences that could not be
gained by the type of code recombination used in this experiment.
Point mutations would be required and very large gaps in function
would need to be crossed before these other functions could be
realized.
In short, I think that this experiment was a setup for success of a
very limited goal and does not explain the evolution of uniquely
functional systems beyond the most elementary of levels. It did end
up producing some "unexpected" solutions to the problem, but that is
only to be expected. There might be many different ways to interfere
with an antibiotic's interaction with a target sequence that might not
be otherwise expected. However, the functional ratio is what is
important here and clearly it is very high as compared to the neutral
sequences (40% beneficial mutations vs. 10% detrimental and only 43%
neutral - Please! Give me a break!). Success was guaranteed by the
way the intelligent designers set up their experiment.
http://www.trnmag.com/Stories/2003/052103/Simulated_evolution_gets_complex_052103.html
> The second paper concerns the emergence of immunity to chloroquine, the
> drug used to kill the parasite that causes malaria. Molecular studies show
> that nine sequential mutations, in a gene which encodes a complex transport
> protein called PfCRT, must accumulate for chloroquine immunity to develop;
> each of these mutations provides gradually increasing resistance, although
> only once the eighth has arisen is the parasite resistant to clinical doses
> of the drug, and only once all nine are in place is there total immunity.
> It took almost 20 years, but that is precisely what has happened. In fact,
> this appears to have happened independently at least four times in
> different geographical locations. You will notice that at no point did this
> step-by-step evolution encounter an uncrossable barrier or have to leap a
> gap of no selective utility.
I have already discussed the topic of chloroquine resistance in this
very thread in response to Von Smith and Bill Rogers.
Again though, like Rogers and Smith, you have overstated your case.
For one thing, most papers use between 6 to 8 mutations (not nine) as
found in many different chloroquine resistant mutants. However, this
really isn't all that important as far as the main issue is concerned.
Neutral gaps of this size are really not a problem for populations
that exist in the wild. The most likely reason why this has not been
observed in the lab is because the lab didn't use a large enough
population size to overcome the neutral gap created by 2 or maybe 3
neutral mutations. However, even a series of 7 neutral mutations in
DNA would create a neutral gap or sea of no more than 16,384
possibilities. In this hypothetical case, even if only one of these
possibilities were "correct", a large population could find it in
relatively short order. In order to find this correct sequence out of
all the other possibilities, the given population of malaria parasites
would have to undergo random walk. This random walk takes time and
this time is dependent upon several factors. Let's say that the
mutation rate was on the order of 10e-8 mutations per base pair per
generation. On average then, it would take around 10e7 generations to
get just one mutation to one of our 7 base pairs of interest. If a
generation time is one day (I'm not exactly sure what the generation
time is for the malaria parasite at this stage of its life cycle), a
steady state population of 10e3 parasites would experience one
mutation in these 7 base pairs every 10,000 days or 27 years on
average. Given this relatively small colony of parasites, it would
take around 500,000 years to develop resistance to chloroquine. If the
colony size were increased to one million parasites, the time required
to evolve resistance would drop to around 5,000 years. If the colony
size were increased to one billion parasites, the time required would
drop to around 5 years.
These rough estimates, based on the time required to cross such a
neutral gap, are very much in line with what we have seen in the
evolution of chloroquine resistance in the wild and they also explain
why this resistance has never been demonstrated in the lab. The lab
experiments simply didn't use a large enough population size or didn't
carry on the experiments for enough generations.
In any case, it is a great example that demonstrates very nicely the
limits that neutral gaps put on the theory of evolution. This only
strengthens my theory.
In real life though, chloroquine resistance (CQR) is a bit more vague,
but still seems to require at least a few mutations (as many as 6 -
but perhaps only two mutations), before at least some beneficial level
of resistance can be realized. It turns out that several of the
mutations seen in CQR are selectively advantageous once the initial
two or three are realized.
The resistance to both mefloquine and chloroquine is achieved via the
blocking or interference of the pre-established interaction of these
drugs with specific target proteins. Again, my prediction that such
interferences are relatively easy to achieve holds up in these cases
as well. No new protein or enzyme is evolved in these cases. The only
thing that happens is a disruption of a specific interaction that was
pre-established (It is just a different way of breaking Humpty Dumpty,
but still relatively easy to do.). As with de novo antibiotic
resistance (via disruption of the antibiotic-target interaction), such
disruptions are relatively easy to achieve and are almost always based
on one or two point mutations, or at most a handful of such mutations
as is potentially the case with chloroquine resistance. Also,
chloroquine resistance has been very difficult to reproduce in the lab
and has taken a bit longer to evolve in the wild than mefloquine
resistance. However, the difference in complexity between these two
drugs is really is rather negligible considering that the mutations
responsible for this difference in complexity can be counted on one
hand. This evidence fits very well with my predictions for the
required time needed to evolve this very low level of complexity that
is based on interfering with a pre-established interaction - not the
creation of anything new as far as an enzyme or some other such
protein of higher complexity.
Specifically though, these are some details about how chloroquine
actually works:
In human red blood cells, P. falciparum supports its growth by taking
up host cell cytoplasm in an acidic digestive food vacuole. Toxic
heme, in its hematin form, is released in the vacuole by hemoglobin
digestion and is crystallized into innocuous hemozoin, or "malaria
pigment". Chloroquine (CQ) interferes with this process by complexing
with hemozoin. This complex prevents hematin from crystallizing into
the innocuous hemozoin form. The "toxic" effects of free hematin are
caused by hematin's ability to increase membrane permeability which
lead to cell lysis and death. Hematin also is known to inhibit
parasite enzymes.
Chloroquine resistant strains of P. falciparum show a reduced
accumulation of CQ in the digestive vacuole. The genetic mutations
associated with this reduced accumulation have been isolated to the
PfCRT (P. falciparum chloroquine resistance transporter) gene. The
gene contains 13 exons that cover 3.1 kb. The PfCRT gene product is a
423 amino acyl ten-transmembrane channel or transporter protein that
catalyzes chloroquine flux and H+ equilibrium across the digestive
vacuole membrane. Many different point mutations have been isolated
in resistant CQR strains of malaria (M74I, N75E, K76T, A220S, Q271E,
N326S, I356T, and R371I). Of these, only the K76T and the A220S
mutations are shared in common between resistant malaria strains on
various affected continents of Asia, Africa, and S. America. The K76T
mutation in particular seems to be the most important marker of CQR.
What is interesting is that the K76T mutation is never seen by itself,
but is always associated with a few other point mutations. However,
in some CQ resistance strains the K76T mutation is absent. One such
strain is the "106/1" strain that has the K76I mutation instead. This
strain has six of the other point mutations, but is has the K76I
instead of the K76T mutation at position 76. Even without the K76T
mutation the 106/1 strain does have a fairly high level of CQR.
However, the level of resistance is not as high as those strains that
do have the K76T mutation. Interestingly enough, Fidock et al.,
performed an experiment with the 106/1 strain where stepwise CQ
pressure was added to the population. The result was a fairly rapid
change at position 76 from the K76I to the more resistant K76T
mutation.
The results of such observations suggest that the K76T mutation is not
selectively advantageous by itself. the A220S may fulfill a
particular requirement in the development of CQR since this mutation
has consistently been found to accompany the K76T mutation in CQR
parasites from the different New and Old World foci. "The suggestion
that K76T cannot occur in the absence of other PfCRT point mutations
may also explain the slow genesis of CQ resistance in the field as
well as the difficulties that have been experienced with attempts to
select CQ resistance in the laboratory."
http://www.dbbm.fiocruz.br/class/Lecture/d24/drug_resistance/mc4404.pdf
> >> No one but you claims that *any* organism, put in *any* new environment
> >> *somehow*, according to evolutionary (due to selection) ideas, *must* be
> >> able to evolve a function that allows it to survive.
> >
> > Actually, this is very much what the theory of evolution is
> > suggesting.
>
> Absolutely not. Nothing about evolution ever said that the first cell was
> required to survive; in fact it's been proposed that life arose more than
> once on the early Earth, but all but one (obviously) of those attempts
> ended in extinction. And the first living things were, so to speak,
> building themselves from the ground up. This is a significant difference
> from an experiment where a well-established species that had grown
> dependent on a particular source of energy suddenly had the rug pulled out
> from under it.
I am saying that as long as the organism is able to survive and
reproduce (i.e., it lives in a non-lethal environment), the theory of
evolution does in fact propose that many new functions of incredible
diversity and complexity WILL evolve - given enough time. I'm not
talking lethal environments here. I'm talking about any organism that
can reproduce over an extended period of time.
> > The very first organism was quite limited indeed and it
> > was in a limited environment as well. And yet, it supposedly evolved
> > many new functions in relatively short order.
>
> Who says? As far as we know the first eukaryotic cell, incorporating many
> new cell structures that do not exist in prokaryotes, did not arise until
> only about 1.5 billion years ago.
In comparison to trillions upon trillions of years to cross even a
small gap of neutral function, a few billion years is nothing.
> > Really, given enough
> > time, any self-replicating organism should be able to morph itself
> > into just about any phenotypic shape and function imaginable, given
> > the proper environment. As long as the new environment is not
> > immediately lethal, and time is allowed for extended growth and
> > competition for survival, then yes, the theory of evolution suggests
> > strongly that new functions will evolve that allow some organisms to
> > survive better than their peers in this new environment.
>
> New functions will evolve, yes. No one ever said (except perhaps
> creationists pushing strawmen) that organisms should be able to evolve into
> "just about any" imaginable configuration.
Yes, this is exactly what is suggested by the theory of evolution.
Given enough time, any life form will be able to evolve almost
unimaginable functions of magnificent variations and complexities over
just a few billion years.
> Doubtless there are many
> configurations that no living thing will ever reach precisely because there
> is no selectable path leading to them.
This is not the point. The point is that evolution proposes that many
such paths do exist. In fact, a huge number of such paths must exist
so that spectacular changes are pretty much inevitable given enough
time for competition. One particular picture might not be realized,
according to the theory, but certainly the picture will change
dramatically. What I am saying is that the picture will change, but
in only the most limited of ways. The theory of evolution claims that
the picture will change almost beyond recognition when compared to its
origin. I think that the neutral gaps surround the picture so
extensively that the picture is pretty much stuck within very limited
boundaries. The theory of evolution really presents no such
boundaries since its supposed paths move out extensively in a huge
number of directions. I propose that after a very few steps, all of
these paths run into significant gaps of neutral function.
> But that is as far as we're
> justified in going, that is the farthest such a line of argument can be
> supported. We, at this moment with our present state of knowledge, are by
> no means justified in saying what specific configurations those might be.
> Whenever we say something is impossible, life tends to surprise us. (Who
> would ever imagine something like a spider, or a firefly, or a bombardier
> beetle, without first seeing one?)
Your problem is that you hypothesize that a mindless process of
evolution created such things as a spider, firefly, beetles, etc.,
without being able to explain how such functions could have evolved
across vast seas of neutral function. Most arguments are based on
morphologic similarities. The more rare arguments that are based on
genetics proposed genetic intermediates between such variations in
morphology. Ian Musgrave, for example, has gone to great lengths to
show how bacterial flagella could have evolved to produce the motility
function. And yet, in his explanations, there are huge neutral gaps
remaining between his islands of intermediate genetic function that he
cannot or at least has not explained. Also, no experiments have been
done to demonstrate his paper hypotheses, not even as far as the
crossing of even one of his proposed intermediate steps.
I mean, obviously the neutral gaps exist and they obviously grow
exponentially with increasing complexity. What do you have that can
explain how these gaps are crossed? Your example of the work of
Lenski et al., is far too limited in that it is set up so that it
doesn't have to cross very many neutral gaps (if any). Your
chloroquine example is in the same boat. Nothing that is of a level
of complexity higher than de novo antibiotic resistance is produce in
either case. Software programmers are certainly not about to loose
their jobs over these "new" discoveries. Why? Because, computers are
still incapable of intelligent design or independent creativity that
goes beyond very limited and very directed situations. These Lenski
software programs could only evolve particular logic functions based
on the recombination of pre-programmed lines of code. In order to
develop new functions beyond this limited parameter (like the opening
of my CD player or the flashing of my computer screen of and on) brand
new lines of code would have to be evolved from scratch via single
point mutations. Also, even the logic functions that were evolved
were dependent upon the proper selective environment being set up
ahead of time by ID. What if there was a gap between one type of logic
function and another type of logic function, such as between the NAND
and the EQU functions that required the evolution of either the AND or
the OR, or the NOR, XOR or NOT functions first? What if these
functions were not recognized by a particular environment as being
beneficial? Then, there would be a neutral gap created by that
environment between the NAND and EQU functions. What are the odds
that the "proper" environment that recognized at least one of these
other functions as beneficial, would come around at the right time?
You see, the random walk not only includes random changes in code, but
also in environment. Without an intelligent mind directing changes in
environment in just the proper way, the organic synthesis of many
different compounds that are made in chemistry laboratories would not
work. The order of the environmental changes is just as important as
the order of the molecules in the "evolution" of new functions or
compounds.
> >> There is no
> >> guarantee that *all* organisms will be able to evolve to *any*
> >> arbitrarily stated conditions.
> >
> > Certainly not. However, what you are basically saying is that the
> > theory of evolution cannot be tested. Experiments cannot be set in a
> > falsifiable way because if they fail, all you have to say is, "Well, I
> > guess we just didn't use the right environment or the right organisms
> > to demonstrate evolution this time." This always leaves you an out.
>
> Yes, and? This is *life* we're dealing with here. It's a complex, messy,
> chance-dependent, sloppy, unpredictable thing.
How do you know if you cannot think of a falsifiable test for your
genetic theory?
> A mutation that could make
> all the difference could be caused by the unintended presence of a
> mutagenic pollutant in extremely small quantities impinging on a cell; it
> could be caused by a cosmic ray arriving from the explosive death of a star
> halfway across the cosmos billions of years ago; it could be caused by a
> background quantum fluctuation, the most intrinsically unpredictable
> phenomenon in existence. This isn't like simple Newtonian physics where you
> can throw a ball up into the air, and given the same initial conditions, it
> will always land in exactly the same spot.
Newtonian physics can be tested in a falsifiable way. Because of
this, it falls under the power of the scientific method. If you
cannot test your theory in a falsifiable manner, then really, you have
entered the realm of blind faith.
> > Without the theory of evolution being falsifiable in such genetic
> > experiments, you can always believe in it no matter what the
> > experiments say. Tell me, what genetic experiments could be done that
> > would falsify the theory of evolution? Really, unless you can detail
> > such an experimental result that would counter the theory of
> > evolution, your theory really is not scientific. You must have a
> > genetic test that is testable and falsifiable. What is it?
>
> Easy: You could test to see if organisms ever undergo beneficial genetic
> changes that can be inherited by their descendants.
This is not enough. There is evidence that neutral gaps grow
exponentially with increasing complexity. It is not enough therefore
to present a case of antibiotic resistance evolution that is based on
the interference of a pre-established interaction, and just
extrapolate this to explain the evolution of functions of higher and
higher complexity. Such an extrapolation is illogical in the light of
increasing neutral gaps. You must be able to present a falsifiable
test that supports your hypothesis about how these growing neutral
gaps are crossed.
> Sorry if you wanted
> something more specific, but evolution is by its very nature a process that
> is partially dependent on chance. Sometimes the right mutations that would
> enable an organism to survive in a given situation just don't come up
> (which is why a rather overwhelming majority of all the species that have
> ever lived are now extinct). It would be absurd to put an organism in a
> situation and demand it evolve in a specific way, and conclude evolution is
> falsified if it doesn't.
I'm not demanding that evolution follow a specific path. What I am
demanding is a demonstration of the evolution of a specific level of
complexity, not a specific type of function. It is the evolution of
increasing levels of complexity that cannot be explained beyond the
most simple levels of function. For example, if I see a cow jump over
a sidewalk, can I automatically assume that this cow can jump over a
6-lane freeway? Obviously not. Why? Because there is evidence that
the cow is fairly limited in its jumping capabilities by both its
genetic inheritance and its current environment. Perhaps if the
environment suddenly changed and gravity was greatly reduced, the cow
might just be able to jump far greater distances, but what are the
odds that just such a "beneficial" environment would happen to come
along at just the right time?
> >> All the "story-telling" pathways
> >> that we present wrt to flagella are pointing out just such pathways
> >> *and* the evidence to support those pathways.
> >
> > Not so. All your story telling about how such pathways must exist
> > don't even work well on paper and they have never been demonstrated
> > experimentally in the case of flagellar evolution (or other bacterial
> > motility systems for that matter). Huge gaps are missing that aren't
> > really discussed beyond a bit of hand waving to cover them up.
>
> This argument cuts both ways. Given our extremely incomplete knowledge of
> the possible configuration space of genes, given our still painfully
> limited ability to calculate how proteins fold and interact, and given the
> immense, incalculable complexity of the system as a whole, why do you feel
> yourself justified in proposing that *no* selective path exists? In what
> substantive way does your argument differ from an argument from ignorance?
Even in my ignorance, I can clearly show how increasing levels of
complexity result in increasing neutral gaps. I can also give real
life examples of how these increasing gaps do in fact translate into
increased time and/or rarity of examples of such levels of functional
evolution. I can only demonstrate conclusively that beyond the most
simple level of single protein functions, there are absolutely no
examples of evolution producing functions of higher levels of
complexity, such as functions that require multiple proteins working
simultaneously (i.e., bacterial motility).
In your ignorance, what do you have to support your position over
mine? Where is your falsifiable evidence?
> >> It has to work via a chain of
> >> events constrained by history and by the necessity of intermediate
> >> functionality.
> >
> > Right again, but what if this chain is broken? What if the links of
> > the chain are separated from each other in all directions by neutral
> > gaps that can only be crossed via random walk?
>
> What if, what if, what if! That does not constitute a scientific argument;
> it is merely handwaving. It is an argument from ignorance and incredulity.
It is a scientific argument if there is testable evidence to support
it, which there is. Where is your evidence for the existence of such
paths beyond the most simple of functions? You are the one doing a
lot of basely claims and hand waving. Where is your evidence for
these hypothesized paths that you so confidently speak of?
> >> *You* are the one who has to demonstrate a *pathway* in which there is
> >> what you misleadingly call "neutral" steps (actually, what you are
> >> proposing is not 'neutral', but what I call 'keystone' or 'group'
> >> selection -- that a function does not appear until a final 'keystone'
> >> mutation plus a bunch of completely inutile changes have occurred) that
> >> lead to the formation of new functions that only appear at the end
> >> point.
> >
> > Actually, if my theory is correct, it would be impossible to
> > demonstrate such evolution because my theory is one that proposes that
> > mindless evolution cannot happen beyond very limited levels of
> > complexity. You are the one who must demonstrate your supposed paths,
> > not I. I don't think they exist, you do. So, demonstrate them.
>
> You said earlier that evolutionary experiments of this sort were
> unfalsifiable.
No, I said that you have yet to suggest a falsifiable experiment to
support your position. There is a difference. So far, it seems to me
that your theory is not falsifiable because you evolutionists have yet
to present something that could actually falsify your theory on a
genetic basis.
> I would now like to turn that argument back on you. If such
> a pathway could be experimentally shown to exist for, say, the bacterial
> flagellum, would you abandon your skepticism, or would you simply move to
> the next gap over and conclude, "Yes, well, I guess that could have evolved
> after all, but *this* one you'll never explain, for sure!" What would you
> accept as falsifying your argument?
Yes, according to my understanding the evolution of any type of
bacterial motility requires multiple proteins all working together at
the same time. According to my calculations such evolution would
require the crossing of neutral gaps via a random walk that would take
a very large population of bacteria trillions of years to cross. So,
yes, if you could demonstrate the evolution of such a multi-protein
system of function I would abandon my skepticism. How about you?
What would it take for you to abandon your skepticism?
Sean
(BigDiscusser)
ridiculous amounts of tme required, plus probabilities about the gaps,
put evolution into the "cows jumping over the moon" catagory. I believe
Jesus IS somehow IN His creation directing it as Colossians Chap 1 v 16
& 17 state. It is all providential. Thanks, and God bless, Jo Jean
I am an 81 year old Christian lady. I am interested in a wide variety of
topics and am a retired RN.
http://community.webtv.net/JOJOYD/BigDiscusser
Jesus loves you.
John Chap 1 v 3
Colossians Chap 1 v 16, 17--defeats evolution with ADAPTATION by Jesus
who is IN His creation (not evolution) plus scientifically untouchable
classic morality, equals the DIVINE SYNTHESIS.
MUSLIMS NEED JESUS CHRIST AS THE SON OF GOD ALMIGHTY
Lilith
> lil...@umich.edu (Lilith) wrote in message news:<75200cbc.03061...@posting.google.com>...
> > > <snip>
> > > bacteria grew just fine without the lactase function, but they would
> > > have done much better in the lactose rich environment if they did have
> > > this function. So, why didn't they evolve this function?
> >
> > If they were growing just fine without the lactase function, why would
> > they need it?
>
> Because, they could survive better than their peers with the lactase
> enzyme. They would become more "fit" in their competition for
> survival.
First, let me point out the obvious. We've seen evolutionary change
happening in bacteria, already, so your argument about "not evolving a
lactase function" speaks more for the tempo and mode of such processes
rather than calling into question the ability for bacteria to evolve
function in the first place.
In other words, we know mutation and selection in bacteria occurs, and
this is not in question. Your complaint can only be seen as calling
attention to the fact that a large change (evolve lactase function
from non-lactase-processing genes) doesn't happen in a laboratory
sample in a short time period.
In order to evolve lactase function, the system must be able to select
on lactase function in the first place. If there is no lactase
function present from any source, there will be no selection to that
effect, and will not be until an E.coli protein mutates in such a way
to bring lactase function within reach.
So, in light of all this information, my challenge to you is this:
design an experiment that could prove your point, conclusively, that
E.coli can never evolve lactase function under any condition, under
any circumstance, under any kind of intermediate step through any kind
of process.
If you can't do that, then tell me why this experiment shows anything
except that this particular limited colony in Hall's lab didn't
succeed in evolving lactase function under those conditions.
> > If they evolved a lactase gene, it would have to arise
> > out of either 2 copies of an extant enzyme with functions within reach
> > (whole gene duplications) or would have to disable working copies of
> > extant enzymes to change over into lactase utilization.
>
> Not exactly true. Some proteins can do multiple functions in
> different systems of function. But, you do have a point here. Too
> many mutations would in fact disable what is already working. This
> limits the genetic real estate that a given bacterium can allow to
> undergo very much random walk, placing yet another limit on the powers
> of evolution.
Nobody is claiming that bacteria suddenly pop a new lactase into
function arbitrarily. That's a creationist point of view, and not
predicted by evolutionary theory.
Evolutionary theory predicts it'd take longer and longer to evolve a
lactase, the further and further away you remove lactase function from
a bacterium, unless there's a surprise lurking in the system somewhere
you didn't account for, like a pseudogene that's lurking a few
mutations away from functionality, or something.
So, why is this a problem for evolutionary theory?
> Also, gene duplication doesn't help much since
> maintaining a duplicated gene is expensive. It costs energy. Unless
> the mutations to this gene happen fast enough to give it some sort of
> advantage really quick like, natural selection will get rid of that
> gene in short order. The gene duplication hypothesis is also quite
> limited.
You make an assumption here. You assume that a gene duplication would
cost energy and would therefore be selected AGAINST once it appears.
So, are you saying that a gene duplication can be selected against?
You say, "Unless the mutations to this gene happen fast enough to give
it some sort of advantage really quick like, natural selection will
get rid of that gene in short order." So, what makes more sense out
of the following:
1) Function evolve sequentially through genome remodeling while all
non-advantageous stuff is lost so that all non-functional evidence of
previous remodeling is quickly lost to later view, or
2)All evidence for change must stick around so that bacterial genomes
would have every evidence for every intermediate available to the eye
and not, say, a mathematical program. All non-advantageous mutations
and selection would have to stick around to be noticed.
Evolutionary theory would mostly predict that if a bacterium doesn't
need the gene and the duplication is not selected for at any time
either way, it'll be lost (become a pseudogene) through the usual
mutational processes that generated it in the first place. It's
signature would eventually vanish back into the bubbling cauldron of
mutations. There is evidence for such pseudogenes in E. coli.
See for example
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12234664&dopt=Abstract
> > The bacteria
> > would have had to decrease the existing abilities to process the
> > useful and optimized metabolic pathways to produce a new one out of
> > existing parts. There's nothing we've seen thus far that suggests that
> > organisms will always evolve that kind of function in ten generations,
> > ten thousand, or ten million. If all available lac-type enzymes are
> > knocked out, what's the chance that they'll evolve a new one?
>
> Not very good at all - Just like it is not very likely that such
> bacteria who don't already have systems of motility would ever evolve
> them. The same holds true about eye spots, abilities to utilize
> radiation energy from the sun, or many other such functions.
My point was that in this setting, in Hall's laboratory, it is
unlikely that a lac+ gene would appear out of nothing in a a short
time given that all lac function was removed. I never said that it
couldn't be done over long periods of time with other intermediate
states.
You're assuming vast gaps between functions. You're not at all
considering stepwise gradual change, or even cumulative change shared
cross-bacteria. There is nothing stopping a million bacterial colonies
from coming in contact in "the wild" and sharing their evolutionary
innovations, because we see that happen in the laboratory. It isn't up
to just one colony to evolve innovations. A species and even other
species have the luxury of taking advantage of all other innovations
from other colonies in other places.
In the end, your argument against such change starts from the
assumption that all change must cross vast gaps, without any evidence
that such vast gaps are required. Without ignorance of the intervening
steps, your argument falls apart, by your own admission. Ignorance,
however, is not an argument against anything. In evolutionary theory's
case, however, ignorance is not used to hold up the theory.
Creation events require de novo bridging of such vast gaps. Evolution,
however, predicts a steady accumulation of change that, once the
intermediates are removed, makes it appear as if vast gaps were
crossed.
The observation in nature are that small, sequential in-reach changes
can add up over time in successive generations. There are more than
point mutations to give those changes, including gene sharing, gene
duplication, gene conversion, etc.
> > Clue: Evolution within the context of the history of the organism is
> > as important as the context in which the organism finds itself.
>
> Certainly this would have to be the case, if it were true.
>
> > In fact, why don't we grow e.coli on a bed of polyester? What's the
> > chance, in 10,000 generations, that they'll evolve a gene to eat
> > polyester? If the organism does not have a context in which it can
> > evolve by sequential steps, a function that will utilize existing
> > pieces to build a polyester-processing system, then it's unlikely to
> > evolve one.
>
> Very true. However, the likelihood that this ability or function
> would be evolved is proportional to the ratio of potential polyester
> enzymes as compared to the total number of potential sequences in
> potential protein space. If the ratio is high, then the likelihood
> that random walk will happen to come upon one of the winning sequences
> is correspondingly high. If the ratio is low, the likelihood that
> random walk will happen to come upon one of the winning sequences is
> correspondingly low.
Let's be precise, here, for I don't want this point to be lost.
Without selection able to act on an existing protein with weak lactase
function (because there isn't any), any weak lactase function would
have to appear through random chance operating as mutations and/or
gene duplication-then-mutation on existing proteins that may already
have a function.
> Of course, as you already noted, the likelihood
> that random walk will succeed is also greatly influenced by the amount
> of genetic real estate that can actually be spared by a particular
> organism to undergo random walk in the first place.
It's actually greatly influenced by the TOTAL AMOUNT of genetic real
estate available to the whole species for all individuals at all
times. A single organism is unlikely to search all "space" for this
kind of mutation. A few million trillion bactera..would that be
enough? How could you show that kind of search space wouldn't be
enough, given horizontal gene transfer and mutational rates?
> > In other words, you're expecting a gap to be crossed. But before you
> > use that as your "AHA" stage, let me tell you this: evolution has its
> > limits. Certain gaps cannot be crossed.
>
> Well, we both certainly agree on this point. But this begs the
> question, if evolution has its limits, then how exactly did we get all
> this variety of fantastically complex functions? I suppose that there
> were no gaps to cross? Really? Can you provide evidence for this
> beyond examples of the evolution of the most simple antibiotic type
> functions and single protein enzymatic type functions?
That IS evidence.
The evidence for evolutionary change IS the small incremental, simple
change. If you mean you'd like to see evidence for gene duplication or
other mechanisms of evolutionary change in bacteria, those are in the
literature for the taking.
See for example, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10417653&dopt=Abstract
But this brings us back to the point that there is no other mechanism
proposed for evolution other than mutation in all its forms, and
selection. That's exactly what evolutionary theory predicts. Small
incremental changes toward fitness along a pathway limited by genomic
history and constrained by current conditions.
> I'll ask you the same thing I asked some others in this forum - Can
> you suggest a genetic experiment that would falsify the theory of
> evolution if it failed? In other words, is the genetic theory of
> evolution falsifiable?
Yes. Let's begin with phylogenetics.
If the genetic theory of evolution was false:
- Within bacteria, we would not see more basic metabolic proteins and
genes as the basis of other gene innovation. We should see that these
proteins do not order themselves across mathematically-calculated
phylogenetic branches of multiple bacterial genes across bacterial
genomes. In other words, we would not see a mathematically-derived
convergence between bacterial core functions leading back to a common
ancestral state.
- Similarly, we would not be able to see bacterial genes as the roots
of the mathematically-calculated tree in multicellular organisms. We
would not find that core metabolic proteins in multicellular organisms
converge back to a bacterial ancestor. There would be no robust tree
to that effect. We should not see bacterial genes reproducibly fitting
into phylogenetic trees using algorithms that have mutation models
built in.
See for instance the tree given here:
http://www.genome.org/cgi/content/abstract/12/7/1080
and here:
http://www.jsbi.org/journal/GIW01/GIW01F16.pdf
> I ask this because I can present evidence for
> vast neutral gaps until the cows come home and all you have to do is
> say, "Well, I guess that the path must have existed somewhere else."
No, that's not true, and if you suppose that, I would consider you, at
the best, ignorant of what the evidence shows.
You're apparently arguing with your own idea of what evolutionary
theory must suppose. At no place do you recognize that these "neutral
gaps" you introduce are proposed after the fact of observation of
processes that obviously appeared a very long time ago.
Do you imagine we only use the theory to bridge the gaps? The theory
is built on evidence. It's not only in the fossil record, but
simultaneously within the genetic/genomic record. That evidence points
to common descent, for not only organisms, but genes.
But suppose for a minute, in the interest of your theory, that we
start introducing briding points within your neutral gaps. When do you
stop calling them 'vast'? What is your metric? How can any measurement
be made to satisfy you that a small sequential change is small enough?
Down to base-mutation?
> You see, you really don't ever have to demonstrate this evolutionary
> path that you are talking about because you can always fall back on
> the idea that evolution does not have to do anything. If something
> doesn't evolve in one way, that doesn't mean that it couldn't have
> evolved some other way given some other type of experiment or
> environment or starting sequence. The problem with this is that your
> little "scientific" theory cannot be falsified.
Except it can be falsified, and it's no little theory. :)
I've given you evidence that could be potentially falsified. Show me
how a reliable, reproducible phylogenetic tree across several species
for individual genes can be built mathematically if common descent
(from ancestral genes) was not the case.
> My theory, on the other hand, can be tested in a falsifiable manner.
> All you have to do is show that functions of increasing complexity do
> not create larger and larger neutral gaps or that such functions can
> be evolved if given the proper environment with the use of beneficial
> intermediate sequences that I hear so much about.
That is shown with the phylogenetic tree, to start. Those are evidence
that the intermediates already existed.
Can your theory do the same?
> For example, if the
> bacterial motility function is so obviously evolvable, then all one
> would have to do to falsify my theory is demonstrate the evolution of
> such functions starting with a colony of bacteria that never had such
> functions.
Your theory can also attempt to fit the phylogenetic data. Does it?
> > The organisms that still live
> > today have been able to leap across reasonable gaps, one small step at
> > a time. THAT is what evolution describes.
>
> Yes, that is what the theory of evolution suggests happened. What you
> have to do is to demonstrate that these intermediate sequences of
> beneficial function actually exist in such common numbers so as to
> make easy stepping-stones for evolution to walk over without falling
> into the vast sea of neutral function.
I have the fingerprints at the crime scene. I can explain their
origin. Can you?
> > Your complaint about large
> > gaps not needing to be crossed is NOT what molecular evolution
> > requires. There is no large, "And here a miracle occurs" that is
> > required by evolutionary theory.
>
> You don't call going from a bacterial-like creature to a human being a
> fantastic transformation?
I don't equate "miracle" with "fantastic transformation". Semantics
aside, there's a big difference between poofing something into
existence and supposing it happened in incremental steps.
> The gaps do obviously exist. What is not
> so obvious, at least when you stop arguing from morphology and start
> trying to argue from genetics, is how such gaps are crossed.
I argue from genetics, at all times.
> You
> suggest that there are intermediate stepping-stones that allow
> evolution to traverse these gaps quite easily. Well then, it should
> be a piece of cake for you to demonstrate these stepping-stones
> experimentally.
I did. Phylogenetic trees are evidence and experimental evidence, at
that. They're forensic evidence, like tire tracks, DNA samples,
fingerprints, blood, hair, and dead bodies at crime scenes. Feel free
to explain the evidence with your theory and explain how it best fits
the evidence, more so than evolutionary theory.
>If you cannot demonstrate them, then the neutral gaps
> really are a problem for you because there is no known mechanism,
> outside of ID, that can explain how such neutral gaps could be
> crossed.
On that topic, your neutral gaps theory suffers from several flaws:
1) Your gaps are merely constructs of missing data.
2) One neutral gap would support your theory. So would a million
neutral gaps.
3) All gaps are without metric. That is, no gap could conclusively be
shown to be non-gap-like EXCEPT in a controlled laboratory setting
under the conditions that allowed an organism to "cross" the gap.
Thus, your challenge sounds impressive, but is basically Hovind-like
at its core.
4) Your gap theory is only falsifiable by standards not required by
even physics experiments.
5) Your gap theory makes no testable predictions, nor does it fit the
data.
> > > These very same bacteria would quickly evolve resistance to penicillin
> > > if it were added to their environment. No more than a handful of
> > > generations would be required.
> >
> > There's a difference. Evolution of lactase function requires a gene
> > duplication of a reasonably closely-related enzyme on demand (which
> > you have noted was certainly not within easy reach anymore as both
> > related enzymes were deleted) and subsequent mutations of several
> > residues within an existing enzyme to acquire lactase function.
>
> You don't seem to have a very good grasp of the experiment in question
> here. Evolution of the lactase function would not or at least did not
> require a gene duplication of a "closely related" enzyme at all.
No, my point was that if you do not have a gene that is not already
within evolutionary reach of lactase function, it is unlikely to
happen in a short period of time. I was not stating that the ebgA
appeared from the lacZ gene. I was stating that in order to quickly
evolve any lactase function de novo, you would have to START with a
gene that, if it has selected function anywhere else, would need to be
both closely related by mutation and also duplicated before it could
mutate and evolve towards a lactase function without simultaneously
decreasing the overall fitness of the organism.
> Also, the ebgA gene (produced a hexamer lactase enzyme) that was able
> to evolve the lactase function was neither closely related to the
> original lacZ gene sequence (produced a tetramer lactase enzyme that
> had very low sequence homology with the protein produced by the ebgA
> gene)
54% similarity and 30% identity is not "very low", especially given
the sequential conservations in some of the amino acid stretches. see
here:
http://www.umich.edu/~lilyth/ebgA.htm
They certainly have all the hallmarks of once sharing a common
ancestor through an ancient gene or genome duplication.
> nor did it require several mutations to achieve the lactase
> function. A single point mutation was all that was needed to turn the
> ebgA gene into one that produced a functional lactase enzyme.
> However, the relatively low ratio of potential lactase sequences was
> soon demonstrated quite nicely when Hall deleted both the lacZ and
> ebgA gene sequences. Without these sequences, no other proteins
> produced by the E. coli bacteria were close enough to any one of the
> potential lactase enzymes to evolve this function back again.
Yes, which brings us back to the question: What is the
independent-to-your-theory significance of this, as evolutionary
theory does not seem to suffer from it?
>
> > As evolution is NOT DIRECTIONAL if it is not directly selected on,
> > Sean, as is certainly known to you, there is a very large "search
> > space" for this kind of evolutionary innovation. Are 10,000
> > generations of millions of e.coli enough to generate that kind of
> > innovation, enough to give a high probability that the search space
> > would be adequately covered? Obviously not.
>
> Obviously not. Again, we agree. So, how are such functions evolved?
Over larger time periods and with larger populations than Hall had at
his disposal, with a greater population of the search space.
> Did the original bacterium have enough genetic real estate to be close
> enough to several much less all of the functions that we see around us
> today? Oh, I know, you will say that the environment changed over
> time in different areas so that stepping stone functions arose to
> supply the needed paths to create these functions.
No, I would say that out of the huge amount of "genetic real estate"
available to a few billion years of selective and competitive
evolution among countless numbers of bacteria, competition and
selection did a leg-up for a lot of the functions we see today.
Environmental change is only one part of that.
> Hmmm . . . What
> are the odds that the proper sequence of environmental changes would
> come along at just the right times to give rise to such things as
> bacterial motility systems, multi-cell groups and creatures, eye
> spots, and a host of other functions that require the simultaneous
> function of hundreds or even thousands of parts? A change in the
> environment might make new islands of beneficial function rise out of
> the sea of neutrality, but it would also make form islands of function
> sink.
And all the time, if you have a large enough simultaneous spread of
mutations over the search space, each peak would be accessible by
sequential mutation, assuming no horizontal gene transfer to cross any
gaps.
> For example, try to evolve the phrase, "Methinks it is like a weasel",
> one letter change at a time, into any other phrase that makes sense in
> English *and* is beneficial in a particular situation. You can change
> the situation/environment at will to help you out if you start getting
> stuck . . . but I really don't think this will help you much because
> the nonfunctional gaps are too large.
In other words, you want to find a subset of all possible sequences in
a random permutation of "Methinks it is like a weasel" given a set of
mutational changes. If I had several million trillion examples of the
phrase, all evolving simultaneously, for a billion years, with the
ability to both increase and shorten its length, as well as introduce
"spaces" for characters I suspect I would find quite a few useful
phrases appearing.
> You see, I know that this is how the paper theory is suppose to work,
> but in light of the neutral gaps involved, I don't see how evolution
> can really get across the gaps.
You have not quantified your gaps. What is a gap? What do you define
what a "gap" is, and what is not? I don't want to hear about the vast
jumps you propose, such as "Zero to Flagella in 30 seconds". I want to
hear about the squishy, intermediate steps. What's a gap down at the
basic molecular level, within reach of normal genomic processes? Is
there a metric for "gaps", and how could we measure 'gaps' and
"gappiness" in a laboratory? How could we tell if a gap became less
gap-like?
> > If there is no selected pathway TO lactase evolution, then it's not
> > gonna happen except by hit or miss. And that's not what evolution's
> > about.
>
> Oh really? So then how does evolution do it? I mean, functions of
> increasing complexity are here. How did they get here? Explain to me
> the genetic changes in light of these exponentially expanding neutral
> gaps in function.
You know the answer to that. I have evidence they evolved. We can
start with the phylogenetic evidence.
>
> > Hit or miss is not what evolutionary theory supposes.
> > Heterogeneity and selection is what evolution supposes.
>
> Heterogeneity? Hmmm, now that's a fancy word. How the heck does that
> word help you? How is it different from "homogeny"? How is
> heterogeneity, as far as differences in functions and levels of
> functional complexity, achieved?
"A fancy word"? Are you reducing arguments now to attack on semantics?
Heterogeneity is achieved by gene duplication, gene conversion, exon
shuffling, mutation, genome duplication, to name a few. Typical
genomic processes observed in nature.
> > If there is no
> > pathway selecting towards lactase evolution, then tell us, Sean, why
> > it would happen?
>
> Yes, why would it happen? That is my whole point. I wouldn't happen
> without either a functional path or an intelligent designer.
Right. And a evolutionary pathway is what evolutionary theory
supposes.
We have hard evidence for that pathway. Shall we begin talking about
the evidence? I suggest you purchase a book, first, "Molecular
phylogenetics" by Nei and Kumar, so we can have an intelligent
conversation on the matter, as I don't have the time to fill you in on
the equivalent of ~300 pages of mathematics and examples.
> > Why would evolutionary theory say it must happen
> > without directed selection (evolutionary pathway) toward development
> > of lactase function?
>
> The theory of evolution doesn't say it happens without a path, it just
> can't detail the path is all. Evolutionary theory suggests that the
> paths are there, but they can't be pointed out.
Except they can be shown to have existed, with the forensic evidence.
> We are simply told
> that they do exist but upon what basis? Where is the evidence for
> them? Where have they ever been demonstrated beyond the shortest
> paths around (i.e., simple functions like antibiotic resistance and
> single protein enzymes)? Oh, it is fine to SAY that they exist, but
> it is another thing entirely to actually test this theory in a
> falsifiable way.
Phylogenetic trees. Buy or borrow the book and we can go to work on
the evidence. Shall we?
> > > Why then is antibiotic resistance so
> > > much easier for them to evolve than the lactase function?
> >
> > Because antibiotic resistance is based on mutation and selection on
> > existing enzymes. That's directed selection, right there.
>
> Actually you are mistaken here. Antibiotic resistance that is based
> on enzymes, such as the penicillinase enzyme, does not evolve de novo.
> The code for the penicillinase enzyme has never been shown to evolve
> de novo in real time experiments. This code was always there whenever
> it is detected as a cause for penicillin resistance. It was either
> inherited vertically or transferred horizontally, but it did not
> evolve de novo.
No, I am not mistaken. You are inferring something I had not said. I
didn't say penicillin enzyme appeared de novo. I said antibiotic
resistance is based on mutation and selection. If you throw a
completely different beta-lactam antibiotic against bacteria, existing
enzymes evolve to process that resistance.
> But, there are several other ways to achieve antibiotic resistance
> besides having access to a preformed enzyme or code. Many such
> methods of antibiotic resistance are based on the specificity of the
> antibiotic and its interaction with a target sequence.
In other words, there are processes operating that are selective.
> Many different
> mutations can interfere with this antibiotic-target interaction.
Selection acts on mutation. If many different mutations can interfere
with that antibiotic - target interaction, then I'd say the bacterium
is doing a good job at exploring its "space" and the antibiotic is not
effective.
> The
> ratio of interfering sequences as compared to non-interfering
> sequences is very high.
I'm not sure of this. A catalytic region is limited to a set of amino
acids that interact with the ligand. Therefore, all possible
non-interfering sequences of the protein are expected to outnumber all
possible interfering sequences of the same protein. That is not
counting non-competitive inhibition disruption on another part of a
protein, however. Do you have references for this claim? Because I'm
curious as to what you mean by "very high".
> This makes the neutral gap very small between
> such sequences. The reason for this is that it is far easier to break
> or interfere with a pre-established function or interaction than it is
> to create a brand new function from scratch.
Yes, far easier, and since a bunch of easy changes is what is
considered to be one of the mechanisms for evolution, why does it stop
there, at easy changes on existing proteins?
> As a result, resistance
> to antibiotics like penicillin can be and are achieved in short order
> even without preformed antibiotic enzymes like penicillinase. The
> very same E. coli bacteria that could not evolve the lactase function
> in tens of thousands of generations would quickly evolve resistance to
> penicillin in a handful of generations using the same level of
> selection pressure.
That was my point in the first place. Remove the lactase and it can't
get to lactase function in ten thousand generations. But you don't
give a nod that 10,000 generations on a small population of bacteria
is less than peanuts as to the availble genetic compliment that has
ever existed for E. coli and its ancestors. It's peanuts all the way
down.
> > > What is it
> > > about the evolution of relatively simple enzymes that is so much more
> > > difficult than the evolution of antibiotic resistance?
> >
> > Because there's no direction that would be given by selection towards
> > lactase function? That's like growing E.coli on a rock and expecting
> > it to start spontaneously eating rock. While the chance of that
> > occuring is not zero, it's certainly not something within reach of
> > ordinary E.coli.
>
> Actually, if the rock was made out of granite, as you suggested
> previously, the chances of E. coli being able to get energy out of it
> are pretty much zero no matter what enzymes were evolved. The lactase
> function is no like this.
If it's "invisible" to E. coli because it has no protein within its
search space, lactase might as well be granite. It's not reachable in
10,000 generations in a laboratory. As far as the E.coli was
concerned, lactase did not exist. It was as meaningful as polyester or
as nylon was (before nylon-eating bacteria figured out how to process
it).
> Any E. coli bacterium that evolved the
> lactase function in a lactose rich environment would instantly gain a
> significant survival advantage for itself.
Any bacteria that figured out how to eat cotton fiber would have a
field day in some of my dresser drawers. That's about the same level
of argument, there.
> Also, the lactase function
> is not all that complex, relatively speaking. It is based on the
> functional potential of a single protein. This is not some
> multi-protein function we're talkin here, like bacterial motility.
> This is just one single protein.
Think about this carefully.
Hall removed lacZ, and discovered ebgA was right there, waiting. It
evolved into a lactose and lactulose function with a few mutations.
Hall then removed ebgA and nothing obviously evolved in 10K
generations.
Therefore, we would say that Hall pushed back the boundary of
evolvability. That's all. Hall showed that it's not probable that it's
going to be evolved de novo -- literally from nothing nearby in
"evolutionary space" -- that it's not likely going to spring up in a
small population over 10,000 generations. And again, this is a problem
for evolutionary theory why?
> > And in the case of the missing lactase enzyme itself, full lactase
> > function would take more than a few changes. It would require the
> > creation of a new enzyme by gene duplication and then evolution.
>
> If gene duplication occurred, the "evolution" would have to happen
> extremely fast and by random walk before nature selected to get rid of
> the non-beneficial duplicated gene that was costing the organism
> energy to maintain. Yes, evolution does have its significant limits
> doesn't it?
Wait, you're again suggesting that natural selection will get rid of
all non-beneficial duplicated genes. There are plenty of pseudogenes
in E.coli that are in evidence.
Then you're suggesting that evolutionary theory present all evidence
for intermediates between your percieved gaps though you yourself
propose that any gene that would not be beneficial to the organism
would be lost.
Which is it that you want? Either genomes reorder themselves enough
to quickly lose duplicated genes (and also all evidence of previous
processes) as evolutionary theory would predict, or these changes hang
around a long time so that all evidence for intermediate states would
be available to your naked eye.
Again, evolution does NOT SUPPOSE de novo generation of genes on
demand. You're utilizing a strawman argument by supposing the
contrary.
> Examples of "evolution" like this are all over the place. While they
> are real examples of evolution in action, they really don't explain
> the evolution of much of anything beyond the most simple of functions
> that have very limited neutral gaps and very high ratios of beneficial
> sequences as compared to the total number of potential sequences.
Give me any mechanism by which small crossings can't add up to big
crossings. Give me a way by which I can test this mechanism.
> Hall demonstrated this same sort of thing in his lactase evolution
> experiments. He showed how the lactase gene (ebgA) could get mutated
> to produce enzymatic activities on several different types of sugars.
> Of course, each of these new functions was achieved with just one
> mutation. One of the enzyme function required two mutations, but this
> is not statistically significant. Likewise, new lactam antibiotics
> will most certainly be within the reach of existing lactamases. The
> target is so specific that any changes to the antibiotics cannot be
> too major. Because of this problem of required specificity, limited
> changes to the antibiotic can be overcome by equally limited changes
> to the antibiotic enzymes.
> Also, even if the bacteria didn't have access to the pre-formed
> beta-lactamase enzyme, they would still evolve resistance to cefepime
> in relatively short order via mutations to target sequences.
The point being, that small changes are extremely rapid. Show me how
small changes are constrained from adding up to selective change over
evolutionary pathways. Give me testable predictions. You haven't done
it thus far.
> > > Also, we have actually seen a few relatively rare real time
> > > demonstrations of enzyme evolution, to include the evolution of the
> > > lactase function in some types of E. coli, but never in other types of
> > > mutant E. coli and never in many other types of bacteria over the
> > > course of 50+ years.
> >
> > Sean, antibiotic resistance IS real-time ENZYME evolution. Do you even
> > know what a beta lactamase (for instance) is? Don't you think you
> > better find out? It's an enzyme. It evolves.
>
> Again, you didn't get this lactamase enzyme de novo. Just because it
> can change slightly to accommodate slight changes in various new
> antibiotics that come out does not mean that this enzyme evolved from
> scratch. Delete the lactamase enzyme and see how quickly you can get
> it back. Then, after that, you can claim that de novo enzyme
> evolution produces antibiotic resistance. For now, this doesn't
> happen. If the preformed enzyme is not already there, it does not
> evolve de novo - period. However, antibiotic resistance still evolves
> de novo. How? Because of mutations to target sequences and the like.
Do you know the origins of penicillin,and how it could have evolved as
an arms race between two organisms? There's no problem in figuring out
how it could have evolved de novo to start with, at least not for me.
It does not assume, however, 'POOF'. So your arguments, have nothing
to do with anything, whatsoever.
> > So, yes, antibiotic resistence is enzyme evolution.
>
> No, it is not. You have to have the enzyme there already preformed to
> a significant degree. Even your example of the evolution of cefepime
> resistance started with a preformed enzyme that was 99.9% identical to
> the "new" enzyme that attacked cefepime. This really isn't what I'm
> talking about here, and you know it. You are trying to blow a smoke
> screen over the main point. The point is that evolving enzymes from
> scratch is much much harder than evolving functions like antibiotic
> resistance that arises de novo, without any preformed enzymes.
No, I'm not blowing a smoke screen. The enzymes evolved. We saw proof
that they evolved towards a new function. You want to define "enzyme
evolution" as "poofs out of nothing nearby" and that's not what
evolution supposes, nor is that how evolution is defined.
And evolving enzymes from scratch the way you demand is NOT supposed
by evolutionary theory. You are proposing a requirement of
evolutionary theory that *does not exist*. Not only are you looking
for evidence for something that doesn't happen nor is supposed to
happen, but you are then attempting use the lack of evidence for this
highly unlikely thing to discredit evolutionary theory.
> > The fact that
> > we've seen real-time evolution of anything is clue one: evolution
> > occurs.
>
> Certainly mindless processes of evolution do occur, but they are very
> very limited in what they can do and explain.
On what basis do you state that? Do you propose a barrier to variation
and selection? What would we do to measure such a barrier?
> The de novo evolution
> of antibiotic resistance in bacteria without preformed enzymes is very
> easy to explain since it involves interference with or the breaking of
> a preformed interaction or function.
That is what all evolutionary change on a genome is supposed to do.
Work within known processes and existing genomic history.
> Again, the principle that it is
> far easier to destroy than to create holds true here. De novo
> antibiotic resistance is really based on the destruction of a function
> and not the creation of a new function from scratch.
You've just solved all our antibiotic problems! I suppose we can go
back and successfully use penicillin on all these bacteria with newly
evolved antibiotic resistances!
Why not?
> > Under selection, the system is perfectly able to move towards
> > the desired, selected state: survival in the presence of an
> > antibiotic.
>
> Yes, even if that bacterial colony does not have access to a
> pre-formed antibiotic enzyme. Again, this is because of the
> specificity of the antibiotic for a particular target. Get rid of the
> target or change it in some way so that the antibiotic cannot bind
> well with it, and resistance is gained - simple. Moving up the ladder
> of complexity though, to the evolution of just one simple enzyme from
> scratch, is a lot more challenging however since the neutral gaps have
> just expanded exponentially.
But at no time does evolution suppose evolution from scratch. I hope i
can repeat this enough times to get you to understand it, but I
suspect you have enough personal investment in this misunderstanding
to carry on the conversation for quite a while.
>
> > That's a basis of Hall's research, up to the present day.
> > He's been able to recently "predict" some aspects of in-the-wild
> > antibiotic resistance by evolving the resistance in the laboratory.
>
> You don't need to evolve anything in the laboratory to successfully
> predict the evolution of antibiotic resistance. I predict that no
> matter which new antibiotic is put on the market that bacteria will
> quickly develop resistance to it. I also predict that if that
> antibiotic is pulled off the shelf for a while, that the bacteria will
> revert back to their wild-type nonresistant state and the antibiotic,
> if used again, will be as effective as it was initially. I suggest
> then, based on this hypothesis of mine, that it would be wise for
> hospitals to get together to start a antibiotic rotation. Use one
> type of antibiotic for a given span of time, and then stop using it
> altogether and start using another type of antibiotic with a different
> target for a while, and then stop using that one and move on to
> another type. Then, after moving on to several different antibiotics,
> start the rotation over again. I am betting that the bacterial
> population will be susceptible to the original antibiotic once again.
Yes, isn't evolutionary theory useful to make predictions, like you
just did?
> > > However, we have never seen a bacterial function
> > > evolve that requires multiple proteins working together at the same
> > > time, such as would be required for the function of bacterial
> > > motility.
> >
> > I don't know of any experiment that's tried to direct that kind of
> > pathway, yet.
>
> Yeah, me either! Perhaps you should suggest this to some of your
> evolutionist buddies?
I have no "evolutionist" buddies. I know several hard-working
scientists. Perhaps you should attempt to become more like them and
develop your experiments yourself and publish them under peer review.
> I'm betting that many have thought of doing
> something like this and perhaps they have tried, but I am betting that
> it just won't work. But, knock yourself out trying - go for it! ; )
My area of expertise is genomics, not microbiology. Thanks for the
permission to try out my own ideas, however.
> > I maintain that there are no barriers to coupled evolution within a
> > complex system given gene duplication and mutation, among other
> > processes.
>
> Yes, you and all other evolutionists "maintain" this position, but
> where is your evidence?
My evidence is in the protein-interaction networks which have evidence
for arising through those exact processes.
See http://www.nd.edu/~networks/ for some papers on this.
>If your gene duplication is not immediately
> advantageous, nature will select to get rid of the duplicated gene.
Nature will NOT select for a non-advantageous gene. It will select for
a detrimental gene, and then only will the gene be slowly disabled, as
you noted, by point mutations or other processes rapidly available to
the bacterium.
Then the gene ends up as a pseudogene when it is enough point
mutations away from being readily accessible.
Through deletion events, some pseudogenes are eventually lost. Some
stay. Evidence of those exist.
> If the neutral gaps between what is and what is needed are too large,
> your duplicated gene will get eliminated before it can undergo very
> much random walk toward much of anything.
Disabling a gene for one function only takes a few mutations, as you
pointed out. That leaves plenty of time for other function to be
established.
How does your theory explain pseudogenes in bacteria?
> Then, where are you? - Back
> to square one? Your mutations need to follow a path of beneficial
> functions. But, what if this path comes to sequences that offer no
> beneficial changes in any direction? What if your island is
> surrounded on all sides by a huge sea of non-function/neutral
> function/detrimental function? What are these "other processes" that
> you would need to save you from this predicament?
Niche change that moves the peaks to the organism's advantage (move
niches when a beneficial niche change presents itself). Genome
duplication, so that every gene is copied, twice...expensive or not,
if the organism survives, it can root change in that way. Exon
swapping, which is more than simple point mutation. Gene duplication.
Gene conversion. Segmental duplication. Horizontal transfer from other
species. Etc.
> > That is the simplest answer: no restriction on evolution at
> > any level. I have seen no evidence that there is any barrier to
> > evolution as evolutionary theory currently presents itself.
>
> Oh really? How do you get across the gaps of nonfunction to produce
> such multi-protein functions as bacterial motility? Please, how,
> exactly, does your current theory of evolution explain this? What
> falsifiable experiments can you put forward in support of this
> statement?
I gave you some. We can move into protein networks, gene duplication
and evolution once we tire of phylogenetic analysis.
> > I have only seen that a couple of knocked-out genes do not poof into
> > appearance out of nothing within ten thousand generations under
> > limited laboratory conditions with no selection along a pathway of
> > intermediate states...an experiment that would certainly take longer
> > than 10,000 generations of E. coli to generate results.
>
> Yes, and you don't find this significant? How so? How do you explain
> the crossing of such gaps that are obviously increasing exponentially
> with each step of increasing complexity?
Increasing time between each step. Sequential (hand in hand)
evolution. Competition. Etc.
> Some functions, such as de
> novo antibiotic resistance, arise rapidly and commonly, while others
> that are only slightly more complex, such as single protein enzymes,
> arise so much less commonly and others, such as multi-protein systems
> of function (i.e., bacterial motility) have never been shown to arise
> de novo. How is this explained?
You keep on repeating yourself, so I'll have to keep on repeating
myself. Let's begin with phylogenetic trees.
> Please, you do seem quite informed.
I'll be happy to oblige.
> I'm curious to hear your answer to why some functions are so easy to
> evolve while others are so much harder to evolve.
Because they provide less advantage to the organism over the
intervening "space"?
> Also, I would be
> curious to hear your predictions on how you would calculate the
> average time needed to evolve such functions as bacterial motility
> starting with a non-motile bacterium. I don't think you can be all
> that specific. I think that you are going to try and be as vague as
> possible by saying that various environmental changes must have come
> along, but you aren't going to even try to detail these changes or the
> average time involved for such changes to produce such levels of
> function.
Well, to start with, I need to know what you're looking for in an
explanation.
To help me, tell me the opposite: Tell me how evolutionary theory is
expected to predict this posthumously, and why it should be able to,
from the extant data with all the missing intermediate steps. You seem
to be well-informed on why evolutionary theory should be able to give
you a complete step-by-step mechanism.
But also, in the same paragraph, tell me how any conjecure on how such
a thing could evolve would satisfy you. To what level would you like
the explanation? Base-by-base mutation? Or would you like the causes
of the mutations? The cosmic rays, the polymerase errors? I don't mean
to be snide here, I'm serious. Tell me what goalposts you have, and
when you'll be satisified with an explanation of the evolution of,
say, motility apparatus. What are the conditions that you'd accept,
and what level of explantion is needed?
> > > Why is this type of multi-protein function so difficult to
> > > evolve in real time? Hmmmmm?
> >
> > I don't understand your complaint. Evolution suggests many changes are
> > evolved within "reach", as in, step-by-step, by action on existing
> > genetic material or mechanisms. I don't see your problem with this.
> > Step-by-step evolution, even in coupled-systems, is perfectly
> > reasonable.
>
> Oh yeah - detail this reasonable explanation for such genetic changes
> in function.
Function is context-dependent. I await your goalposts.
>
> > > I look forward to finally hearing from someone in the know as to why
> > > antibiotic resistance evolves so much faster than the functions of
> > > enzymes and why enzymes evolve at least on some rare occasions, but
> > > functions with multiple proteins working together at the same time,
> > > never seem to evolve in real time.
> >
> > Um, Sean, antibiotic resistance IS evolution within enzymes.
>
> Not really - see above
>
> > The
> > enzymes are themselves evolving better function in respect to new
> > antibiotics.
>
> Um, Deanne, this is not the de novo evolution of an enzyme. Such
> enzyme changes always start with a pre-existing enzyme that is very
> similar. Beta-lactamases have never been shown to evolve de novo
> (i.e., in a population that didn't have some pre-formed beta-lactamase
> to begin with).
And never has evolutionary theory proposed such a thing. And I'm sure
you know this by now. :)
> > The enzymes are in some cases changing their function to
> > adjust to the presence of a new antibiotic. Therefore, new antibiotic
> > resistance IS the change of an enzyme's function.
>
> See above - You are trying to dodge the issue.
No, I'm trying to make it clear to you that small changes in enzymes
are not blocked from occurring. You are missing the point and accusing
me of dodging the issue.
>
> > For instance, from Hall's recent paper: "The TEM family of
> > beta-lactamases has evolved to confer resistance to most of the
> > beta-lactam antibiotics, but not to cefepime"
> >
> > A refresher from your biochemistry class, the "-ase" at the end of
> > that word means it's an enzyme. If you still don't believe me, go
> > here:
> >
> > http://us.expasy.org/cgi-bin/nicezyme.pl?3.5.2.6
> >
> > That's the page for beta-lactamases in the ENZYME nomenclature
> > database. Yea, they're enzymes.
>
> LOL - Oh really? I didn't know!? Shocker! Please Deanne - get with
> the program and stop trying to blow smoke.
Again, my point is missed. So you're telling me that you define
"enzyme evolution" as "de novo appeareance of an enzyme from nothing",
yet you give no particular mechanism by which you would expect this
enzyme to appear from nothing.
>
> > And as to why we don't "see" multiple protein evolution, show me a
> > study where someone has done work on multiple-protein evolution
> > (coupled evolution). I can't seem to find studies like that. Maybe you
> > know of some. Until someone digs deeply into that kind of study, I'd
> > say that your complaint is premature.
>
> Fine - But until such studies and successes can be demonstrated by
> you, I'm saying that your belief in evolution is a poorly supported
> belief that is based on a whole lot of faith a not much else. But, I
> do admire great faith in a person. Hang in there . . . Perhaps the
> experiments you need will come along just before cows start hopping
> over the moon.
Wrong. I have plenty of evidence. Care to start examining it? Let's
talk phylogenies.
> > >I mean, if it is so easy, as you
> > > seem to be saying, then evolution should proceed rapidly, should it
> > > not?
> >
> > No. Evolutionary theory does not say that genes should poof out of
> > nothing without known processes. If there was no replacement for the
> > lacZ gene, or any gene within evolutionary "reach" even with gene
> > duplication, then why would we expect it to evolve lacZ function?
>
> Evolution claims that a lot of new functions did arise via purely
> mindless natural processes.
But NOT sudden de novo appearence of enzymes from scratch. Tell me
where anyone says this.
> If there were no neutral gaps to slow
> this process of evolution down, these functions that did arise would
> have arisen far faster than they did. Millions and billions of years
> would not have been required. Without neutral gaps, the evolutionary
> forces would "poof" a great many things into existence.
That's why life evolves along reasonable pathways. That's what
evolutionary theory supposes. No poofing required.
> > Do you have evidence that there are any enzymes less than a few
> > handfuls of mutations away from lacZ that the bacteria could have
> > evolved but didn't?
>
> LOL - No!!!! That is the whole point. There is a average gap
> between functional lactase sequences that is apparently quite large
> given the potential sequence space of 10e1300. The ratio of lactase
> sequences in this space seems to be fairly small indeed.
First, you pointed out that lacZ and ebgA were significantly different
in sequence by your own claim.
Then you say that the lacZ function is limited in sequence space,
though you understood that the two proteins were not similar in
sequence.
Then you claim that 10e1300 is all sequence space for lacZ (the length
of the lacZ protein is only about 1000), don't you mean 20e1000?
Actually, we're talking about genetics, not protein codons, so the
numbers change to something like 4^3000 which would be reduced
somewhat for codon degeneracy.
You base your argument against evolution on the fact that 10,000
generations of a lab quantity of E.Coli couldn't evolve a new protein
sequence for lac+ function...YET, you turn around and try to argue
against the chances of this evolution occuring.
So, what is it, Sean? Either you admit that 10,000 generations of a
limited set of E.coli was not enough to do a random walk to explore
the number of possibilites you require for your "proof" of evolution
so your entire objection to Hall's experiment is moot...
...OR that you expect 10,000 generations of this limited number of
E.coli to do quite a good job at exploring all your proposed 10^1300
combinations, and THAT is what you are objecting to. I would ask you
to do the calculation on 10,000 generations of a fixed colony of
bacteria to see how many mutations that colony could generate on its
own genome, and the number of mutations needed to generate an enzyme
de novo locally on that genome, and figure out where your goalposts
really are. From the numbers you're using here, I'd say somewhere in
the vicinity of Jupiter.
So, anyway, which is it? You can't use both arguments on the same
system. Either you object to Hall's results because E.coli SHOULD have
evolved something de novo, or you are mocking evolutionary theory for
suggesting that protein sequences will evolve de novo despite
astronomical odds.
Either:
- Acknolwedge the odds for de novo evolution are astronomical and
cannot happen in the wild, and use that to support your position, or
- Acknowledge that de novo evolution of a full enzyme is theoretically
possible over 10,000 whole generations of E.coli and the fact that it
didn't appear in that time in that population is evidence for your
position.
And once again, for the record, evolutionary theory never supposes de
novo appearence of proteins -- nothing appears 'from scratch' on a
genome.
> > > If there were no neutral gaps to slow the process of evolution
> > > down, then given the proper environment, the evolution of beneficial
> > > functions, such as the lactase function in a lactose rich environment,
> > > should proceed very quickly.
> >
> > Just like nylonase seemed to just spring out of nowhere but it was
> > really a selected copy of a differently-expressed, already-existing
> > gene.
>
> Yes - The nylonase function arose via frame-shift mutation. I
> wouldn't call this anything like the previous gene.
It's a mutation, therefore it's a selected copy of a gene that already
existed but was just read in another context.
> The coding
> sequence was entirely new. Of course, there may be a higher ratio of
> nylonases out there as compared to lactases, but the point is the
> same. The ratio of even nylonase sequences is far lower than the
> ratio of antibiotic resistance target sequences in E. coli. The gap
> is wider. And, this gap increases in size as one moves up the ladder
> of functional complexity.
It doens't matter what the ratio is. It's been observed and it
occurred. It only has to happen once to enable an advantage.
> > How do you know that the knock-out E.coli had all the right conditions
> > to evolve a lactase function out of existing parts? If it had no
> > "within reach" enzyme to utilize as a weak lactase it could get a
> > foothold with, and then select for lactase function, then it wouldn't
> > be any more able to generate that lactase function than it could eat
> > rock. Frankly, to demand anything like that is silly.
>
> You are on the verge of understanding the problem I think, but you do
> not yet understand that the limits to evolution are more widespread.
My question was rhetorical, not a "wondering" question. There are a
lot of non-evolved functions that we don't know about because they
didn't evolve. There are many more non-evolved, possible functions
than there are evolved functions.
For instance, cellulose is a wonderful structural protein as it seems
to be outside of the reach of ordinary bacterial enzymes to break
down. Why not? Why can't bacteria evolve the ability to munch on the
long-chain sugar that is cellulose? Some actually have -- don't get me
wrong, but I mean, why can't E.coli for instance evolve cellulose
eating abilities? What would it have to do to evolve that?
It would need to have a protein that would have a weak processing
ability to chop cellulose up into sugar molecules. But cellulose
likely evolved to its present form for just this reason...it was in a
"space" that was unaccessible to bacterial enzymes.
> Increasing gaps with increasing complexity means that if evolving a
> relatively simple lactase function is as hard as eating rock for some
> creatures, that evolving anything more complex than this would be all
> that much harder.
> The genetic real estate of a given creature is
> severally limited, as no is its environment. The odds that it is
> close to ANY enzyme of the complexity of lactase or nylonase or
> penicillinase is pretty low.
I have no idea where you get "pretty low" from, since you have nothing
to state "pretty low" against. I base my "pretty low" from knowledge
of genomic remodeling processes. But "pretty low" does not mean
"none".
> Occasionally though, the odds are still
> within range so that one or two of such enzymes may come around at
> just the right time. But, this is quite rare.
Once in three billion years is the minimal needed.
> Given the rarity of
> such events, consider how rare it would be for such creatures to
> evolve anything more complex, like a motility function or other such
> multi-protein functions where all the proteins work together at the
> same time.
Argument from incredulity. I see no evidence for a barrier.
>Remember, just because all the needed parts are being made
> by the same creature as parts of other systems of function does not
> mean that they will spontaneously self-assemble to produce a new
> function.
You are completely, absolutely misunderstanding protein-protein
interaction dynamics which is more chemical and statistical than the
simple picture you seem to have to make this kind of conclusion. You
are thinking of assembly here in terms of Lego blocks. Protein
assembly is statistical and non-specific protein interactions are
rife. You can get assembly of lots of wacky combinations as a matter
of every day function in a bacterial cell. You can select on those,
too.
> For example, all the amino acids are present in a cell
> doing many different functions. They could make many new functions as
> well, but they just don't know how to self-assemble themselves. All
> the parts are there, but ordering them is important. How is this
> done?
Not only can you have various parts associating randomly in the very
early stages of forming a complex, but you can also select for better
interactions based on point mutations back on the genome level.
I think you underestimate the "selection space" available.
>
> > > This lactose environment ain't outer
> > > space and it ain't granite you know.
> >
> > It might as well be if there's no enzyme that has significant lactase
> > activity. It makes the enzyme effectively "blind" to evolutionary
> > change in that direction.
>
> Yes! I'm so glad that you recognize this point.
Yes, but obviously this is not a problem in my understanding. This is
standard evolutionary theory stuff.
> > What's your evidence that it had any kind of
> > weak lactase function at the end of the experiment? Did it?
>
> What? I don't exactly understand your question here. The ebgA gene
> produced a protein with beneficial lactase function. But, no other
> gene was able to produce such an enzyme with a beneficial level of
> lactase activity.
Right, so if you couldn't find any bacteria with weak lactase
function, then clearly it had nothing to select for function, so it
didn't evolve lac+ ability, so the bacteria were essentialy blinded to
the fact that lactose was present. If it had weak lactase function and
then it disappeared, I'd be worried. But we don't expect that to
happen.
> > > One little enzyme is all that is
> > > needed to use this new environment in a more advantageous way. And
> > > yet, many different types of bacteria seem unable to evolve the
> > > lactase enzyme despite hundreds of thousands and even millions of
> > > generations of time. What then, exactly, is slowing this process
> > > down? Please, you seem so knowledgeable . . . what is the answer?
> >
> > The answer is that 10,000 generations of e.coli in a laboratory under
> > fixed experimental conditions were not enough to evolve, through
> > selection, a weak lactase activity.
>
> Yes, that is the conclusion that I came to as well.
But given the statistics you understand to be true (10^1300 sequence
space), what makes you think this is somehow problematic for
evolution?
I am worried that you are laboring under the misconception that
evolution is deterministic, that E.coli growing on a rich bed of
lactose should know the lactose is there and available. There's no
such requirement for its survival, and if it was starved to death on a
rich bed of lactose,granite, or polyester, if its "evolutionary space"
couldn't reach lactase in short order, it would starve. This is
natural selection. It's thought to be the source of many extinctions
-- change of environment around fitness. Too quick a change and the
animal dies. Or in this case, the bacteria starve.
Again, the molecular details of evolution are there in the gene
record. I invite you to discuss phylogenetics.
Deanne
Lilith
mean "cellulose is a wonderful structural molecule" in my previous
post. I do realize that cellulose is a polysaccharide formed by the
action of enzymes. :)
Sean Pitman
> Also, even the logic functions that were evolved
> were dependent upon the proper selective environment being set up
> ahead of time by ID. What if there was a gap between one type of logic
> function and another type of logic function, such as between the NAND
> and the EQU functions that required the evolution of either the AND or
> the OR, or the NOR, XOR or NOT functions first? What if these
> functions were not recognized by a particular environment as being
> beneficial? Then, there would be a neutral gap created by that
> environment between the NAND and EQU functions. What are the odds
> that the "proper" environment that recognized at least one of these
> other functions as beneficial, would come around at the right time?
> You see, the random walk not only includes random changes in code, but
> also in environment. Without an intelligent mind directing changes in
> environment in just the proper way, the organic synthesis of many
> different compounds that are made in chemistry laboratories would not
> work. The order of the environmental changes is just as important as
> the order of the molecules in the "evolution" of new functions or
> compounds.
Now that I have the original Lenski et al., article from "Nature" (vol
423: 8 May 2003), I found something very interesting on the very last
page. Consider the following passage from the "Different
environments" section of the article:
"At the other extreme, 50 populations evolved in an environment where
only EQU was rewarded, and no simpler function yielded energy. We
expected that EQU would evolve much less often because selection would
not preserve the simpler functions that provide foundations to build
more complex features. Indeed, none of these populations evolved EQU,
a highly significant difference from the fraction that did so in the
reward-all environment (P = 4.3 x 10e-9, Fisher's exact test).
However, these populations tested more genotypes, on average, than did
those in the reward-all environment (2.15 x 10e7 versus 1.22 x 107;
P<0.0001, Mann-Witney test), because they tended to have smaller
genomes, faster generations, and thus turn over more quickly.
However, all populations explored only a tiny fraction of the total
genotypic space. Given the ancestral genome of length 50 and 26
possible instructions at each site, there are ~5.6 x 10e70 genotypes;
and even this number underestimates the genotypic space because length
evolves."
Isn't that just fascinating? When the intermediate stepping stone
functions were removed, the neutral gap that was created successfully
blocked the evolution of the EQU function. Now, isn't this what I've
been saying all along? This experiment was successful because the
intelligent designers in this case were capable to defining what
sequences or functions were "beneficial" for their evolving
"organisms." If enough sequences or functions are defined as
beneficial, then certainly such a high ratio will result in rapid
evolution, as we saw here. However, a gap of just 16 neutral
mutations effectively blocked the evolution of the EQU function.
Just for those who are curious, here are the detailed "Experimental
Conditions" listed by the authors:
Avida software was used.
"Every population started with 3,600 identical copies of an ancestral
genotype that could replicate but could not perform any logic
functions. Each replicate population that evolved in the same
environment was seeded with a different random number. The
hand-written ancestral genome was 50 instructions long, of which 15
were required for efficient self-replication; the other 35 were tandem
copies of a single no-operation instruction (nop-C) that performed no
function when executed. Copy errors caused point mutations, in which
an existing instruction was replaced by any other (all with equal
probability), at a rate of 0.0025 errors per instruction copied.
Single-instruction deletions and insertions also occurred, each with a
probability of 0.05 per genome copied. Hence, in the ancestral genome
of length 50, 0.225 mutations are expected, on average, per
replication. Various organisms from nature have genomic mutation
rates higher or lower than this value. Mutations in Avida also
occasionally cause the asymmetrical division of copied genome, leading
to the deletion or duplication of multiple instructions. Each digital
organism obtained 'energy' in the form of SIPs at a relative rate
(standardized by the total demand of all organisms in the population)
equal to the product of its genome length and computational merit,
where the latter is the product of rewards for logic functions
performed. The exponential reward structure shown in Table 1 was used
in the reward-all environment, whereas some functions obtained no
reward under other regimes. An organism's expected reproductive rate,
or fitness, equals its rate of energy acquisition divided by the
amount of energy needed to reproduce. Fitness can also be decomposed
into replication efficiency (ratio of genome length to energy required
for replication) and computational merit. Each population evolved for
100,000 updates, an arbitrary time unit equal to the execution of 30
instructions, on average, per organism. The ancestor used 189 SIPs to
produce an offspring, so each run lasted for 15,873 ancestral
generations. Populations existed on a lattice with a capacity of
3,600 individuals. When an organism copied its genome and divided, the
resulting offspring was randomly placed in one of the eight adjacent
cells or in the parent's cell. Each birth caused the death of the
individual that was replaced, thus maintaining a constant population
size."
Sean
Dunno
I think you have effectively shown that a complex function
can't always be built by an evolutionary process if the
building blocks used in construction said complex function are
removed.
What a suprise.
Dunk
wrote:
<snip>
> In order to evolve lactase function, the system must be able to select
> on lactase function in the first place. If there is no lactase
> function present from any source, there will be no selection to that
> effect, and will not be until an E.coli protein mutates in such a way
> to bring lactase function within reach.
urmmm this gets amended in various ways throughout the lengthy post,
but some clarification is needed right here just to be on the safe
side.
In general it is _not_ necessary to be able to select on a function in
the first place in order to evolve it.
Often enough it is the other way around.
As a first example recall the Lenski et al. paper (0).
They were not able to evolve the final function by selecting on it in
the first place. The only way was to select on various other things
until the final function was almost in place.
Life can be like that. Selection on a, b, c sets up function d.
Then selection can improve d. The functions can be slightly
different than d, moderately different or unrelated.
In any case these discrete 'functions' are as conceived by us. To the
organism reproduction is the function. Thus the functions (in the
observer's mind) can be as similar as rates of the same reaction, or
as different as coopting an enzyme as the lens of your eye. Thus a
function can evolve before it exists, and depending on how
nitpickingly you define your functions, they always do. Oh oh, is
that a philosopher I hear whiffling through the tulgey wood?
It is not uncommon for a protein to have, potentially, more than one
talent. If there is a need for something else a protein can do, and
a duplication occurs, one copy may be improved for the new function.
In the other posts here, and even in this nice new paper (1), they
only refer to selection setting in 'soon after' duplication. But,
(and it's not so surprising when you think about it, and there are
refs I could dig up if necessary) in those duplications that last,
dual selection was often the case before duplication.
There are lots of duplications. However, many are called but few are
chosen. About 1 in 10,000. Otherwise, by now we wouldn't be able
to stand up under the weight of our genome.
<snip>
> Heterogeneity is achieved by gene duplication, gene conversion, exon
> shuffling, mutation, genome duplication, to name a few. Typical
> genomic processes observed in nature.
This is also a partial list of routes to new functions. I want to add
one more important one - changes in gene regulation. It's common and
important; why wouldn't it be? The crystalin lens protein mentioned
above is one example. The protein was always transparent (as many
are). But transparency didn't exist as a biological function until
gene regulation made it so.
Of course all your proteins are needed at just the right time and
place. What about a bacterium? Regulation of gene expression still
matters big time. Aside from the precise timing of the cell cycle,
enzymes in general don't last. They get degraded and have to be
replaced. That's why you not only have to eat every day, you have to
eat something besides sugar. Some proteins are needed all the time,
but it is important not to waste resources on others when they are not
needed. For instance a lactase enzyme, in a well adjused microbe,
would only be produced when lactose is detected.
What does this have to do with new functions? Consider
pentachlorophenol (PCP) degradation. PCP is a man made chemical that
is very toxic to bacteria and other living things. It's been around
for about 60 years. Some bacteria now have a system to break it down
and eat it (2). (it's IC by the way). The key mutation that makes
this possible is a change in the expression of one of the necessary
enzymes. It is normally produced only in some other unrelated
circumstance. The mutation made it available all the time. When
you're in PCP you're in PCP all the day if you are a bacterium. You
have be able to deal with PCP all the time or it will deal with you.
This protein took up a completely new function. Another protein in
the process had previously acted on other milder chlorophenols and
luckily was produced in response to chlorophenols in general. It took
on a slightly new function. In both cases the (potential) function
evolved before it became a biological function, hence before there
could be any selection of it. Both of them have subsequently evolved
to deal with PCP a bit faster than the corresponding enzymes in other
bacteria can, even when artificially produced in the right
circumstance. But they still are not very fast.
0.
http://www.antievolution.org/cgi-bin/ikonboard/ikonboard.cgi?s=3ec079805b4bffff;act=ST;f=2;t=64
1. Hooper SD, Berg OG. (2003) On the nature of gene innovation:
duplication patterns in microbial genomes.
Mol Biol Evol. 2003 Jun;20(6):945-54. Epub 2003 Apr 25.
PMID: 12716994 [PubMed - in process]
2. Copley SD. (2000) Evolution of a metabolic pathway for
degradation of a toxic xenobiotic: the patchwork approach.
Trends Biochem Sci. 2000 Jun;25(6):261-5. Review.
PMID: 10838562 [PubMed - indexed for MEDLINE]
Dunk
snipity snip
>Deanne, who knows about these things, but dunk wanted to be sure certain points were clear.
Von Smith
Great! So now all you have to do is demonstrate that such neutral
gaps are pervasive enough to preclude evolution of various biological
functions, given likely precursors and known mechanisms of genetic
change. Otherwise, your argument is (still) irrelevant.
Sean Pitman
I'll even go along with this nomination as long as a link to my
follow-up response(s) is included.
Sean
Howard Hershey
reply to me, I became frustrated at the repetitiveness and length, so I
decided to try to get at what I see as the crux of the argument more
directly.
This is a summary of the argument that Sean is making, as I see it, and why
I think the core features of his argument is based on a strawman version of
nature, which includes a whopping dose of teleological thinking (the
assumption that a current function was an intended and necessary end goal),
the usual inability of creationists to see that evidence from nature
includes more than direct experimentation (specifically, it also includes
evidence that shows that nature worked through certain specific mechanisms
rather than others), as well as other problems, and the usual overestimation
of the amount of change needed to produce the amount of evolution observed
in nature (most evolutionary change does not involve the 'invention' of any
new genes, but merely allelic variation of existing ones or their regulatory
regions, and via that, the modification of the quantitative traits). His
argument also fails to distinguish between absolutely *necessary* (aka,
minimal) requirements for life itself and *useful* changes (changes which
are useful or necessary to exploit materials and conditions in certain
environments and not necessary or useful in others). There is actually very
little function and structure that is *necessary* in the sense of being
necessary for life under all (including the initial) conditions of
existence. DNA is probably not *necessity* for life in this sense of
*necessary* because it probably was a secondary addition to a simpler form
of 'life' that was still capable of self-reproduction of a genetic material
and had enzymatic functionality that supported that. Multicellularity is
*certainly* not a *necessary* condition for life, since the earth happily
existed with no multicellularity for more time than it has existed with
multicellularity (3.5 billion years of life compared to 0.75 or so billion
years of multicellular life). Eucaryotic sexual cycles are not a
*necessary* condition for life. The only *necessary* requirements are those
that are the minimal requirements for life (self-reproduction and the
ability to extract energy from the environment to accomplish
self-reproduction) under conditions where there is no competition.
Everything else that organisms exhibit are *useful* (and often *necessary*
for the current organism), but are not required for the minimal functions of
life in all environments, but merely the current one.
Sean recognizes that it is quite possible for a gene to be modified so that
a new 'function' can be produced. In fact, he points out many examples of
just this type of change occurring in both experimental and natural
settings. That includes the conversion of the ebg gene to lactase activity,
the changes that lead to clinically significant resistance to chloroquine,
various forms of antibiotic resistance. The latter also can be used as an
estimate of the speed at which, in nature, a reasonably 'significant gap' of
phenotypically unchanged 'required steps' can occur. [N.b. It is
important to remember that the phenotype used, absence of clinical effect,
is not the same as 'differential reproductive success' of malarial
parasites. The latter can occur under sub-clinical conditions.] Note that
the 'evolution' of this selective change occurred across a non-selective gap
of 7 to 9 events and occurred in 40 years. So, it is quite clear that *in
principle* it is quite possible for selection to produce 'new functions'
even in Sean's world (since there do exist evolutionary changes that produce
'new' functions that do not require his hypothesized many 'neutral' steps)
*and* that it is even possible to cross *reasonable* sized gaps in
functionality.
Given this recognition that it is indeed possible to evolve 'new' functions
without having to cross his hypothetical large seas of multiple neutral
steps, Sean is left arguing that these observed cases do not represent the
normal cases. He instead tries to refocus our attention on the cases where
this does not happen and tries to convince us (by asserting without
presenting evidence) that the 'normal' situation is the one he posits: That
most new functions require his hypothetical ocean of completely useless
intermediate steps. This is a strawman argument and the biochemical
equivalent of the distinction between microevolution (evolution that can be
observed experimentally) and macroevolution (evolution that cannot be
directly observed and can be plausibly denied). Usually the latter is put
in terms of "we need to see a lizard give birth to a bird" or "where are all
the intermediates between amoeba and man?" or "if you start with a
completely random sequence of DNA, you need x gazzillion changes to get the
one (or small number of) sequence that has y function (teleologic function),
and none of the intermediates have y function".
Sean points out that if you remove all possibility of easy transition to a
new function by only looking at bacteria that lack ebg or other such genes,
then one cannot evolve lactase by *directly* selecting for lactase function
within the time constraints of human designed experimentation. That is, he
points out that evolution is not a mechanism which has the ability to
generate whatever function he chooses to generate, in whatever organism with
whatever genome he chooses (and he chooses genomes without any sequences
closely similar to lactase), in whatever time frame he thinks is sufficient
when the only thing being selected is the teleological or end result he
thinks exists.
Note that Sean's argument is merely a restatement of the "you can't evolve a
wing because the intermediate stages of a wing is useless as an instrument
of flight" argument transferred to molecules. "You can't evolve a lactase
directly (if you start with certain conditions involving apparently random
sequences -- and *if*, of course, you arbitrarily exclude all those cases
where it has been empirically demonstrated that you can indeed evolve a
lactase directly ;-) -- going *directly* toward the teleologically
determined end function Sean arbitrarily chooses) because, yawn!, the
half-way intermediates do not function as a useful (selectable) lactase.
Notice that Sean's argument also includes a restatement (in molecular terms)
of the idea that evolution can explain *micro*evolution (the evolution of
the differences between very closely related individual) but cannot explain
*macro*evolution, which is defined as a gap big enough that it cannot be
crossed in one step: "a cat giving birth to a dog" or differences between
very distantly related organisms, such as "amoeba to man". In Sean's
argument this is the gap between some random sequence of DNA and his
teleologically determined final sequence. Again the assumption is that no
intermediate states can have any selective value or that the gap cannot be
crossed in the amount of time available to experiment. And, of course, it
is true that sometimes a gap cannot be crossed or crossed in the time
available.
I agree entirely in one sense. Evolution cannot cross every possible gap
*directly* aiming for some teleological set goal (the terminal functionality
of Sean's arbitrary choice). In fact, evolution, because of the mechanism
by which natural selection works, cannot proceed toward teleological goals
at all. Evolution's selection mechanism can only focus on reachable local
goals. If no bacteria in a particular environment can utilize lactose, then
no bacteria will use it and there is no selective advantage to any bacteria
on this basis. If no bacteria in a particular environment can use nylon or
some other plastic polymer (and there are man-made plastic polymers that
could potentially be useful carbon sources but which are not used precisely
because no current bacteria can cleave a particular chemical bond), then no
bacteria has a selective advantage on that basis. When or if a bacteria
produces a variant able to cleave, say, the bond in polyvinyl chloride and
also deal adequately with the chlorine atoms, it will certainly have a
selective advantage over bacteria that cannot do this in certain
environments (those that contain significant amounts of polyvinyl polymers).
There is no guarantee that such a variant will occur anytime soon. There is
also no guarantee that it won't happen.
But, of course, the key word in all this is *directly*. Evolution, properly
understood, does not often produce things *directly* from some random
starting sequence to some final teleological functionality under the "need"
for such functionality. In fact, it cannot do so (although Lamarck -- and
Sean -- would disagree). Instead, there must usually be some intermediate
utility, but not *necessarily*, nor for any long or involved sequence of
changes (which we will define as more than 7-9 events, since it is quite
clear, from chloroquine resistance, that such gaps can be rather easily
crossed in human time-frames), *usually*, via intermediates with the
teleological end functional utility.
So what we are really arguing about are two different views of the
biochemical nature of how 'functions' arise in organisms. In Sean's view,
evolution can indeed account for the existence of those 'functions' which
can be reached by no more than a few steps in the normal way that biologists
describe. But his claim is basically that such steps are exceedingly rare
and irrelevant. His argument is that most 'new' functions in organisms
involve multiple changes through a wasteland of *no utility at all* until
the final moment when it all falls into place and we have selection for the
final teleological function. Given this view, he cannot see how 'new'
functions can arise by selection, since it would require direct teleological
selection for that final function from an essentially unrelated sequence
without any affinity for or relationship to the final sequence.
That is, he is using his (what I regard as a strawman) idea of how 'new'
functions arise in order to then argue that they cannot arise that way. And
then use the fact that they cannot arise that way to claim that "goddidit"
is a better explanation. One must always keep this attempted switcheroo,
the attempted focusing on (asserted but unsupported) claims that the failure
of natural selection to work under all and any conditions to produce a
teleologic end point somehow obviates the fact that natural selection does
work to produce new function when the clearly described requisite conditions
*are* present.
*If* it were the case that evolution by selection has to produce new (but
currently existing) functions in living organisms by a process that requires
crossing large sweeps of selective neutrality for *any* function or that
only the teleological function is important in selection, and *if* the
sequences that make up the proteins of life *commonly* had to pass through
vast wastelands of functionlessness (not just for the end function, but also
for any intermediate function that differs from the end function) to reach
the desired teleological end, then it would indeed be nearly impossible for
these functions to exist via known evolutionary mechanisms.
But this view of how organisms work also implies that currently living
organisms should exhibit certain predictable features:
1) If what Sean claims is true, *most* proteins in organisms should be
structurally *isolated* wrt their sequences from all other proteins in an
organism. This is because, if each of these majority of protein functions
(in Sean's vision of biology) had to be created essentially from scratch
through multiple functionless steps rather than via a few steps from closely
related already existing proteins, there should be little evidence of
sequence similarity between proteins that perform different functions.
OTOH, if most protein functions in organisms arose via duplications and
divergence from proteins that serve related functions, one would expect to
be able to see, often, and especially for recently evolved new functions,
sequence evidence that indicates that the 'new' enzyme or function came from
a structurally related precursor. That is, proteins should exist in
families. So here we have a genetic 'test' of Sean's vision of what is
required for 'new' function (crossing large gaps) and what my vision of how
'new' functions arise (by modification of related enzymes). I would expect
that many genes would be found in gene families. I would expect that genes
like the globins of hemoglobin should share similar sites for introns with
each other and with myoglobin. I would expect that many 'novel' genes would
appear to be 'chimeric' (due to fusion of different protein domains, of
which there is a limited number) events rather than via 'construction from
completely random sequences'. I would expect enzymes and other proteins to
have secondary activities and to bind to other proteins, sometimes without
that interaction or secondary activity having biological meaning in the
current environmental setting. I would expect this evidence to be clearer
for 'recently' evolved proteins than for the most ancient proteins.
2) I would expect, if Sean's vision of how evolution works -- changes are
due to specific genes that have to have many, multiple changes to produce a
new phenotypic effect -- that humans and chimps would have certain genetic
sequences that code for proteins that are dramatically different from each
other. I would expect that different dog breeds, likewise, should have
certain genes that are dramatically different from each other and from other
canids by many, many, sequence changes. These involve, after all, large
phenotypic changes and current differences that occurred relatively rapidly
even in the standard time chronology. If these differences are not due to
'new' functions that have to cross large seas of inutility, perhaps, just
perhaps, Sean's model of evolution, which implies just such events as being
frequently necessary, is not an accurate description of how evolution works.
Perhaps, just perhaps, much evolution does not, in fact, involve the
invention of new proteins at all. This would be a genetic test of the
expectation that protein sequence changes crossing large seas of inutility
are a necessary requirement for most evolutionary change.
Needless to say, I cannot think of a single gene in humans that is so
different from the equivalent in chimps (or is not present in one or the
other species at all) that it cannot be recognized rather easily as an
simple allelic difference largely commensurate with the amount of time since
divergence and even, for the most part, ignoring selection completely. [It
is not that selection didn't happen and wasn't important, only that the
amount of change and difference due to selection is minor compared to the
amount of change due to drift.]
Taken to a larger scale, it is noteworthy that significant numbers of genes
are held in common by large groupings of organisms, at least as members of
families of genes. That is, the 'invention' of novel genes and gene
functions is indeed relatively rare. The duplication and divergence of
pre-existing genes is relatively common. The selection of chimeric genes is
relatively common. The retention of structure while changing function is
relatively common. Overlapping function and redundancy is relatively
common. In short, living organisms do not look like creatures which contain
functions that had to cross large gaps of inutility. They look like
organisms that have considerable similarity wrt the proteins and functions
they perform.
3) I would expect, if Sean is right, complex multi-protein systems to show
no evidence of subsystem utility nor the ability to be generated in a
step-wise fashion, either ontologically or phylogenetically. OTOH, if Sean
is wrong, I would expect an ontological process that would indicate that the
final 'teleological in hindsight' product was actually composed of amplified
recursive systems or composed of subsystems that are related to functions
that the subsystem can have independently of the teleological 'end function'
that Sean posits. That is, my claim is that the solution that nature uses
for the three-body problem is to produce two two-body events.
When I look at systems like the clotting system of vertebrates, I see a
system of repeated and self-recursive cascades using proteins that are
clearly related to each other. It is quite easy to see how such a system
can evolve in a step-wise fashion with functional utility at each step. In
the case of the bacterial flagella, where Sean sees huge gaps of complete
non-function, I see subsytems and even ontologically immature systems that
perform a different function that the end system still performs (the
bacterial flagella is *still* a protein-export device in addition to being a
motility device. The motor subsystem is also used in many other parts of
the cell independently of its use in the flagella. That is, the flagella
problem is not a case of all-or-nothing utility, focused solely on the
motility function as the only possible utility. There is actual *evidence*
that sub-parts of the flagella have functional utility beyond that of being
a motility device. There is actual *evidence* that certain subsytems are
independently constructed (with independent utility) and only later come
together via protein-protein interaction to produce the motility function.
Sean merely asserts that the flagella is necessarily an all-or-nothing event
that must come together by sheer randomness. He does that because such a
strawman version of how evolution works is necessary for his claim that
evolution must work randomly through large completly useless gaps to be
accepted in the face of evidence that the genetic structure of organisms
belies his strawman model.
I could go on, but why bother. It is clear that Sean is asserting a
strawman version both of what is required of evolutionary change and of what
actually exists in nature in order to claim that, because his strawman
vision cannot occur by known evolutionary mechanisms, that evolution is
false. That is what creationists do.
Von Smith
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03062...@posting.google.com>...
> > lil...@umich.edu (Lilith) wrote in message news:<75200cbc.03061...@posting.google.com>...
> > > > <snip>
<snip>
OK, it's "Humor the Liberal Arts Major" time again. If I understand
things correctly, the simple fact that we can construct a robust
phylogenetic tree for gene families at all *directly* falsifies Dr.
Pitman's claims about biological functions being little Pacific
fitness islands separated by vast oceanic stretches uncrossable by
evolution.
The point I think I see here does not even depend on whether such
robust trees with high relevance scores are good evidence for common
descent per se. Here's my reasoning:
Dr. Pitman's argument AIUI proceeds something like this:
P1. The phase space for any gene sequence of substantial length is
almost unimaginably huge, as is the sequence space for any protein for
which it might code.
P2. The total number of biologically possible functional sequences
are a tiny tiny subset of the total number of sequences in the space
(I've seen Dr. Pitman make up -er, estimate- numbers on the order of 1
in 10^10^1300).
P3. These functional sequences are randomly distributed throughout
the sequence space, and are therefore generally very sparsely
scattered in it.
P4. The functional sequences we observe in life today are a
representative subset of the total population of all possible
functional sequences, and should thus be similarly scattered, failing
some drastic and unidentified sampling bias.
P5. The intervening phase space between any two functions (whether
possible or actual), in addition to being large, will generally tend
to be selectively neutral in most if not all historically possible
fitness landscapes.
Conclusion: For any two functional sequences, it is vanishingly
unlikely that evolution from one to the other will be selected for, or
will occur via neutral drift within available time.
IIUC, one can construct the following lemma (or corrolary, or
whatever) concerning gene phylogenies:
P5. If functional molecular sequences are sparsely and randomly
scattered throughout the sequence space, the degree of sequence
similarity among them should also be random.
P6. Phylogenetic trees from random data will not be robust or have
high relevance scores.
Lemma: It will not be possible to construct robust, parsimonious
trees with high relevance scores for hypothetical gene families.
And nonetheless, here we are with exactly the sort of trees that
should not be possible if Dr. Pitman's South Pacific characterization
of the fitness landscape were correct. That such phylogenies are
possible *directly* falsifies his neutral gaps hypothesis, regardless
of what they indicate about common descent or evolutionary pathways
per se.
ISTM that relaxing or challenging any of the premises seriously
undermines Dr. Pitman's argument. And if we adhere to them, it is
hard to escape the lemma: We shouldn't be able to construct
statistically significant phylogenies for gene families at all unless
Dr. Pitman is seriously wrong about something.
Please tell me what I have missed. I don't have much ego invested in
this, because I don't even pretend to have any relevant expertise.
Von Smith
The wise make fools, and proverbs garble them.
William
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>I'll even go along with this nomination as long as a link to my
>follow-up response(s) is included.
>
>Sean
>
>www.naturalselection.0catch.com
The above site contains a lot of confused thinking. The author appears
to confuse the facts of evolution (the fossil record, common descent
etc) with the theory that explains the facts (natural selection,
genetic drift etc). And his language rather gives away his theological
bias (natural processes are called 'mindless' processes - implying
that there must be some 'mindful' processes).
William
catshark
<hers...@indiana.edu> wrote:
>After working for some time in the usual 'call and response' mode on Sean's
>reply to me, I became frustrated at the repetitiveness and length, so I
>decided to try to get at what I see as the crux of the argument more
>directly.
POTM. Seconds?
---------------
J. Pieret
---------------
Cogito sum, ergo sum, cogito.
- Robert Carroll -
Von Smith
> On Tue, 24 Jun 2003 15:06:38 +0000 (UTC), Howard Hershey
> <hers...@indiana.edu> wrote:
>
> >After working for some time in the usual 'call and response' mode on Sean's
> >reply to me, I became frustrated at the repetitiveness and length, so I
> >decided to try to get at what I see as the crux of the argument more
> >directly.
>
> POTM. Seconds?
He's already got another post in the same thread nominated that covers
a lot of the same ground. Maybe we could merge them as a POTM?
Von Smith
The wise make fools, and proverbs garble them.
>
Sean Pitman
> This is a summary of the argument that Sean is making, as I see it, and why
> I think the core features of his argument is based on a strawman version of
> nature, which includes a whopping dose of teleological thinking (the
> assumption that a current function was an intended and necessary end goal),
As I have said multiple times before, I do not make this
"teleological" assumption at all. Certainly the theory of evolution
proposes that no particular goal was necessary or intended by the
mindless workings of nature. That is precisely the problem. If
everything is a potential, then natural changes tend toward homogeny.
Obviously it is impossible to detail the entirety of the potential
sequence space for a living organism in its environment. However, I
think that it is possible to show that the neutral sequences within
this potential space grow exponentially with increasing functional
complexity. What does this mean? It means that on average, the
neutral gaps between various functions of increasing complexity start
to grow exponentially. This means that existing functions start to
become surrounded, on EVERY side, by neutral sequences. At this
point, it really doesn't matter which way evolution tries to go, it
will be blocked by the surrounding ocean of neutral sequences. No
teleological goal is needed since all goals, except for the most
simple, are blocked.
I have used this example before, but it bares repeating: Try evolving
a sentence or paragraph, one letter at a time with each change or
"mutation" being beneficial in a given scenario. See how far you can
get. It is a lot harder than one might think. Certain changes can be
done that might change meaning in beneficial way, but very quickly
neutral gaps are reached no matter which direction one tries to go.
The same thing happens with random mutations and natural selection.
Since the genetic real estate of a given organism or population is
limited and the environment is also limited in resources and options,
these limits severely limit the number of potential beneficial
sequences that could be used by a given organism. Such limits put
significant constraints upon the evolution of new functions since new
beneficial functions of increasing complexity become extremely rare
relative to all the neutral and detrimental sequences.
Can this be absolutely proven? No, as nothing can be absolutely
proven this side of eternity. One has to look at the weight of
evidence. I think that the weight of evidence is clearly in favor of
the idea that vast oceans of neutral sequences surround very tiny
islands of function and that these oceans grow exponentially faster
than the relative number of islands grow as the level of functional
complexity increases.
You and other evolutionists, who are actually considering this
problem, suggest that the neutral ocean is not nearly as big as I am
proposing. You are suggesting that there are a lot more functional
paths between these potential islands. You do not think that one path
in particular can be detailed, since this would be "teleological", but
you believe that there is very good evidence for the existence of
common pathways none-the-less. Of course, this is a must for your
position. Without these supposed paths, evolution is sunk and you
know it. Your problem is that you cannot demonstrate these paths.
Your position is not falsifiable. If you set up a test to find a path
and you do not find it, all you have to say is, "gee, I guess this
particular path does not exist, but that doesn't mean that there isn't
another path somewhere else." This is a fine position since it is not
falsifiable. No test could be set up that could absolutely disprove
this position. Since no one knows all about the potential sequence
space for any particular organism in any particular environment, it
would take an eternity to demonstrate a lack of all potential
pathways. So, since your position cannot be completely disproved this
side of eternity, you can feel safe in your faith regardless of the
mountains of evidence that remove one path after another. As long as
a potential for some unknown path exists, you faith can take hold of
the unknown that holds a potential answer to save your theory.
However, since you claim to be a man of science and not of blind
faith, and since you cannot test for all pathways, there must be some
testable way to support your position that these pathways are common
enough to save your theory. What evidence do you have for this
position? Where is your "weight of evidence" for the existence of
these common pathways toward not just one (teleological) but many
potentially different functions of higher complexity?
> the usual inability of creationists to see that evidence from nature
> includes more than direct experimentation (specifically, it also includes
> evidence that shows that nature worked through certain specific mechanisms
> rather than others),
All "evidences" must be interpreted. Such interpretations must be
supported by direct experimentation that can falsify the
interpretation. If the interpretation or hypothesis is not
falsifiable, then no one can say that their interpretation is any
better than anyone else's interpretation. All non-falsifiable
interpretations become equal. You cannot say that someone who
disagrees with your interpretation is "wrong" because you have no
predictive value until you can test your hypothesis in a falsifiable
way.
> as well as other problems, and the usual overestimation
> of the amount of change needed to produce the amount of evolution observed
> in nature (most evolutionary change does not involve the 'invention' of any
> new genes, but merely allelic variation of existing ones or their regulatory
> regions, and via that, the modification of the quantitative traits).
Why are not talking about what most point to as evidence of evolution
in action. Certainly most examples of evolution are extremely simple
to explain with the mindless processes of nature alone. The examples
of allelic variation that have been demonstrated to occur in real time
are extremely simple indeed. But, we are not talking quantity here,
but quality. If the only question was, "Which type of changes occur
most often?" then there would be no ball game here. However, there
really is no overestimate on the amount of change that is required to
produce many functions of high complexity. A historically non-motile
bacterium requires truly vast changes before any motility system could
be realized (not just one specific teleological type of motility
system such as a flagellar apparatus, but any type of motility
system). This is not an overestimate. Other functions of increasing
complexity also require significantly increasing changes to occur to
produce them. You really cannot make such blanket statements such as
this without some sort of evidence to back yourself up.
> His
> argument also fails to distinguish between absolutely *necessary* (aka,
> minimal) requirements for life itself and *useful* changes (changes which
> are useful or necessary to exploit materials and conditions in certain
> environments and not necessary or useful in others).
This is complete nonsense and a wonton misrepresentation of my
position. Many beneficial functions are not vital for life, but they
are still beneficial. I could certainly live without my right arm,
but this fact doesn't make my right arm unnecessary. If by the term
"necessary" you mean, "vital for life", then very few things are
absolutely necessary for life. This really is not the issue. The
issue is, how do organisms evolve new functions of increasing
complexity that give them an advantage over their peers in a given
environment. Certainly these new functions would not have to be
"vital" for life itself, but they would be vital for *improved*
survival.
> There is actually very
> little function and structure that is *necessary* in the sense of being
> necessary for life under all (including the initial) conditions of
> existence. DNA is probably not *necessity* for life in this sense of
> *necessary*
And where, exactly, did I say otherwise?
> because it probably was a secondary addition to a simpler form
> of 'life' that was still capable of self-reproduction of a genetic material
> and had enzymatic functionality that supported that.
Yes . . . That certainly is the theory of how functions of increasing
complexity came about.
> Multicellularity is
> *certainly* not a *necessary* condition for life, since the earth happily
> existed with no multicellularity for more time than it has existed with
> multicellularity (3.5 billion years of life compared to 0.75 or so billion
> years of multicellular life).
Again, where did I ever argue that multi-cellularity was "necessary"
for life?
> Eucaryotic sexual cycles are not a
> *necessary* condition for life.
No, they aren't. And your point is?
> The only *necessary* requirements are those
> that are the minimal requirements for life (self-reproduction and the
> ability to extract energy from the environment to accomplish
> self-reproduction) under conditions where there is no competition.
Ok . . . and I hope you are going somewhere with this because I really
don't remember arguing this point.
> Everything else that organisms exhibit are *useful* (and often *necessary*
> for the current organism), but are not required for the minimal functions of
> life in all environments, but merely the current one.
So how did these new functions that might not be necessary for life
itself (such as the lactase function in a lactose-enriched
environment) evolve if there were neutral gaps in the way? How does
competition for survival provide the pathways across these neutral
gaps so that the resources of new environments can be used in newly
beneficial ways of increasing complexity? Again, I'm not looking for
specific teleological examples, but I am looking for specific examples
of any function within a given *level* of complexity. For example, if
you could show how any type of bacterial motility could evolve or if
you could demonstrate the evolution of bacterial motility, that would
be very convincing to me. Or, if the category of bacterial motility
is still too teleological for you, then I would be satisfied with the
demonstration of the evolution of any multi-protein function where all
the parts are required to work at the same time. That is the *level*
of functional complexity that I am looking for evolutionists to
explain or demonstrate.
> Sean recognizes that it is quite possible for a gene to be modified so that
> a new 'function' can be produced. In fact, he points out many examples of
> just this type of change occurring in both experimental and natural
> settings. That includes the conversion of the ebg gene to lactase activity,
> the changes that lead to clinically significant resistance to chloroquine,
> various forms of antibiotic resistance. The latter also can be used as an
> estimate of the speed at which, in nature, a reasonably 'significant gap' of
> phenotypically unchanged 'required steps' can occur. [N.b. It is
> important to remember that the phenotype used, absence of clinical effect,
> is not the same as 'differential reproductive success' of malarial
> parasites. The latter can occur under sub-clinical conditions.] Note that
> the 'evolution' of this selective change occurred across a non-selective gap
> of 7 to 9 events and occurred in 40 years.
Here you are mistaken. The neutral selective gap for chloroquine
resistance was most likely more on the order of 3 or 4 mutations.
Many of the other observed mutations found in chloroquine resistant
parasites are not required. Many different point mutations have been
isolated in resistant CQR strains of malaria (M74I, N75E, K76T, A220S,
Q271E, N326S, I356T, and R371I). Of these, only the K76T and the
A220S mutations are shared in common between resistant malaria strains
on various affected continents of Asia, Africa, and S. America.
Several of the rest of the mutations are thought to be sequentially
beneficial, but not necessary for the development of selectable
chloroquine resistance to begin with. Thus, the neutral gap here is
still very small indeed, although greater than the one step gap needed
for mefloquine resistance. However, even if the gap were 7 to 9
neutral steps wide, for population sizes and reproduction rates that
exist naturally, such a gap would not be much of a problem in the 20
or so years that it took for these populations to develop significant
levels of chloroquine resistance. The reason why this evolution has
never been demonstrated in the lab is most likely due to the limited
population size under study in the lab and the limited time of
observation.
I detail the statistical basis for these statements at:
> So, it is quite clear that *in
> principle* it is quite possible for selection to produce 'new functions'
> even in Sean's world (since there do exist evolutionary changes that produce
> 'new' functions that do not require his hypothesized many 'neutral' steps)
> *and* that it is even possible to cross *reasonable* sized gaps in
> functionality.
New functions do evolve, but "reasonable" gaps are NOT crossed in the
process. The gaps always involve the crossing of less than a handful
of neutral mutations and usually require only one or two mutations.
Even chloroquine resistance only requires 3 or 4 specific mutations,
but even if 7 or 9 were required, this would not be a significant gap
given the population size that exists in the wild. In determining
what is or what is not a significant gap, you must look at not only
the absolute gap involved, but the population size, the mutation rate,
and the generation time. The problem here is that with every doubling
of the neutral gap, the population would have to grow by a factor of
two to keep up. In short order, growing neutral gaps outpace any
population's ability to keep up with the exponentially growing random
walk required to cross the gap.
> Given this recognition that it is indeed possible to evolve 'new' functions
> without having to cross his hypothetical large seas of multiple neutral
> steps, Sean is left arguing that these observed cases do not represent the
> normal cases. He instead tries to refocus our attention on the cases where
> this does not happen and tries to convince us (by asserting without
> presenting evidence) that the 'normal' situation is the one he posits: That
> most new functions require his hypothetical ocean of completely useless
> intermediate steps.
Again, you are arguing from a position of quantity instead of quality.
You are arguing that since you can demonstrate a huge number of
examples of evolution in action where new functions are in fact
evolved, that you really do not need to look at the level of function
that these very common examples demonstrate. For you, absolute
numbers are convincing. You don't need to know anything about the
quality. All you want in quantity. Clearly, I do have very good
"evidence" for the exponential decrease in examples of evolution as
the level of functional complexity increases. When you start out with
the lowest level of functional complexity, such as that required for
de novo antibiotic resistance via one or two mutations, then it is
very easy to find tons of examples. However, when you move up the
ladder a little bit to functions that require the crossing of 3 or 4
neutral steps, as with chloroquine resistance, the number of examples
drops off dramatically. Then, when you move up to the de novo
evolution of complete enzymes in real life organisms, such as lactase
evolution in E. coli, the number of examples drops off even more
dramatically. Then, when you move up to the de novo evolution of
multi-protein functions, such as bacterial motility, the number of
examples is ZERO. Its an interesting progression isn't it?
> This is a strawman argument and the biochemical
> equivalent of the distinction between microevolution (evolution that can be
> observed experimentally) and macroevolution (evolution that cannot be
> directly observed and can be plausibly denied). Usually the latter is put
> in terms of "we need to see a lizard give birth to a bird" or "where are all
> the intermediates between amoeba and man?" or "if you start with a
> completely random sequence of DNA, you need x gazzillion changes to get the
> one (or small number of) sequence that has y function (teleologic function),
> and none of the intermediates have y function".
Of course, I'm trying to point out that the problem really isn't one
that can be determined morphologically. The problem really is one of
genetic gaps, not phenotypic gaps. There are in fact very significant
gaps between functions that rely on single proteins alone. It only
gets worse from here on out.
> Sean points out that if you remove all possibility of easy transition to a
> new function by only looking at bacteria that lack ebg or other such genes,
> then one cannot evolve lactase by *directly* selecting for lactase function
> within the time constraints of human designed experimentation. That is, he
> points out that evolution is not a mechanism which has the ability to
> generate whatever function he chooses to generate, in whatever organism with
> whatever genome he chooses (and he chooses genomes without any sequences
> closely similar to lactase), in whatever time frame he thinks is sufficient
> when the only thing being selected is the teleological or end result he
> thinks exists.
Not at all. These teleological examples only demonstrate that the
average neutral gaps do in fact grow exponentially with increasing
functional complexity. The functions do in fact become more and more
rare relative to the total number of potential sequences in "sequence
space". Given this fact, it is not up to you to demonstrate the
commonality of functional paths that traverse this open ocean of
neutrality as functional complexity increases. After all, these same
bacteria that could not evolve the lactase function in a lactose rich
environment would evolve antibiotic resistance to just about any
antibiotic in short order - even if exposed to sublethal levels of an
antibiotic. In other words, even if it was not absolutely "necessary"
for life, these bacteria would still rapidly evolve antibiotic
resistance to many different types of antibiotics, but they would not
rapidly evolve the lactase function. Why? The reason for this
difference in evolvability is not based on the level of selection
pressure, but upon the level of functional complexity (the relative
rarity of beneficial sequences in sequence space).
> Note that Sean's argument is merely a restatement of the "you can't evolve a
> wing because the intermediate stages of a wing is useless as an instrument
> of flight" argument transferred to molecules.
Yes it is. However, it is far easier for evolutionists to argue from
morphology than from genetics. Where the morphological steps seem
apparently small, the genetic steps involved are not necessarily so
simple.
> "You can't evolve a lactase
> directly (if you start with certain conditions involving apparently random
> sequences -- and *if*, of course, you arbitrarily exclude all those cases
> where it has been empirically demonstrated that you can indeed evolve a
> lactase directly ;-)
Which is just one case. Again, what Hall's experiment demonstrates is
the relative rarity of functional sequences as one moves up the ladder
of functional complexity.
-- going *directly* toward the teleologically
> determined end function Sean arbitrarily chooses) because, yawn!, the
> half-way intermediates do not function as a useful (selectable) lactase.
You really don't see the relevance here? I'm truly mystified.
> Notice that Sean's argument also includes a restatement (in molecular terms)
> of the idea that evolution can explain *micro*evolution (the evolution of
> the differences between very closely related individual)
Extremely closely related indeed! I mean, when statistical gaps as
small as 20 or so differences in genetic functions effectively block
the evolution of those functions by any reasonable sized population of
life forms of any type, then I call those changes that can actually
evolve VERY closely related or "micro" indeed. My definition of
"macro"evolution is actually very "micro".
> but cannot explain
> *macro*evolution, which is defined as a gap big enough that it cannot be
> crossed in one step: "a cat giving birth to a dog" or differences between
> very distantly related organisms, such as "amoeba to man".
LOL - Not at all. The macro-evolution limiting boundary that I would
draw need not look at such large morphologic differences as you note
here, but on much much smaller differences in functional complexity -
such as the difference between single protein functions that those
functions that require multiple proteins all working together
simultaneously. This is the "cat-dog difference" I'm talking about.
> In Sean's
> argument this is the gap between some random sequence of DNA and his
> teleologically determined final sequence. Again the assumption is that no
> intermediate states can have any selective value or that the gap cannot be
> crossed in the amount of time available to experiment. And, of course, it
> is true that sometimes a gap cannot be crossed or crossed in the time
> available.
Again, what if these gaps turn existing functions into islands that
are surrounded in all directions by neutral sequences? No
teleological sequence target is needed, only target levels are needed.
Hitting any target within a particular level of functional complexity
is what I am talking about - not any one target in particular.
> I agree entirely in one sense. Evolution cannot cross every possible gap
> *directly* aiming for some teleological set goal (the terminal functionality
> of Sean's arbitrary choice).
Can evolution cross the gap between one *level* of function and the
next higher *level* of function. That is the question. We are not
talking specific targets here. Examples of specific targets being
missed are used to demonstrate the relative rarity of such targets as
complexity increases, but this is really not the main point or
challenge. The challenge is to hit ANY target within such a level of
increasing complexity (i.e., the level of multi-protein functions).
> In fact, evolution, because of the mechanism
> by which natural selection works, cannot proceed toward teleological goals
> at all. Evolution's selection mechanism can only focus on reachable local
> goals. If no bacteria in a particular environment can utilize lactose, then
> no bacteria will use it and there is no selective advantage to any bacteria
> on this basis.
The fact is though, they could utilize the lactose if they only had
only little relatively simple lactase protein. They would gain an
advantage in this environment if they were able to evolve the lactase
function just as these same bacteria would quickly evolve the
antibiotic function in sublethal levels of many different antibiotics.
> If no bacteria in a particular environment can use nylon or
> some other plastic polymer (and there are man-made plastic polymers that
> could potentially be useful carbon sources but which are not used precisely
> because no current bacteria can cleave a particular chemical bond), then no
> bacteria has a selective advantage on that basis.
Basically, what you are saying is that if evolution is impossible due
to neutral gaps, then evolution will not occur. Well duh! That is
what I've been saying all along.
> When or if a bacteria
> produces a variant able to cleave, say, the bond in polyvinyl chloride and
> also deal adequately with the chlorine atoms, it will certainly have a
> selective advantage over bacteria that cannot do this in certain
> environments (those that contain significant amounts of polyvinyl polymers).
In other words, if evolution can occur, then evolution will occur.
Well duh again!
> There is no guarantee that such a variant will occur anytime soon. There is
> also no guarantee that it won't happen.
LOL - No guarantee and no testable predictions either. It's nice to
believe in a non-falsifiable position - isn't it? "It could happen
even if I have no clue how or when or where." You can always fall
back on that one in order to maintain your unshakable faith in the
powers of Darwinian evolution. Please . . . Even though there are no
"guarantees" as you say, there certainly is very good evidence to
support reasonable estimates about how long it would take on average
given all known information about a given genome, population, mutation
rates, reproduction rates, and current environment. At least I can
make a testable prediction based on this information. You can't even
make a stab in the dark prediction, because as soon as your prediction
for some sort of reasonable time frame fails, you can say, "Oh well, I
guess evolution must have happened a different way."
> But, of course, the key word in all this is *directly*. Evolution, properly
> understood, does not often produce things *directly* from some random
> starting sequence to some final teleological functionality under the "need"
> for such functionality. In fact, it cannot do so (although Lamarck -- and
> Sean -- would disagree).
I don't know about Lamarck, but I never did say that the proposed
process of evolution was teleological. What evolution does claim to
be able to do is to produce vastly different functions of increasing
*levels* of complexity if given enough time and competition in a
non-lethal environment. I disagree with the suggested *levels* of
functional complexity that evolution is supposed to be able to
achieve. As I see it, the evidence suggests that only the very
simplest of functions can be evolved in the limited time frame
suggested by the theory of evolution (i.e., only 4 or 5 billion
years).
> Instead, there must usually be some intermediate
> utility, but not *necessarily*, nor for any long or involved sequence of
> changes (which we will define as more than 7-9 events, since it is quite
> clear, from chloroquine resistance, that such gaps can be rather easily
> crossed in human time-frames), *usually*, via intermediates with the
> teleological end functional utility.
Yeah yeah yeah . . . yadda yadda yadda. You keep saying this over and
over and over again. But simply saying it over and over and over
again doesn't make it true. Where is your evidence? You go on and on
discussing how things are supposed to work. I get it already! I
understand how evolution is supposed to work! Where is your evidence!
Stop making these blanket statements of how things must have happened
and start backing these statements up with something!
> So what we are really arguing about are two different views of the
> biochemical nature of how 'functions' arise in organisms. In Sean's view,
> evolution can indeed account for the existence of those 'functions' which
> can be reached by no more than a few steps in the normal way that biologists
> describe. But his claim is basically that such steps are exceedingly rare
> and irrelevant.
Not all such steps to new function are rare. Some are quite common.
But this commonality rapidly decreases as one move up the ladder of
functional complexity until functions of higher and higher complexity
get extremely rare indeed.
> His argument is that most 'new' functions in organisms
> involve multiple changes through a wasteland of *no utility at all* until
> the final moment when it all falls into place and we have selection for the
> final teleological function.
Not entirely true. You are misstating my position. My position is
not so much concerned with quantity as it is with the quality of the
evolved functions. Most new functions of a very low level of
functional complexity are separated by a very small "wasteland."
However, this wasteland grows dramatically with just a few steps up
the ladder of functional complexity until it becomes true that "most
new functions" at such higher levels of complexity "involve multiple
changes through a wasteland of no utility at all until the final
moment when it all falls into place and we have selection for . . . "
something, anything, of benefit at that level of functional
complexity.
> Given this view, he cannot see how 'new'
> functions can arise by selection, since it would require direct teleological
> selection for that final function from an essentially unrelated sequence
> without any affinity for or relationship to the final sequence.
Again, you misrepresent my position as requiring teleological
demonstrations, which I do not require - as detailed above.
> That is, he is using his (what I regard as a strawman) idea of how 'new'
> functions arise in order to then argue that they cannot arise that way.
How would you say that new functions of increasing complexity arise?
Now, after you make your paper statements again, as you have done
before, you need to be able to back your descriptions of how this
process occurs with some testable evidence or repeatable demonstration
of some kind. If you cannot do this, you certainly can believe
whatever you want, but I don't see how you can hope to call your
belief scientific.
> And
> then use the fact that they cannot arise that way to claim that "goddidit"
> is a better explanation. One must always keep this attempted switcheroo,
> the attempted focusing on (asserted but unsupported) claims that the failure
> of natural selection to work under all and any conditions to produce a
> teleologic end point somehow obviates the fact that natural selection does
> work to produce new function when the clearly described requisite conditions
> *are* present.
And what would these "clearly described requisite conditions" be?
This is the whole issue. You say that these conditions are possible
and that given these conditions, that evolution proceeds just fine.
Well then, if these conditions are so clear, you must be able to
describe what they are. What are they? I've been waiting a long time
for someone to stop just saying that they are there and actually
demonstrate them with some evidence. It is easy to simply SAY that
something is "clear" . . .
> *If* it were the case that evolution by selection has to produce new (but
> currently existing) functions in living organisms by a process that requires
> crossing large sweeps of selective neutrality for *any* function or that
> only the teleological function is important in selection, and *if* the
> sequences that make up the proteins of life *commonly* had to pass through
> vast wastelands of functionlessness (not just for the end function, but also
> for any intermediate function that differs from the end function) to reach
> the desired teleological end, then it would indeed be nearly impossible for
> these functions to exist via known evolutionary mechanisms.
Certainly true. This is my whole point. . .
> But this view of how organisms work also implies that currently living
> organisms should exhibit certain predictable features:
This should be interesting . . .
> 1) If what Sean claims is true, *most* proteins in organisms should be
> structurally *isolated* wrt their sequences from all other proteins in an
> organism. This is because, if each of these majority of protein functions
> (in Sean's vision of biology) had to be created essentially from scratch
> through multiple functionless steps rather than via a few steps from closely
> related already existing proteins, there should be little evidence of
> sequence similarity between proteins that perform different functions.
You make the mistake of arguing that the existence of similarities
prove common descent with modification of the entire organism. There
are many designed things that use similar or even identical parts in
very different systems of function. The demonstration of similarities,
even common similarities, of parts within different systems of
function does not explain the differences that do exist. For example,
all proteins use the same identical amino acids. Does this fact, in
and of itself, mean that all proteins must have descended from a
common ancestor? Just because all of the words in this thread us all
the same letters or "parts" does not mean that this thread arose or
even could have arisen via the mindless processes of Darwinian style
evolution. If life were designed, as I think it was, by some
intelligent mind, who is to say that this intelligence could not have
used the same or similar parts for the performance of different
functions?
You see, the theory of ID is not ruled out by appealing to
similarities nor is the idea of common descent ruled in by appealing
to similarities. The determination of ID vs. evolution can only be
determined based on the differences. Can the differences be explained
by mindless naturalistic processes? If they can be explained by such
processes, then ID cannot be supported. However, if mindless
processes are limited to such an extent that certain differences
cannot be explained except by comparison to or correlation with other
intelligently designed creations, then ID is the only reasonable
conclusion.
Another thing, phylogenetic trees that demonstrate differences between
such functional proteins as cytochrome c sequences in various
creatures, cannot necessarily be used to demonstrate or estimate
evolutionary relationships. The reason for this is because if the
differences were truly neutral then they would become scrambled very
rapidly. The only way that the differences in cytochrome c in
bacteria and fruit flies and fish and bats and horses and humans etc.,
is if the differences were actually functional differences that were
maintained by natural selection over the course of many generations.
Such functional differences cannot then be used to estimate orders of
divergence over variations in functional needs in particular life
forms and environments. For further discussion of this point see:
http://naturalselection.0catch.com/Files/geneticphylogeny.html
> OTOH, if most protein functions in organisms arose via duplications and
> divergence from proteins that serve related functions, one would expect to
> be able to see, often, and especially for recently evolved new functions,
> sequence evidence that indicates that the 'new' enzyme or function came from
> a structurally related precursor. That is, proteins should exist in
> families.
Also, if similar internal functions were required by different systems
of function, with only slight variations on functional needs or
requirements, we would also expect to have such clustering of protein
"families". Such clustering could just as easily be explained on the
basis of function requirement, and not necessarily on evolutionary
relationship. Again, just because ever protein uses the same 20 amino
acids does not in itself give evidence of common ancestry of all of
these different proteins. In the same way, just because a particular
protein has similarities or is even identical to another protein
elsewhere in another system of function does not mean that these two
proteins must have arisen via a common evolutionary ancestor. I use
the same exact words in many different sentences all the time. This
does not mean that these words evolved outside of ID. Very different
cars also use very similar parts. This does not mean that these parts
evolved via mindless processes from the same ancestor part. And, even
if they did, this does not mean that the different cars evolved via
mindless processes. Just because some simple parts can be shown to
evolve into other simple parts does not mean that an extrapolation to
include all parts and all functions in such an evolutionary process is
warranted or reasonable.
> So here we have a genetic 'test' of Sean's vision of what is
> required for 'new' function (crossing large gaps) and what my vision of how
> 'new' functions arise (by modification of related enzymes).
This is hardly a test to separate my position from yours since both of
our positions propose that such "families" of similar proteins are to
be expected. There is absolutely no reason for you to propose that if
my idea of limiting gaps were a true problem that we would not see
such protein families. Upon what is this suggestion based? What
makes you think this would be a requirement or even likely? - assuming
of course the "correctness" of my position?
> I would expect
> that many genes would be found in gene families.
So would I if live were actually the result of ID. It is called,
"conservation of design." Why redesign the wheel for each new
function that you want to create? It is only reasonable to use what
works, with slight modifications, to do similar things as a part of
different functions. Each of the 20 different amino acids still does
the same job in the various different proteins that are formed. Brand
new amino acids are not needed to perform very different functions.
The same is true for larger systems of function. Brand new protein
sequences are not needed to give rise to many different larger systems
of function.
> I would expect that genes
> like the globins of hemoglobin should share similar sites for introns with
> each other and with myoglobin.
So would I. If I were the designer, I wouldn't think of making a
completely different protein sequence to do a similar job just because
it is in a different location or part of a different system of
function. That would be illogical. These two different proteins do a
similar job in different larger systems of function. Why then
wouldn't one expect for them to be similar in structure and underlying
code?
> I would expect that many 'novel' genes would
> appear to be 'chimeric' (due to fusion of different protein domains, of
> which there is a limited number) events rather than via 'construction from
> completely random sequences'.
Likewise, if I were the designer, why would I think to make many
different independent proteins or genetic sequences in widely spaced
areas of the genome if the needed collective function were isolated to
a small area? Why not just combine the sequences into one and make a
single protein with multiple functions or "domains"? I have a
pocketknife like that. It has multiple functional tools all stuck
together in one place - very handy.
> I would expect enzymes and other proteins to
> have secondary activities and to bind to other proteins, sometimes without
> that interaction or secondary activity having biological meaning in the
> current environmental setting.
So would I. Many secondary activities can be realized by my car that
were not intended or which do not have beneficial meaning in my
current environment.
> I would expect this evidence to be clearer
> for 'recently' evolved proteins than for the most ancient proteins.
Certainly I would agree, unless there was an ancient function
(designed or evolved) that was maintained the entire time by natural
selection.
> 2) I would expect, if Sean's vision of how evolution works -- changes are
> due to specific genes that have to have many, multiple changes to produce a
> new phenotypic effect -- that humans and chimps would have certain genetic
> sequences that code for proteins that are dramatically different from each
> other.
Not if humans and chimps were independently designed by the same
designer or if the same common ancestor was very similar to both.
> I would expect that different dog breeds, likewise, should have
> certain genes that are dramatically different from each other and from other
> canids by many, many, sequence changes.
I wouldn't expect this at all since most of the differences between
various breeds of dogs are based on the Mendelian variation potential
of a fairly static gene pool. Certain phenotypic differences, such as
the very short legs of some breeds, are of course the result of new
mutations that affect pre-existing alleles in a new way.
Certainly some traits in certain breeds of dogs are the result of
novel mutations. However, the vast majority of the most significant
phenotypic differences are not the result of such mutations at all.
As expected, the ones that are the result of mutation are usually
achieved with just one or two point mutations. Lets use the "dwarf"
cats for example. Achondroplasia dwarfism is characterized by
abnormal body proportions. I'm not sure about cats, but achondroplasia
in humans can be caused by a single point mutation in a number of
different locations. For example, a point mutation, Gly380Arg, in the
transmembrane domain of fibroblast growth factor receptor 3 (FGFR3)
leads to achondroplasia in humans. The achondroplasia mutation G380R
uncouples ligand-mediated receptor activation from down-regulation at
a site where the levels and kinetics of FGFR3 signals are crucial for
chondrocyte maturation and bone formation. In other words, this
mutation destroyed the ability to down-regulate the G380R receptor
protein. Because of this, the receptor lost its ability to be turned
off and so it stays on all the time. This leads to defective
chondrocyte maturation and bone formation . . . resulting in the
achondroplasia phenotype.
So you see, again, these "new" traits in "new" dog or cat or human
"breeds or races" are not really all that special.
> These involve, after all, large
> phenotypic changes and current differences that occurred relatively rapidly
> even in the standard time chronology. If these differences are not due to
> 'new' functions that have to cross large seas of inutility, perhaps, just
> perhaps, Sean's model of evolution, which implies just such events as being
> frequently necessary, is not an accurate description of how evolution works.
Again, most of these "large" phenotypic changes can be explained with
the use of the potential of genetic recombination of pre-existing
options within a fairly static gene pool of options. Very dramatic
phenotypic changes are made possible in this manner, starting with
just two dogs or cats or whatever. As described above, the new
allelic traits that do evolve into the gene pool are not really all
that special (no more spectacular than the de novo evolution of
antibiotic resistance).
The problem here is, using genetic recombination alone, you cannot get
a cat to evolve into a dog. New functions are needed. How are these
new functions gained? Some very simple functions are no problem, but
this is not the issue. We are talking about functions of increasing
complexity.
Dr. Walter Veith, zoologist, former evolutionist, and senior professor
at the University of the Western Cape, says, "By selecting from the
built-in natural variation of the gene pool, various breeds of dogs
and domestic cattle were produced. Great changes in physiology and
morphology are involved, and evolution is here certainly excluded."
Darwin had no idea since he was not capable of understanding the
genetics involved, so he can be excused for assuming some sort of
evolutionary process here. However, for us in this modern age of
increased enlightenment we can no longer use Darwin's finch beaks or
other minor variations within a "kind" as examples of evolution in
action. Why? Because in none of these examples has anything that is
actually genetically new or unique evolved!
http://naturalselection.0catch.com/Files/methinksitislikeaweasel.html
http://www.amazingdiscoveries.org/evolution.html
> Perhaps, just perhaps, much evolution does not, in fact, involve the
> invention of new proteins at all.
Oh really? So where did new proteins come from? Oh, I know, the
sequential changes were so small along the evolutionary path that no
one could say at any point that a "new" protein had evolved from the
one before. Now of course, all these intermediate proteins have been
lost so we have the appearance of "new" proteins. What a great story!
Any evidence?
> This would be a genetic test of the
> expectation that protein sequence changes crossing large seas of inutility
> are a necessary requirement for most evolutionary change.
Again, quantity vs. quality. We are not talking "most", we are
talking "type". How does your "most" explain the existence of the
"type" of functions that I am talking about? These functions of
increasing complexity do exist. How did they evolve?
> Needless to say, I cannot think of a single gene in humans that is so
> different from the equivalent in chimps (or is not present in one or the
> other species at all) that it cannot be recognized rather easily as an
> simple allelic difference largely commensurate with the amount of time since
> divergence and even, for the most part, ignoring selection completely. [It
> is not that selection didn't happen and wasn't important, only that the
> amount of change and difference due to selection is minor compared to the
> amount of change due to drift.]
Ah . . . The differences between humans and chimps debate. Really, I
don't have much of a problem with humans and chimps sharing a common
ancestor. I don't think that we did, but it wouldn't bother me IF we
did. We have just recently sequenced the entire human genome, but we
don't really know much about what it says or how it works. In the
light of the fact that humans and chimps cannot produce viable much
less fertile offspring, I would hold off on making any definite
conclusions of common ancestry. However, even though I think it
unlikely that humans and chimps shared a common evolutionary ancestor,
I do not believe that there is enough knowledge concerning the
differences between our species to completely rule out this idea. In
any case, even though we don't know enough about the differences
between us and chimps to make any definite conclusions about specific
evolutionary or ID scenarios, we do know a lot more about the workings
of other genomes, such as E. coli. The evidence here for the limits
of evolution are more clearly delineated.
For further discussion of this topic see:
http://naturalselection.0catch.com/Files/donkeyshorsesmules.html
> Taken to a larger scale, it is noteworthy that significant numbers of genes
> are held in common by large groupings of organisms, at least as members of
> families of genes. That is, the 'invention' of novel genes and gene
> functions is indeed relatively rare.
Could this rarity of novel evolution of increasing complexity be due
to neutral gaps?
> The duplication and divergence of
> pre-existing genes is relatively common.
Again, this has never been observed in real time. You are only able
to ASSUME that gene duplication and divergence is relatively common if
you take your theory of evolution as an a priori assumption of truth.
Is it logical to argue that something is true based upon the assumed
truth of what the position in question? Isn't this called "circular
reasoning"?
> The selection of chimeric genes is
> relatively common. The retention of structure while changing function is
> relatively common. Overlapping function and redundancy is relatively
> common.
Again, you assume what you are trying to defend here. The positive
selection of chimeric genes is not observed all that "commonly" in
real life. It is assumed to be common based only on evolutionary
assumptions.
> In short, living organisms do not look like creatures which contain
> functions that had to cross large gaps of inutility.
Yes they do. You only deal with those functions and sequences that
are already very similar but you carefully avoid the gaps between
those sequences and functions that are not very similar. Even the
similar sequences that you can detail as parts of different systems of
function cannot be said to have arisen via gene duplication and
selective divergence. If a gene duplicates and is not immediately
selectable as advantageous, natural selection will select to get rid
of that gene since it costs energy to maintain non-beneficial genetic
real estate. Gene duplication really explains very little.
> They look like
> organisms that have considerable similarity wrt the proteins and functions
> they perform.
Not at all. Vast differences in structure and function exist within
creatures as simple as single celled bacteria. How are these
differences explained? You tend to dwell on similarities, most of
which you cannot explain or which do not help your position out much,
and completely ignore the major differences that do exist and that
never evolve in real time.
> 3) I would expect, if Sean is right, complex multi-protein systems to show
> no evidence of subsystem utility nor the ability to be generated in a
> step-wise fashion, either ontologically or phylogenetically.
First off, you cannot or at least have not shown that such systems can
be "generated in a step-wise fashion". This sort of demonstration has
simply never been done. Also, if a multi-amino acid protein shows
evidence of subsystem utility, why wouldn't a multi-protein system
show evidence of subsystem utility? Again, it is conservation of
design.
> OTOH, if Sean
> is wrong, I would expect an ontological process that would indicate that the
> final 'teleological in hindsight' product was actually composed of amplified
> recursive systems or composed of subsystems that are related to functions
> that the subsystem can have independently of the teleological 'end function'
> that Sean posits. That is, my claim is that the solution that nature uses
> for the three-body problem is to produce two two-body events.
This is a fine theory, but where is your evidence? I'm saying that
any collection of items, parts, or systems can be categorized
according to shared similarities, but this does not necessarily mean
common descent or any sort of actual relationship. Certainly I would
expect that if the evolutionary scenario where true that such
intermediate steps would be quite evident in hindsight. However, just
because something can be categorized along some sort of continuum does
not mean that this continuum is by necessity an evolutionary
relationship or any other sort of particular relationship. There must
be other evidence and some sort of detailed mechanism. Also, arguing
from morphology is always easier than arguing from code or genetics
since what seems like a short step morphologically can be quite a leap
genetically.
> When I look at systems like the clotting system of vertebrates, I see a
> system of repeated and self-recursive cascades using proteins that are
> clearly related to each other. It is quite easy to see how such a system
> can evolve in a step-wise fashion with functional utility at each step.
First off, this is a cascading system. All the parts are not working
together at the same time here. Even so, it is an extremely complex
system that cannot be easily explained by appealing to the
similarities of SOME of the parts involved. Many of the parts are
very different. Not all of them are serine proteases. Also, it is
good to note that no one has ever demonstrated even one of the
proposed steps in the evolution of the clotting cascade.
> In
> the case of the bacterial flagella, where Sean sees huge gaps of complete
> non-function, I see subsytems and even ontologically immature systems that
> perform a different function that the end system still performs (the
> bacterial flagella is *still* a protein-export device in addition to being a
> motility device. The motor subsystem is also used in many other parts of
> the cell independently of its use in the flagella. That is, the flagella
> problem is not a case of all-or-nothing utility, focused solely on the
> motility function as the only possible utility. There is actual *evidence*
> that sub-parts of the flagella have functional utility beyond that of being
> a motility device. There is actual *evidence* that certain subsytems are
> independently constructed (with independent utility) and only later come
> together via protein-protein interaction to produce the motility function.
> Sean merely asserts that the flagella is necessarily an all-or-nothing event
> that must come together by sheer randomness.
This is an outright lie. You have read my discussions with Ian
Musgrave about this very topic so I am sure that you know my position
quite well. You know then that I never asserted that the flegellar
system of function is "necessarily an all-or-nothing event that must
come together by sheer randomness." I do clearly recognize that the
flagellar system of motility is made up of parts that do in fact have
other functions within many different types of bacteria. This is not
the issue. Obviously many parts have many different functions within
living things. The problem is that these various parts, that could in
fact be arranged to perform many different joint functions, such as
bacterial motility, simply do not know how to self-assemble themselves
properly. Even if all the required parts for a functional flagellum
are being made within a given cell, this does not mean that the
flagellum will self-assemble. The order of the parts is also
important. Putting them together in the proper sequences is vital to
the motility function. The fact is that all the parts are not present
in any given cell and even if they were, they would not necessarily
self-assemble to produce the motility function. Also, it should be
noted yet again that not even one of the proposed evolutionary steps
in flagellar evolution have been demonstrated to be crossed in real
time, much less any complete motility system.
> He does that because such a
> strawman version of how evolution works is necessary for his claim that
> evolution must work randomly through large completly useless gaps to be
> accepted in the face of evidence that the genetic structure of organisms
> belies his strawman model.
You continually misrepresent my position in order to make it appear
like I am building a straw man. It is actually you who are building
the straw man to represent my position because you know that I am
actually correct in my understanding and description of the Darwinian
process. It is a lot easier for you to attack me if you misrepresent
me. Next time, please, try and be more honest in your representations
of my views. I know you understand what they are, so I find it
difficult to think that you just don't understand what you are doing.
I think you are deliberately trying to confuse the issue here.
> I could go on, but why bother. It is clear that Sean is asserting a
> strawman version both of what is required of evolutionary change and of what
> actually exists in nature in order to claim that, because his strawman
> vision cannot occur by known evolutionary mechanisms, that evolution is
> false. That is what creationists do.
Nice try. You build a straw man to represent my position and then you
claim that I built it. Good one . . . but pretty much transparent for
anyone familiar with my posts.
Sean
catshark
wrote:
>> >After working for some time in the usual 'call and response' mode on Sean's
>> >reply to me, I became frustrated at the repetitiveness and length, so I
>> >decided to try to get at what I see as the crux of the argument more
>> >directly.
>>
>> POTM. Seconds?
>
>He's already got another post in the same thread nominated that covers
>a lot of the same ground. Maybe we could merge them as a POTM?
Hot damn! I even seconded the previous nomination 11 days ago. Well, at
least I might use this to begin to chart the course of my Alzheimer's . . .
OTOH, it *still* is a post worthy of consideration . . .
Dunno
> Howard Hershey <hers...@indiana.edu> wrote in message news:<BB1DD0E6.C783%hers...@indiana.edu>...
>
>> This is a summary of the argument that Sean is making, as I see it, and why
>> I think the core features of his argument is based on a strawman version of
>> nature, which includes a whopping dose of teleological thinking (the
>> assumption that a current function was an intended and necessary end goal),
>
> As I have said multiple times before, I do not make this
> "teleological" assumption at all. Certainly the theory of evolution
> proposes that no particular goal was necessary or intended by the
> mindless workings of nature. That is precisely the problem. If
> everything is a potential, then natural changes tend toward homogeny.
> Obviously it is impossible to detail the entirety of the potential
> sequence space for a living organism in its environment.
If you aim to show descendants of horses wont have feathers or
exoskeletons I would tend to agree.
> However, I
> think that it is possible to show that the neutral sequences within
> this potential space grow exponentially with increasing functional
> complexity.
Ok, I'll bite. Show.
> What does this mean? It means that on average, the
> neutral gaps between various functions of increasing complexity start
> to grow exponentially. This means that existing functions start to
> become surrounded, on EVERY side, by neutral sequences. At this
> point, it really doesn't matter which way evolution tries to go, it
> will be blocked by the surrounding ocean of neutral sequences.
Now if you could narrow this down a bit more.
Which functional differences between organisms in a monophyletic
clade would you consider simple, and complex?
> No
> teleological goal is needed since all goals, except for the most
> simple, are blocked.
>
What functional differences between say goats, sheep and
elk are simple, and which complex? They are ruminants, have
hair, produce milk, have nearly identical teeth, cloven
hooves, all the same organs, same bones, etc. Which one
has a function that the others cannot possibly achieve
because of this vast surrounding ocean of neutral sequences?
Snip remainder of this monster on the assumption it is a rerun.
Forgive if it is not.
Lilith
Von: You are correct. Robust, reconstructable trees made from many
proteins (in this case within a species) should not appear UNLESS the
sequences themselves shared a common ancestor -- a commonly-shared
earlier "protein state". While some of the gene families are separated
by vast gulfs of evolutionary time, there are many gene families and
superfamilies which have obvious sequence similarity, enough that
they're graced by the title 'paralogs'.
Howard Hershey said it well, too, at :
Deanne
Adam Marczyk
>
> > Also, even the logic functions that were evolved
> > were dependent upon the proper selective environment being set up
> > ahead of time by ID. What if there was a gap between one type of logic
> > function and another type of logic function, such as between the NAND
> > and the EQU functions that required the evolution of either the AND or
> > the OR, or the NOR, XOR or NOT functions first? What if these
> > functions were not recognized by a particular environment as being
> > beneficial? Then, there would be a neutral gap created by that
> > environment between the NAND and EQU functions. What are the odds
> > that the "proper" environment that recognized at least one of these
> > other functions as beneficial, would come around at the right time?
> > You see, the random walk not only includes random changes in code, but
> > also in environment. Without an intelligent mind directing changes in
> > environment in just the proper way, the organic synthesis of many
> > different compounds that are made in chemistry laboratories would not
> > work. The order of the environmental changes is just as important as
> > the order of the molecules in the "evolution" of new functions or
> > compounds.
[...]
> Isn't that just fascinating? When the intermediate stepping stone
> functions were removed, the neutral gap that was created successfully
> blocked the evolution of the EQU function. Now, isn't this what I've
> been saying all along?
If you seriously believe that this constitutes a problem for
evolution, you are, to put it charitably, suffering from some very
severe misunderstandings about the way evolution is supposed to work.
Of course that happened; that is exactly what we should expect. If the
fitness landscape for a given adaptation is completely flat except for
one single vertical peak - if there are no hills to be climbed - then
of *course* an evolutionary algorithm will, on average, do no better
than blind search. Evolution absolutely requires that there exist a
gradually increasing selective advantage between the beginning point
of no function and the end point of full functionality.
I believe I understand what your problem is now. You're still dragging
around a misconceived teleological view of how evolution is supposed
to work. You begin with no function, end with a complex,
multi-component function, and then you survey the path between them
and conclude that it is fantastically improbable that a random walk
could deliver a population from the beginning to the end. This is the
same as my above example of a fitness landscape that has one single
peak and is otherwise completely flat.
But what you've failed to recognize is that we are *not* dealing with
a simple random walk through all possible configurations from
beginning to end. The way evolution works is this: You begin with no
function, then explore the immediate vicinity until you come up with a
slight, selectable improvement. You do not then continue your random
walk from the beginning; you explore *from that point onward*, until
you get to the next selectable improvement, then explore from there,
and so on. That is the definition of an evolutionary algorithm, and it
is far more efficient than a random walk for the precise reason that
the points of intermediate selectable functionality allow most of the
dead-end possibilities to be cut out. Your hypothetical sea of neutral
mutations may well exist - but evolution has a path of stepping stones
by which to cross it.
(In an article on genetic algorithms I'm working on, I point out that
one such algorithm designed an improved jet turbine that outperformed
configurations selected by a human engineer and by an expert system;
the algorithm took approximately two days of computation on a desktop
workstation to navigate a solution space containing more than 10^387
possibilities. Again, the point is precisely that a gradually
increasing fitness slope allows evolutionary algorithms to exclude a
vast majority of the inviable solutions.)
Of course, had the evolving population taken a slightly different
branching at any of these stepping stones, the end result could have
been the same function, but operating in a completely different way
and reached through a completely different path - or even a completely
different function, but one that performs some *other* valuable
utility to the organism. I alluded to this before when I pointed out
that you have no way of knowing how many different functional
configurations are out there. Your argument in a nutshell is this: You
are, without justification, concluding that the job an organism is
doing is the only one it could do; you are then, similarly without
justification, concluding that the particular configuration we see is
the only one that could do that job; you then go on to calculate what
the odds are of striking across it by pure chance, and when you find
them to be formidable, you conclude that evolution has been falsified.
This is a gross misrepresentation of the way the evolutionary process
actually works, and until you get past it, you will make little
progress.
Chris Ho-Stuart
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03062...@posting.google.com>...
>> Isn't that just fascinating? When the intermediate stepping stone
>> functions were removed, the neutral gap that was created successfully
>> blocked the evolution of the EQU function. Now, isn't this what I've
>> been saying all along?
>
> If you seriously believe that this constitutes a problem for
> evolution, you are, to put it charitably, suffering from some very
> severe misunderstandings about the way evolution is supposed to work.
> Of course that happened; that is exactly what we should expect. If the
> fitness landscape for a given adaptation is completely flat except for
> one single vertical peak - if there are no hills to be climbed - then
> of *course* an evolutionary algorithm will, on average, do no better
> than blind search. Evolution absolutely requires that there exist a
> gradually increasing selective advantage between the beginning point
> of no function and the end point of full functionality.
Evolution does not require gradually increasing selective advantage.
There are many problems with that notion.
(1) Change involving loss of fitness can occur, and become fixed,
by drift. This is still evolution.
(2) There is no consistent fitness landscape. The fitness landscape
often changes faster than phenotypes.
(3) Mathematical models for population genetics have shown the
"Punctuated equilibrium" effect arising in a fitness landscape
with many "peaks". Some random factors may take a population
"down" a peak; selection will tend to direct further change back
to a peak again, but it might be a different peak.
"Punctuated Equilibrium Is Now Old hat"
by Roger Lewin
in Science vol 231, pp 672-673 (14 Feb 1986)
Apart from this, I basically agree.
Cheers -- Chris
Adam Marczyk
And your point is what, exactly? Is this not a suitable analogy of how
sexual reproduction actually works in living organisms? Crossover *is*
the main source of variation in such organisms; point mutations are
certainly not the reason why you're not an exact clone of your
parents.
[...]
> So, there are several interesting constraints to this experiment. For
> one thing, the ultimate functional goal was predetermined as with
> Dawkins's "Methinks it is like a weasel" computer evolution
> experiment.
That is not a severe constraint when no predetermined route to
reaching that goal was specified. Evolution, of course, is not a
teleological process, but if you take a population of
fast-reproducing, evolving organisms (such as bacteria, or malaria
parasites) and then expose them generation over generation to a toxin
designed to kill them, it's all but guaranteed that some sort of
resistance will show up eventually.
[...]
> Like the evolution of
> antibiotic resistance this function was easy to evolve given the
> restraints used by the scientists because the neutral gaps were set up
> to be so small.
Sorry? Living things use only 20 amino acids. This experiment had 26
different possible instructions. By what reasoning do you conclude
that the number of non-selectable changes is larger in living things
than it was in this experiment?
> Also, the success of the experiment was dependent on
> pre-established lines of code that were set up to work together to
> solve logical problems of a specific type. I suggest however that
> this particular setup would not be able to evolve other types of
> functions, like the ability to open the CD-drive or the ability to
> cause the monitor to blink off and on.
You should feel free to suggest that, though what your reasoning
behind that conclusion is, I confess I have no idea. Because the
program succeeded at one task, you conclude that it would fail at a
different task?
> The gaps involved would
> require different types of starting code sequences that could not be
> gained by the type of code recombination used in this experiment.
> Point mutations would be required and very large gaps in function
> would need to be crossed before these other functions could be
> realized.
I'm noticing that you have a persistent tendency to retreat to the
gaps (as in "God of the gaps", not the neutral kind you refer to) when
faced with evidence of complex selectable functions evolving in
experimental conditions.
> In short, I think that this experiment was a setup for success of a
> very limited goal and does not explain the evolution of uniquely
> functional systems beyond the most elementary of levels. It did end
> up producing some "unexpected" solutions to the problem, but that is
> only to be expected. There might be many different ways to interfere
> with an antibiotic's interaction with a target sequence that might not
> be otherwise expected. However, the functional ratio is what is
> important here and clearly it is very high as compared to the neutral
> sequences (40% beneficial mutations vs. 10% detrimental and only 43%
> neutral - Please! Give me a break!). Success was guaranteed by the
> way the intelligent designers set up their experiment.
You have just made an elementary blunder. The reason that the final
organisms had such a high ratio of beneficial mutations is *precisely
because* they were the most successful line. They are winners and the
descendants of winners. At each step, the starting organisms mutated
(through crossover); the unsuccessful offspring of these changes were
discarded, while the successful ones became the seeds of a new
generation. The numbers you quote most assuredly do not represent the
overall ratio of mutations for every single organism in the
experiment.
[...]
> In any case, it is a great example that demonstrates very nicely the
> limits that neutral gaps put on the theory of evolution. This only
> strengthens my theory.
I have discussed your misunderstandings in this regard in another
post.
> The resistance to both mefloquine and chloroquine is achieved via the
> blocking or interference of the pre-established interaction of these
> drugs with specific target proteins. Again, my prediction that such
> interferences are relatively easy to achieve holds up in these cases
> as well. No new protein or enzyme is evolved in these cases.
How is the mutated PfCRT not a "new" protein? Are you now resorting to
elementary creationist mischaracterizations of evolution which demand
that completely new sequences with no relation to anything that came
before them simply spring full-formed out of the genetic ether in one
step?
> The only
> thing that happens is a disruption of a specific interaction that was
> pre-established (It is just a different way of breaking Humpty Dumpty,
> but still relatively easy to do.).
Ah, now we change tactics and switch to, "But it's not really a *real*
new function" (with the inevitable implication that a "real" new
function is simply something the questioner knows when he sees it).
But in fact, chloroquine resistance has been considerably more
difficult to achieve than most drug resistance. I quote from the
Nature article:
"Chloroquine acts by binding to heme molecules released from the
hemoglobin that is digested by malaria parasites as they grow within
their host red blood cells. This binding interferes with the process
by which heme is normally incorporated into inert crystals and
detoxified, thereby essentially poisoning the parasite. Because heme
is not a parasite-encoded molecule that can mutate under drug
pressure, malaria parasites have had to solve the difficult problem of
chloroquine's toxicity by evolving a mechanism either to prevent
drug-heme interactions or to control the damage from these complexes."
> As with de novo antibiotic
> resistance (via disruption of the antibiotic-target interaction), such
> disruptions are relatively easy to achieve and are almost always based
> on one or two point mutations, or at most a handful of such mutations
> as is potentially the case with chloroquine resistance. Also,
> chloroquine resistance has been very difficult to reproduce in the lab
> and has taken a bit longer to evolve in the wild than mefloquine
> resistance. However, the difference in complexity between these two
> drugs is really is rather negligible considering that the mutations
> responsible for this difference in complexity can be counted on one
> hand. This evidence fits very well with my predictions for the
> required time needed to evolve this very low level of complexity that
> is based on interfering with a pre-established interaction - not the
> creation of anything new as far as an enzyme or some other such
> protein of higher complexity.
I believe your predictions are missing something. You said that with a
population size of one billion, CQ resistance should take about 5
years to evolve. But it has taken 20, and the malaria vector is a
single-celled parasite. By comparison, the number of cells in a single
human body is easily greater than one trillion, a difference of a
factor of one thousand. Considering that malaria is endemic across
most tropical regions of the world and causes millions of deaths per
year, I would think we're talking about a population size enormously
greater than a billion, and therefore resistance should have popped up
almost instantly. Care to explain?
[...]
> > Absolutely not. Nothing about evolution ever said that the first cell was
> > required to survive; in fact it's been proposed that life arose more than
> > once on the early Earth, but all but one (obviously) of those attempts
> > ended in extinction. And the first living things were, so to speak,
> > building themselves from the ground up. This is a significant difference
> > from an experiment where a well-established species that had grown
> > dependent on a particular source of energy suddenly had the rug pulled out
> > from under it.
>
> I am saying that as long as the organism is able to survive and
> reproduce (i.e., it lives in a non-lethal environment), the theory of
> evolution does in fact propose that many new functions of incredible
> diversity and complexity WILL evolve - given enough time. I'm not
> talking lethal environments here. I'm talking about any organism that
> can reproduce over an extended period of time.
That is also false. Evolution does not demand that new functions
arise. In fact, an evolutionary trend can often be toward greater
simplicity, stripping out as much as possible, to make reproduction as
fast as possible. After all, what matters in the end, for evolution's
purposes, is how many offspring you leave behind. A very simple
organism with a hellaciously fast reproductive rate may well
outcompete more complex organisms with fancy defenses that consume
energy that could otherwise have been spent on having more babies. (Do
you think we humans are at the top of the heap because we have
fripperies like eukaryotic cells and specialized organs? Betcha you
leave a lot fewer offspring than any given bacterium living in your
digestive tract.)
> > > The very first organism was quite limited indeed and it
> > > was in a limited environment as well. And yet, it supposedly evolved
> > > many new functions in relatively short order.
> >
> > Who says? As far as we know the first eukaryotic cell, incorporating many
> > new cell structures that do not exist in prokaryotes, did not arise until
> > only about 1.5 billion years ago.
>
> In comparison to trillions upon trillions of years to cross even a
> small gap of neutral function, a few billion years is nothing.
You'll have to make up your mind. First you say a small gap of neutral
function like that crossed for CQ resistance should take 5-10 years;
now you say it takes trillions of years. Or does the definition of
"small" vary depending on where in your post you use it?
> > > Really, given enough
> > > time, any self-replicating organism should be able to morph itself
> > > into just about any phenotypic shape and function imaginable, given
> > > the proper environment. As long as the new environment is not
> > > immediately lethal, and time is allowed for extended growth and
> > > competition for survival, then yes, the theory of evolution suggests
> > > strongly that new functions will evolve that allow some organisms to
> > > survive better than their peers in this new environment.
> >
> > New functions will evolve, yes. No one ever said (except perhaps
> > creationists pushing strawmen) that organisms should be able to evolve into
> > "just about any" imaginable configuration.
>
> Yes, this is exactly what is suggested by the theory of evolution.
You seem determined to cling to your misconceptions, so I won't
belabor the point.
[...]
> > >> There is no
> > >> guarantee that *all* organisms will be able to evolve to *any*
> > >> arbitrarily stated conditions.
> > >
> > > Certainly not. However, what you are basically saying is that the
> > > theory of evolution cannot be tested. Experiments cannot be set in a
> > > falsifiable way because if they fail, all you have to say is, "Well, I
> > > guess we just didn't use the right environment or the right organisms
> > > to demonstrate evolution this time." This always leaves you an out.
> >
> > Yes, and? This is *life* we're dealing with here. It's a complex, messy,
> > chance-dependent, sloppy, unpredictable thing.
>
> How do you know if you cannot think of a falsifiable test for your
> genetic theory?
How do I know what? Are you arguing that life is not complex,
chance-dependent, or unpredictable?
> > A mutation that could make
> > all the difference could be caused by the unintended presence of a
> > mutagenic pollutant in extremely small quantities impinging on a cell; it
> > could be caused by a cosmic ray arriving from the explosive death of a star
> > halfway across the cosmos billions of years ago; it could be caused by a
> > background quantum fluctuation, the most intrinsically unpredictable
> > phenomenon in existence. This isn't like simple Newtonian physics where you
> > can throw a ball up into the air, and given the same initial conditions, it
> > will always land in exactly the same spot.
>
> Newtonian physics can be tested in a falsifiable way. Because of
> this, it falls under the power of the scientific method. If you
> cannot test your theory in a falsifiable manner, then really, you have
> entered the realm of blind faith.
There are many different ways to test and falsify evolution. What you
have proposed, because of the intrinsically unpredictable nature of
evolution, is not one of them.
> > > Without the theory of evolution being falsifiable in such genetic
> > > experiments, you can always believe in it no matter what the
> > > experiments say. Tell me, what genetic experiments could be done that
> > > would falsify the theory of evolution? Really, unless you can detail
> > > such an experimental result that would counter the theory of
> > > evolution, your theory really is not scientific. You must have a
> > > genetic test that is testable and falsifiable. What is it?
> >
> > Easy: You could test to see if organisms ever undergo beneficial genetic
> > changes that can be inherited by their descendants.
>
> This is not enough. There is evidence that neutral gaps grow
> exponentially with increasing complexity.
Only in your flawed view of how the process works. I have explained my
"stepping stones" model and corrected your teleological
misunderstandings in another post.
[...]
> I'm not demanding that evolution follow a specific path. What I am
> demanding is a demonstration of the evolution of a specific level of
> complexity, not a specific type of function.
Before you can be shown that, you'll have to give a rigorous and
objective definition of complexity, such that anyone could apply your
metric to tell whether complexity has increased. (Otherwise it simply
becomes another pointless exercise in "I know it when I see it". Your
metric is likely to be tested against the following real-world
conditions: whether a dog is more complex than a cat; whether a finch
with a long, thin beak is more complex than a finch with a shorter,
thicker beak; whether a human being is more complex than a
chimpanzee.) Once you've done that, then you can move on to explaining
what level of increased complexity would be required to establish
evolution in your mind.
[...]
> > I would now like to turn that argument back on you. If such
> > a pathway could be experimentally shown to exist for, say, the bacterial
> > flagellum, would you abandon your skepticism, or would you simply move to
> > the next gap over and conclude, "Yes, well, I guess that could have evolved
> > after all, but *this* one you'll never explain, for sure!" What would you
> > accept as falsifying your argument?
>
> Yes, according to my understanding the evolution of any type of
> bacterial motility requires multiple proteins all working together at
> the same time. According to my calculations such evolution would
> require the crossing of neutral gaps via a random walk that would take
> a very large population of bacteria trillions of years to cross. So,
> yes, if you could demonstrate the evolution of such a multi-protein
> system of function I would abandon my skepticism.
I'm going to have to ask you to clarify yourself a bit. What do you
mean by "demonstrate"? How could such a demonstration be achieved?
> How about you?
> What would it take for you to abandon your skepticism?
You could show, for example, that a single, consistent nested
hierarchy relating various groups of living things could not be built
up by doing genetic comparisons. (I here exclude single-celled
organisms for whom horizontal gene transfer is known to be a major
method of reproduction.)
Pokemoto
>Path:
>lobby!ngtf-m01.news.aol.com!ngpeer.news.aol.com!newsstand.cit.cornell.edu
!lnsnews.lns.cornell.edu!newsfeed.stanford.edu!darwin.ediacara.org!there.i
s.no.cabal
>From: seanpi...@naturalselection.0catch.com (Sean Pitman)
>Newsgroups: talk.origins
>Date: Wed, 25 Jun 2003 19:20:26 +0000 (UTC)
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>
>
>Howard Hershey <hers...@indiana.edu> wrote in message
>news:<BB1DD0E6.C783%hers...@indiana.edu>...
>
>> This is a summary of the argument that Sean is making, as I see it, and why
>> I think the core features of his argument is based on a strawman version of
>> nature, which includes a whopping dose of teleological thinking (the
>> assumption that a current function was an intended and necessary end goal),
>
>As I have said multiple times before, I do not make this
>"teleological" assumption at all. Certainly the theory of evolution
>proposes that no particular goal was necessary or intended by the
>mindless workings of nature. That is precisely the problem.
This statement is false on your part. What do you think your broken window
analogy is? From the second sentence it looks like you've been convinced you
that your broken window analogy is bogus, but the first sentence is false due
to your repeated use of this analogy. In fact you never retracted it or
admitted that it was bogus, until now.
If
>everything is a potential, then natural changes tend toward homogeny.
>Obviously it is impossible to detail the entirety of the potential
>sequence space for a living organism in its environment. However, I
>think that it is possible to show that the neutral sequences within
>this potential space grow exponentially with increasing functional
>complexity. What does this mean? It means that on average, the
>neutral gaps between various functions of increasing complexity start
>to grow exponentially.
This does not follow. You know this. The number of neutral mutations is
dependent on the sequences available and the selectivity of the environment
that the organism is living in. You can't claim exponential growth of neutrals
because you do not know the conditions that you are talking about. Your Hall
example does one thing very clearly. It tells you that your neutral gaps do
not have to exist. Hall got his trick to work in three different species and
other researchers got it to work too. Where is your evidence for exponential
increase? Your only evidence indicates that neutral gaps can exist, but they
don't have to. Demonstrate that there were too many neutral gaps in the
evolution of the flagellum, and that they were needed in groups large enough to
matter between selective events.
This is your problem and why your argument is bogus. Untestable assertions are
worthless. They may give you some goal or point of view, but you can't use
them for anything useful until you can find some means of testing them to tell
you if you are wrong or right.
Rest of the same old same old snipped:
Ron Okimoto
John Harshman
Dunno wrote:
> On Wed, 25 Jun 2003 19:20:26 +0000 (UTC), Sean Pitman wrote:
>
>>Howard Hershey <hers...@indiana.edu> wrote in message news:<BB1DD0E6.C783%hers...@indiana.edu>...
[snip]
> Now if you could narrow this down a bit more.
>
> Which functional differences between organisms in a monophyletic
> clade would you consider simple, and complex?
I would like to interrupt this thread for a bit of curmudgeonly
pedantry. It's always been grating to me when somebody says
"monophyletic clade". It's redundant. All clades are monophyletic;
that's the definition of a clade. I find this happening more and more.
At the just finished SSE/SSB meeting, it was all I could do to restrain
myself when several speakers used this term. Fortunately, restraint is
unnecessary on TO.
And to answer your question, simple functions are those that are
observed (in real time) to arise by evolution; complex functions are
those that are not. The list of simple functions will expand over time,
and the list of complex ones contract accordingly, as new experiments
are done.
Adam Marczyk
news:3efa...@news.qut.edu.au...
> Adam Marczyk <ebon...@hotmail.com> wrote:
>> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in
>> message news:<80d0c26f.03062...@posting.google.com>...
> [snip]
>>> Isn't that just fascinating? When the intermediate stepping stone
>>> functions were removed, the neutral gap that was created successfully
>>> blocked the evolution of the EQU function. Now, isn't this what I've
>>> been saying all along?
>>
>> If you seriously believe that this constitutes a problem for
>> evolution, you are, to put it charitably, suffering from some very
>> severe misunderstandings about the way evolution is supposed to work.
>> Of course that happened; that is exactly what we should expect. If the
>> fitness landscape for a given adaptation is completely flat except for
>> one single vertical peak - if there are no hills to be climbed - then
>> of *course* an evolutionary algorithm will, on average, do no better
>> than blind search. Evolution absolutely requires that there exist a
>> gradually increasing selective advantage between the beginning point
>> of no function and the end point of full functionality.
>
> Evolution does not require gradually increasing selective advantage.
> There are many problems with that notion.
>
> (1) Change involving loss of fitness can occur, and become fixed,
> by drift. This is still evolution.
You're right, I misspoke myself. Not every change in a process of evolving
some feature has to be strictly beneficial - I even mentioned this myself
earlier on, when I pointed out that the final and most complex logic
function in this experiment, EQU, was not achieved until an earlier
mutation knocked out AND, the second-most-complex function. Though this
change was deleterious at first, it proved to be necessary in the end for
achieving EQU. What I should have said is that evolution requires there be
a fitness landscape of smooth hills that can be climbed, not a flat plain
punctuated by an occasional vertical spike.
> (2) There is no consistent fitness landscape. The fitness landscape
> often changes faster than phenotypes.
This is true, but I don't consider it an important qualification. There
must still be a selective advantage to every trait that is ultimately
selected for, even if the landscape changes during the process of evolving
that trait.
> (3) Mathematical models for population genetics have shown the
> "Punctuated equilibrium" effect arising in a fitness landscape
> with many "peaks". Some random factors may take a population
> "down" a peak; selection will tend to direct further change back
> to a peak again, but it might be a different peak.
> "Punctuated Equilibrium Is Now Old hat"
> by Roger Lewin
> in Science vol 231, pp 672-673 (14 Feb 1986)
I think this is the same thing we agreed on in the first point.
> Apart from this, I basically agree.
--
Sean Pitman
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03062...@posting.google.com>...
> > The "breeding" or evolving a "bit string" in the Alife program is not
> > based on "randomly swapping bits" but on the "Standard Genetic
> > Algorithm." In this algorithm, a crossover point is selected
> > randomly, then the left portion of one string is "mated" or
> > "recombined" with the right portion of another string (and vice
> > versa). This allows chunks of circuitry, which work well together, to
> > have some chance of not being disrupted. Some random flipping of
> > single bits is also used, but this is relatively rare.
>
> And your point is what, exactly? Is this not a suitable analogy of how
> sexual reproduction actually works in living organisms? Crossover *is*
> the main source of variation in such organisms; point mutations are
> certainly not the reason why you're not an exact clone of your
> parents.
Genetic recombination does not evolve anything new as far as the gene
pool of pre-established options is concerned. Gregor Mendel, not
Darwin, first discovered this method of change which explains much of
what Darwin used as a basis for his theory of evolution. Although
natural selection is most certainly involved in this process, there
are definite limits to the changes that can be accomplished with
Mendelian genetics/genetic recombination alone. In order for the gene
pool itself to evolve, mutations are required to make new alleles.
Certainly new alleles can be made and added to the gene pool, but the
new functions that result are always of a very low complexity. As one
moves up the ladder of complexity, fewer and fewer example of the
evolution of novel functions can be found. I believe that the reason
for this phenomenon is that functions that are part of increasing
levels of complexity are surrounded by an exponentially expanding
ocean of neutral sequences in sequence space.
> > So, there are several interesting constraints to this experiment. For
> > one thing, the ultimate functional goal was predetermined as with
> > Dawkins's "Methinks it is like a weasel" computer evolution
> > experiment.
>
> That is not a severe constraint when no predetermined route to
> reaching that goal was specified.
Actually, the route was established as well, before the experiment
took place. The stepping stones were set in place. Certainly the
order of which stepping stones would be used first, second, third
etc., was not predetermined, but the fact remains that the minimum
number of steps required was certainly estimated to within a very
close proximity. The designers knew that the EQU function was only 16
steps away from the original function (and there was an original
function). They also knew that each of the other functions that they
defined as "beneficial" were also only one or two steps away, in an
ascending sequence, from the steps that came before. Given this set
up, even I would predict that this sort of "evolution" would proceed
very quickly, as it did in such an intelligently designed environment.
However, when the environment was changed so that some of the
intermediate stepping stones were removed, the EQU function did not
evolve at all in the time allotted.
This is my entire position. If the stepping stones can be
demonstrated to be as close together in real life as they were in this
set-up experiment, then I will become an evolutionist. Currently
though, it seems most evident to me that as one moves up the ladder of
complexity the intermediate sequences of beneficial function become
very rare very quickly. Just as quickly evolution looses the power to
make much of anything at that level of complexity or higher.
> Evolution, of course, is not a
> teleological process, but if you take a population of
> fast-reproducing, evolving organisms (such as bacteria, or malaria
> parasites) and then expose them generation over generation to a toxin
> designed to kill them, it's all but guaranteed that some sort of
> resistance will show up eventually.
This is because most if not all "toxins" are very specific in their
interaction with their target sequences. There is a relatively high
ratio of target sequences that do not bind as well to the toxins as
compared with those sequences that do. Because of this high
specificity of the toxin-target interaction, many different mutations
can interfere or break-up this interaction and produce resistance.
However, take a different environment where survivability is just as
crucial or dependent upon the evolution of the proper function, and
rapidly generating organisms will still not evolve the needed
function. The lactase function is a fine example of this problem.
You can culture many different types of bacteria in an environment
that starts out with glucose or other types of sugars and then
gradually shifts to lactose as the only sugar. No matter how
prolonged this shift is and no matter how vital for ultimate survival
it is to evolve the lactase function. These particular types of
bacteria will not be able to evolve the lactase function before it is
required. However, take these same bacteria and put them into an
environment where the level of a particular antibiotic (any antibiotic
really) is gradually increased, and they will rapidly evolve
resistance to it. Don't you find this phenomenon most interesting?
Increasing the level of functional complexity dramatically reduces the
odds that evolution will occur. It also dramatically increases the
average time required for evolution to occur. I find this fact most
interesting.
> > Like the evolution of
> > antibiotic resistance this function was easy to evolve given the
> > restraints used by the scientists because the neutral gaps were set up
> > to be so small.
>
> Sorry? Living things use only 20 amino acids. This experiment had 26
> different possible instructions. By what reasoning do you conclude
> that the number of non-selectable changes is larger in living things
> than it was in this experiment?
It depends upon the function in question. There are 26 letters of the
alphabet. Using these 26-letters as part of the English language
system or environment, it is very easy to evolve a list of functional
3-letter words since they have been arbitrarily defined in such as way
that the neutral gaps between each new function are relatively small.
However, it becomes much much harder to evolve a new 6-letter word,
much less a new "beneficial" sentence using random mutation and
function based selection. The same thing is true of the 20 amino
acids in living things. Some functions based on these 20 amino acids
are extremely simple to evolve (i.e., antibiotic resistance). Other
functions are not so easy to evolve (de novo enzyme evolution like
lactase or nylonase), and other functions have never been observed to
evolve (multi-protein functions like bacterial motility).
> > Also, the success of the experiment was dependent on
> > pre-established lines of code that were set up to work together to
> > solve logical problems of a specific type. I suggest however that
> > this particular setup would not be able to evolve other types of
> > functions, like the ability to open the CD-drive or the ability to
> > cause the monitor to blink off and on.
>
> You should feel free to suggest that, though what your reasoning
> behind that conclusion is, I confess I have no idea. Because the
> program succeeded at one task, you conclude that it would fail at a
> different task?
It succeeded at one task because the intermediate steps were designed
ahead of time so that that particular task could evolve
(teleologically I might add). However, I am betting you that no
matter how long you run this program, it will not come up with the
ability to perform other relatively simple tasks like telling the
CD-player in the computer to open or telling the monitor to flip the
screen off and on. The "evolution" of this experiment was very
limited just as the degree of changes that are dependent upon genetic
recombination of static gene pool options is very limited in the
degree and type of changes that can be produced.
> > The gaps involved would
> > require different types of starting code sequences that could not be
> > gained by the type of code recombination used in this experiment.
> > Point mutations would be required and very large gaps in function
> > would need to be crossed before these other functions could be
> > realized.
>
> I'm noticing that you have a persistent tendency to retreat to the
> gaps (as in "God of the gaps", not the neutral kind you refer to) when
> faced with evidence of complex selectable functions evolving in
> experimental conditions.
What are you talking about here? I'm saying nothing different here
than my usual argument of neutral gaps. The scientists in this
particular case used their powers of intelligent design to design the
proper environment and to define all the intermediate steps that would
be required to "evolve" a particular predetermined function of higher
complexity. What I am saying is that without such predetermined
design that no such program capable of reproduction and random
mutation/recombination, would be able to evolve new function of higher
complexity or even similar complexity all by itself - despite the
potential for such evolution (i.e., It is possible to produce a code
that would in fact open the CD-player or cause the monitor screen to
flip off and on).
> > In short, I think that this experiment was a setup for success of a
> > very limited goal and does not explain the evolution of uniquely
> > functional systems beyond the most elementary of levels. It did end
> > up producing some "unexpected" solutions to the problem, but that is
> > only to be expected. There might be many different ways to interfere
> > with an antibiotic's interaction with a target sequence that might not
> > be otherwise expected. However, the functional ratio is what is
> > important here and clearly it is very high as compared to the neutral
> > sequences (40% beneficial mutations vs. 10% detrimental and only 43%
> > neutral - Please! Give me a break!). Success was guaranteed by the
> > way the intelligent designers set up their experiment.
>
> You have just made an elementary blunder. The reason that the final
> organisms had such a high ratio of beneficial mutations is *precisely
> because* they were the most successful line. They are winners and the
> descendants of winners. At each step, the starting organisms mutated
> (through crossover); the unsuccessful offspring of these changes were
> discarded, while the successful ones became the seeds of a new
> generation. The numbers you quote most assuredly do not represent the
> overall ratio of mutations for every single organism in the
> experiment.
Actually, you are technically correct here. I should have explained
my point more clearly than I did here. The overall ratio of
beneficial mutations as compared with neutral and detrimental
mutations was predetermined to be very high indeed. As I recall, the
potential sequence space was calculated to be around 10e70. The
minimum number of neutral steps to the EQU function was predetermined
to be around 16. However, several intermediate sequences were
inserted in a pre-determined way so that the average neutral step
between each of these intermediate functions was only one or two steps
wide. This produced a ratio of beneficial mutations vs. neutral or
detrimental mutations that was no less than 1 in 1,500 or so. Because
of this extraordinarily high rate of beneficial mutations, the
relatively small steady state population was able to cross this
intelligently designed bridge in ~15,000 generations. Out of 50 of
the starting genomes, a whopping 23 of them were able to evolve the
most complex EQU function in only 15,000 generations?! AMAZING!!!!!
Not! This extremely fast rate of evolution across a minimum gap of 16
steps was made possible by a closely spaces series of stepping stones
that we simple do not find so commonly in the real natural world
between functions beyond the most simple.
snip
> > The resistance to both mefloquine and chloroquine is achieved via the
> > blocking or interference of the pre-established interaction of these
> > drugs with specific target proteins. Again, my prediction that such
> > interferences are relatively easy to achieve holds up in these cases
> > as well. No new protein or enzyme is evolved in these cases.
>
> How is the mutated PfCRT not a "new" protein? Are you now resorting to
> elementary creationist mischaracterizations of evolution which demand
> that completely new sequences with no relation to anything that came
> before them simply spring full-formed out of the genetic ether in one
> step?
No. Such "new" sequences are in fact "new" proteins that do have "new"
functions. As such, they are examples of real evolution in action.
However, one must also consider the type of function that has been
evolved and the level of complexity that was required to achieve this
*type* of function. The fact of the matter is, it is a whole lot
easier to come up with a new sequence whose only function is to
disrupt a pre-established function. Many different sequences would be
capable of doing this. So, the odds are very high that at least one
of these relatively common sequences will just happen to come along
via random drift. The problem, of course, is that many function
cannot be achieved via the blocking of other pre-established functions
(i.e., lactase, nylonase, bacterial motility etc).
> > The only
> > thing that happens is a disruption of a specific interaction that was
> > pre-established (It is just a different way of breaking Humpty Dumpty,
> > but still relatively easy to do.).
>
> Ah, now we change tactics and switch to, "But it's not really a *real*
> new function" (with the inevitable implication that a "real" new
> function is simply something the questioner knows when he sees it).
Not at all. I think that you are deliberately trying to miss the
point here. Certainly this is a new function and it certainly did
evolve, as I have said very clearly many times before in this thread
and to you directly. Again though, the level of function here is
about as low on the ladder of complexity that you can get. It is
basically the bottom rung, the bottom of the barrel - so to speak. My
point is that such functions are easy to evolve because the ratio of
sequences that can achieve such functions is extremely high compared
to the total number of potential sequences in sequence space.
However, this ratio drops dramatically with each step up the ladder of
complexity.
> But in fact, chloroquine resistance has been considerably more
> difficult to achieve than most drug resistance. I quote from the
> Nature article:
>
> "Chloroquine acts by binding to heme molecules released from the
> hemoglobin that is digested by malaria parasites as they grow within
> their host red blood cells. This binding interferes with the process
> by which heme is normally incorporated into inert crystals and
> detoxified, thereby essentially poisoning the parasite. Because heme
> is not a parasite-encoded molecule that can mutate under drug
> pressure, malaria parasites have had to solve the difficult problem of
> chloroquine's toxicity by evolving a mechanism either to prevent
> drug-heme interactions or to control the damage from these complexes."
The reason why Chloroquine resistance took a bit longer is not because
it is based on some other mechanism that the interference of a
pre-established function or interaction (as described in great detail
already). It is based on such interfering mutations and as such, the
ratio of such potential sequences is relatively high. The only
difference here is that the ratio is not as high as it is in other
types of situations involving antibiotic or drug resistance. It seems
as though there is actually a neutral gap here that is at least 2
mutations wide, but probably more on the order of 3 or 4 mutations
wide. The crossing of such a gap would take a given population a lot
longer to achieve, but it could still be done in a reasonable amount
of time given the population number that exist in nature.
> > As with de novo antibiotic
> > resistance (via disruption of the antibiotic-target interaction), such
> > disruptions are relatively easy to achieve and are almost always based
> > on one or two point mutations, or at most a handful of such mutations
> > as is potentially the case with chloroquine resistance. Also,
> > chloroquine resistance has been very difficult to reproduce in the lab
> > and has taken a bit longer to evolve in the wild than mefloquine
> > resistance. However, the difference in complexity between these two
> > drugs is really is rather negligible considering that the mutations
> > responsible for this difference in complexity can be counted on one
> > hand. This evidence fits very well with my predictions for the
> > required time needed to evolve this very low level of complexity that
> > is based on interfering with a pre-established interaction - not the
> > creation of anything new as far as an enzyme or some other such
> > protein of higher complexity.
>
> I believe your predictions are missing something. You said that with a
> population size of one billion, CQ resistance should take about 5
> years to evolve. But it has taken 20, and the malaria vector is a
> single-celled parasite.
My calculations where not intended to be more than rough examples to
show that neutral gaps would limit a labs ability to demonstrate
evolution where it might be more easily done in nature owing to higher
populations sizes, which in fact is true here. Also, in my
calculations, I used generous numbers of mutation rates and generation
times. The mutation rates and generation times are most likely a bit
lower than I estimated in my calculations. But, the point still
remains.
> By comparison, the number of cells in a single
> human body is easily greater than one trillion, a difference of a
> factor of one thousand. Considering that malaria is endemic across
> most tropical regions of the world and causes millions of deaths per
> year, I would think we're talking about a population size enormously
> greater than a billion, and therefore resistance should have popped up
> almost instantly. Care to explain?
Aside from the comments made above about this, once a particular
function does evolve somewhere in one organism, it takes time for that
organism to produce offspring and spread its newly evolve code around.
Depending on the selective advantage gained and a host of other
factors, such as the availability of vectors and intermediate life
cycle times, it might take a bit longer to make such a new code wide
spread. In any case, what happened is far more consistent with my
theory that neutral gaps do in fact limit evolution and that even a
few neutral steps dramatically curtail the evolution of even vital
"teleological" functions. I mean really, it took at least 10 years
for even a detectable level of chloroquine resistance to be realized!
It doesn't take nearly this long for a significant level of penicillin
resistance to be realized. The obvious reason for this can be found
in the number of neutral gaps involved. Imagine if the required
random walk was wider than 3 or 4 steps. What would have happened
then? If it took 10 years to cross a gap of only 3 or 4 steps, how
many years would it take to cross a neutral gap of 6 or 7 steps? - And
by the way, not all the mutations in the evolution of chloroquine
resistance were neutral. Only 2 are required and most of the other 5
or 6 common mutations are thought to be sequentially beneficial. So,
doubling the neutral gap would cause the average time involved to
increase by a factor of 2. Instead of 20 years, 400 years would be
required. A gap of 10 or 12 would require 160,000 years and a gap of
only 20 would require 25,600,000,000 years.
> > I am saying that as long as the organism is able to survive and
> > reproduce (i.e., it lives in a non-lethal environment), the theory of
> > evolution does in fact propose that many new functions of incredible
> > diversity and complexity WILL evolve - given enough time. I'm not
> > talking lethal environments here. I'm talking about any organism that
> > can reproduce over an extended period of time.
>
> That is also false. Evolution does not demand that new functions
> arise.
It certainly strongly suggests this. On your own website you also
suggest this when you said that, ". . . perhaps four or five billion
years ago, the first primitive bacteria came into existence. They
gained energy through photosynthesis, they grew, they lived, they
evolved. Ever more complex forms began to arise." Certainly then, the
only requirements for such complex forms to arise is a non-lethal
environment and increasing competition for resources. What else is
there that produces such an increase in complexity according to the
theory of evolution? Changing environments? No necessarily true as
long as the resources currently available lend themselves to novel
uses for those who are able to evolve in such a way as to use these
already present resources in a more effective way in a competitive
environment.
> In fact, an evolutionary trend can often be toward greater
> simplicity, stripping out as much as possible, to make reproduction as
> fast as possible.
Yes, this is true. But, it is far easier to destroy than to create.
It is far easier to remove, hinder or destroy pre-established
functions that it is to create them. Although examples of loss of
information are still examples of evolution via mutation and natural
selection, this is a far lower level of complexity than the turning
the process around and explaining how increasing levels of complexity
could possibly have been evolved via mindless natural processes.
Again, it easy to explain how Humpty Dumpty got broken, but it is
another thing to figure out how to put him back together again or to
explain how he got put together to begin with.
> After all, what matters in the end, for evolution's
> purposes, is how many offspring you leave behind.
This is not all that matters for the evolution vs. ID debate however.
As an evolutionist, you must be able to present a mechanism whereby a
process that is only interested in how many offspring are left behind
or how well these offspring survive can actually give rise to
functions of increasing complexity that we do actually see around us
today. Obviously, if evolution did happen, it didn't just sit on its
butt or stick content itself with removing pre-exiting functions. New
functions must have been made along with new functions of dramatically
increasing complexity. The most simple of such functions are easy to
explain since the ratios for such functions are so high. However,
start trying to explain the arrival of higher levels of complexity.
That is what you have yet to do although you certainly have done a
whole lot of hand waving and smoke blowing. As Ron Okimoto likes to
say, the mere fact that you say something is true over and over again
is nothing until you can show some evidence to support yourself.
Where is this evidence? What falsifiable test can you put forward to
support your position?
> A very simple
> organism with a hellaciously fast reproductive rate may well
> outcompete more complex organisms with fancy defenses that consume
> energy that could otherwise have been spent on having more babies. (Do
> you think we humans are at the top of the heap because we have
> fripperies like eukaryotic cells and specialized organs? Betcha you
> leave a lot fewer offspring than any given bacterium living in your
> digestive tract.)
And your point is?
> > > > The very first organism was quite limited indeed and it
> > > > was in a limited environment as well. And yet, it supposedly evolved
> > > > many new functions in relatively short order.
> > >
> > > Who says? As far as we know the first eukaryotic cell, incorporating many
> > > new cell structures that do not exist in prokaryotes, did not arise until
> > > only about 1.5 billion years ago.
> >
> > In comparison to trillions upon trillions of years to cross even a
> > small gap of neutral function, a few billion years is nothing.
>
> You'll have to make up your mind. First you say a small gap of neutral
> function like that crossed for CQ resistance should take 5-10 years;
> now you say it takes trillions of years. Or does the definition of
> "small" vary depending on where in your post you use it?
LOL - Are you trying to be dense? Obviously I am not saying that a
"small gap of neutral function" should take trillions of years to
cross. Obviously I'm saying that with just a little bit larger of a
gap, say around 25 or 30 DNA mutations, that trillions of years would
be required for even huge populations like that of plasmodium
parasites. What I am saying is that larger gaps do exist and that
these gaps grow exponentially with each step up the ladder of
complexity that you climb.
snip
> > Newtonian physics can be tested in a falsifiable way. Because of
> > this, it falls under the power of the scientific method. If you
> > cannot test your theory in a falsifiable manner, then really, you have
> > entered the realm of blind faith.
>
> There are many different ways to test and falsify evolution. What you
> have proposed, because of the intrinsically unpredictable nature of
> evolution, is not one of them.
Again, saying that something is true is far different from putting
yourself out there and actually giving an example of a genetic test
that would in fact be capable of falsifying evolution. What exactly
are these many different tests that could falsify evolution?
snip
> > > > You must have a
> > > > genetic test that is testable and falsifiable. What is it?
> > >
> > > Easy: You could test to see if organisms ever undergo beneficial genetic
> > > changes that can be inherited by their descendants.
> >
> > This is not enough. There is evidence that neutral gaps grow
> > exponentially with increasing complexity.
>
> Only in your flawed view of how the process works. I have explained my
> "stepping stones" model and corrected your teleological
> misunderstandings in another post.
You have yet to demonstrate that they stepping-stones exist in the
number needed for evolution to work. This is the basis for this
entire debate here. You hypothesize that these
stepping-stones/evolutionary paths exist, but where is your testable
evidence? Can this blanket statement of yours be falsifiably tested?
> > I'm not demanding that evolution follow a specific path. What I am
> > demanding is a demonstration of the evolution of a specific level of
> > complexity, not a specific type of function.
>
> Before you can be shown that, you'll have to give a rigorous and
> objective definition of complexity, such that anyone could apply your
> metric to tell whether complexity has increased. (Otherwise it simply
> becomes another pointless exercise in "I know it when I see it".
I have given an easily demonstratable definition of increasing
complexity. It starts off with very low levels of complexity, such as
those functions that arise via that interference of pre-established
functions (i.e., many forms of antibiotic resistance). It them moves
up the ladder to those functions that require the simultaneous
interaction of multiple amino acids in single protein systems of
function (i.e., enzymes such as lactase, nylonase, penicillinase
etc.). It them moves up the ladder to a level where multiple proteins
are required all working together simultaneously to produce a given
function (i.e., bacterial motility, phagocytosis, muscle contraction
etc.) And, the ladder moves on from here. So far, evolution seems
have the power to commonly produce functions of the lowest level of
complexity mentioned here. Occasionally, evolution will actually come
up with some function from the level of complexity of enzymes and
other single protein functions that are not based on interfering with
a preformed function. However, no new function of a higher level than
this has ever been demonstrated or even adequately theorized (in a
falsifiable manner) as to how even a relatively simple function that
requires multiple proteins could even evolve.
>Your
> metric is likely to be tested against the following real-world
> conditions: whether a dog is more complex than a cat; whether a finch
> with a long, thin beak is more complex than a finch with a shorter,
> thicker beak; whether a human being is more complex than a
> chimpanzee.) Once you've done that, then you can move on to explaining
> what level of increased complexity would be required to establish
> evolution in your mind.
I don't need cats turning into dogs or monkeys into humans to have
evolution "established" in my mind. All I need is some way to explain
the evolution of functions as simple as the most simple multi-protein
function that you can think of. Your problem is that you cannot think
of a way to test your hypothesis that such things happened in a
falsifiable manner.
> > Yes, according to my understanding the evolution of any type of
> > bacterial motility requires multiple proteins all working together at
> > the same time. According to my calculations such evolution would
> > require the crossing of neutral gaps via a random walk that would take
> > a very large population of bacteria trillions of years to cross. So,
> > yes, if you could demonstrate the evolution of such a multi-protein
> > system of function I would abandon my skepticism.
>
> I'm going to have to ask you to clarify yourself a bit. What do you
> mean by "demonstrate"?
Demonstrate - a : to prove or make clear by reasoning or evidence b :
to illustrate and explain especially with many examples
(Merriam-Webster)
> How could such a demonstration be achieved?
Take a bacterium, or any other life form, and reproduce, in real time,
the evolution of a new function that is dependent upon multiple
proteins all working together at the same time (i.e., any motility
system or other such system dependent upon the simultaneous action of
multiple-proteins). If this would take too long, then demonstrate
each of the proposed steps between theorized intermediate sequences
that would be required. Ian has suggested various potential pathways
for the evolution of such systems of motility, like the flagellar type
of motility, and yet he has failed to actually test his hypothesis or
even demonstrate the crossing of just one of his proposed intermediate
steps.
> > How about you?
> > What would it take for you to abandon your skepticism?
>
> You could show, for example, that a single, consistent nested
> hierarchy relating various groups of living things could not be built
> up by doing genetic comparisons. (I here exclude single-celled
> organisms for whom horizontal gene transfer is known to be a major
> method of reproduction.)
You are asking me to prove a negative. You are asking me to
demonstrate an absolute absence of a possibility. This cannot be done
this side of eternity. This position of yours is not a falsifiable
position. You must present something that can actually be tested in a
falsifiable manner. One test, one result, hypothesis falsified. What
test, if it were done and your predictions did not hold, would
absolutely disprove your position? For example, if you demonstrated
the evolution of a bacterial motility system, I would accept that
demonstration as an absolute disproof of my position. What genetic
test and outcome would absolutely disprove your position?
You also present something that has been done and ask me to show that
it can't be done. That is a logical impossibility, like showing that
the Empire State Building cannot be built when it is already built.
In order to have your position tested, you must predict something that
has not been done in a way that your prediction can be disproved.
Sean
P.S. Also, the finding of nested hierarchies does not necessarily
support the idea of common descent via the mindless processes of
evolution over the idea of ID based on the functional needs of
different creatures in different environments. Certainly, if these
differences in similar proteins (like cytochrome c - for example) were
not based on differences in the functional needs of different
creatures (making the differences neutral), then random mutations
would quickly destroy the nested differences that we find in different
creatures. Evolutionary "clocks" that are based on such differences
only work over the course of relatively short periods of time
(thousands and not millions of generations).
More discussion of this concept at:
http://naturalselection.0catch.com/Files/geneticphylogeny.html
Pokemoto
>Path:
elay.ihug.net!ihug.co.nz!logbridge.uoregon.edu!newsfeed.stanford.edu!darwi
n.ediacara.org!there.is.no.cabal>Date: Fri, 27 Jun 2003 18:17:15 +0000 (UTC)
snip
>
>ebon...@hotmail.com (Adam Marczyk) wrote in message
>news:<3285a60d.03062...@posting.google.com>...
>> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message
>news:<80d0c26f.03062...@posting.google.com>...
>
Snip:
>>
>> And your point is what, exactly? Is this not a suitable analogy of how
>> sexual reproduction actually works in living organisms? Crossover *is*
>> the main source of variation in such organisms; point mutations are
>> certainly not the reason why you're not an exact clone of your
>> parents.
>
>Genetic recombination does not evolve anything new as far as the gene
>pool of pre-established options is concerned.
As Sean as acknowledges in other posts this is false. When recombination puts
two mutations together in the same gene and they do something different that is
something new. The two mutations existed in the population, but they did not
exist as a unit and the new function did not exist in the population until the
recombination occurred. This is essentially the same thing as if the second
mutation occurred in the same gene as the first mutation. We also have what we
call abberant recombination because it occurs between two nonhomologous
sequences. These produce new genes making chimeric genes. This type of
recombination has been documented. Sean will have to demonstrate that what he
considers to be "new" really means anything.
Gregor Mendel, not
>Darwin, first discovered this method of change which explains much of
>what Darwin used as a basis for his theory of evolution. Although
>natural selection is most certainly involved in this process, there
>are definite limits to the changes that can be accomplished with
>Mendelian genetics/genetic recombination alone. In order for the gene
>pool itself to evolve, mutations are required to make new alleles.
We observe new mutations and new alleles all the time. In your own model of
"all variation present from the start" you have to generate many new alleles by
recombination. How can you tell your recombined new alleles from alleles that
happened due to mutation? The answer is that you can't, and you can't even
begin to generate the genetic diversity that we see in humans let alone all the
other species that have much more genetic variation than humans do. Before
you use this argument again, back it up. Sure it all could be done by
recombination if you could get two individuals to survive with all those
mutations in their genes (I'd like to see Sean demonstrate an example) and you
had enough time to recombine the starting chromosomes, but Sean only has 6000
years and recombination between two mutations in the same gene can be as rare
or rarer than the mutation rate.
>Certainly new alleles can be made and added to the gene pool, but the
>new functions that result are always of a very low complexity. As one
>moves up the ladder of complexity, fewer and fewer example of the
>evolution of novel functions can be found. I believe that the reason
>for this phenomenon is that functions that are part of increasing
>levels of complexity are surrounded by an exponentially expanding
>ocean of neutral sequences in sequence space.
>
This is bogus. Design an experiment that we can do you your lifetime to
demonstrate that you could be correct. You admit that we readily observe the
"simple" things, but how long would it take to observe the complex things and
how much would it cost in time and money. If you can design such an experiment
and want to carry it out for a few million years you can try and get someone to
do it and fund it.
Demonstrate that such limits exist in the evolution of an ape like creature
into a human. Where are these gaps and how did you determine that they exist?
These mutations occurred over a period of at least 5 million years. Where are
the impossible mutations?
Snip:
I'm not going to bother with most of the rest, and AOL can't paste the whole
piece so I'll have to quote the last bit.
[Sean ends.]
Sean
P.S. Also, the finding of nested hierarchies does not necessarily
support the idea of common descent via the mindless processes of
evolution over the idea of ID based on the functional needs of
different creatures in different environments.
[Ron]: This is an example of Sean trying to put the clothes that we have
demonstrated that our emperor is wearing on his emperor without justification.
He never gets around to telling us how the clothes fit and what they look like
on his emperor. It is really weird, on the one hand he claims that our emperor
is naked, but he wants to borrow clothes from our emperor.
[Sean continues]: Certainly, if these
differences in similar proteins (like cytochrome c - for example) were
not based on differences in the functional needs of different
creatures (making the differences neutral), then random mutations
would quickly destroy the nested differences that we find in different
creatures. Evolutionary "clocks" that are based on such differences
only work over the course of relatively short periods of time
(thousands and not millions of generations).
[Ron]: The tragedy is that these things were all worked out before Denton
wrote his first bogus book in the mid 1980's and if Sean were to read a real
science text on the subject he would realize that this argument is about as
bogus as they can possibly get.
The signal is expected to degrade because genes are finite. This is exactly
what we observe. People have spent a lot of time to tell us that once around
10% of the sites have been mutated the error of second hits at already mutated
positions becomes significant and you have to have more sequence to overcome
this error and get a reasonable answer. The laughable thing is that we observe
this degredation in the signal and it matches theory. If multiple mutations
were not happening randomly why would we observe this signal degredation? Why
is it that a gene like hemoglobin is pretty much out the window in accuracy
past around 200 million years. It is pretty accurate in estimates involving
mammals and their phylogenetic associations, but it becomes very inaccurate for
things like fish where the radiations occurred over 300 million years ago. Why
doesn't Sean's idea of similar lifestyles meaning more similar genetics not
work for the different groups of fish? Not only that but hemoglobin works just
fine for within specific groups of fish like teleosts (guppies to marliin)
because they evolved relatively recently, but predictably, not so well between
the major groups of different types of fish that evolved hundreds of millions
of years before the teleost radiation. So why would guppies have more similar
DNA to a marlin than it would to a gar or ceolacanth?
This has all be worked out and if Sean knew the data he would know that it is
all consistent with biological evolution, but not with his stop gap "me too"
models.
[Sean continues]: More discussion of this concept at:
http://naturalselection.0catch.com/Files/geneticphylogeny.html
[Ron]: Yes, go to this web site and read the first home page bull pucky about
the Emperor and no clothes. You will find the rest of the web site
demonstrates that the scientific emperor has lots of clothes on, but Pitman
doesn't like the style. He would drool over anything as good that he could
hang on his emperor, but he doesn't have anything as good. What is really
ridiculous is that he takes some of the scientific clothes and claims that they
would fit his emperor, but he never gets around to seeing if they really fit
(like the genetic similarity argument above). It is like, so what if you have
these clothes, my emperor could wear the same clothes. Pitman's problem is
that he can't demonstrate that his emperor has these clothes on, and science
observes these clothes on their emperor. Such is the dishonest creationist
mind set.
Pitman claims that honest creationist arguments exist, but he never gets around
to presenting any. He has claimed several times that such arguments exist, but
he has yet to present one that he has confirmed to be honest. Remember that
when you read his web site. Pitman acknowledges that the creationist arguments
are mostly bogus, he just hasn't determined that the ones on his web site are
bogus enough for him not to continue using them. He knows that once he checks
them out they all have problems, but his answer is to not check them out.
The real damning thing is that when pressed to present an honest creationist
argument, he has never put forward something from his own web site.
Ron Okimoto
Howard Hershey
seanpi...@naturalselection.0catch.com wrote on 6/25/03 7:20 PM:
> Howard Hershey <hers...@indiana.edu> wrote in message
> news:<BB1DD0E6.C783%hers...@indiana.edu>...
[I apologize in advance for the length of this reply.]
>
>> This is a summary of the argument that Sean is making, as I see it, and why
>> I think the core features of his argument is based on a strawman version of
>> nature, which includes a whopping dose of teleological thinking (the
>> assumption that a current function was an intended and necessary end goal),
>
> As I have said multiple times before, I do not make this
> "teleological" assumption at all.
You are simply unaware of or have not seriously considered the implications
of *any* creationist argument. Basically all creationist arguments choose
an end result that exists, such as a bacterial flagella, and assumes or
asserts that that existing function is the ultimate or end function for
which the designer constructed the current structure. This is usually
embedded in a (generally false) dichotomous explanation for how such a
"function" cannot arise via (a usually false view of) 'evolution'.
In your argument, both the teleology of the current function/structure (it
was designed for that end purpose) and the false dichotomous argument are
quite evident. Basically, you argue:
1) Some outside intelligent entity poofs it into existence directly from
nothing (or at least from an always unspecified substance). Usually the
poofing is *independent* for each organism the individual considers a
created 'kind'.
Notice that the above is *inherently* a teleological argument. The only
reason why 'flagella' exists at all is because it is *the* structure that
some entity envisioned and made for an ultimate function (motility). To
function as a motility device is not just the ultimate purpose of the
flagellar structure, to a creationist it is the sole purpose. If motility
were not the ultimate purpose of the structure, but merely a side
consequence or a modification of a structure evolved for different purposes,
but with some motility function, the case for the *necessity* of a designer
to achieve the end purpose falls apart.
Your particular false vision of evolution states:
2) The 'end or teleological purpose' stated in 1) comes from a random
sequence without *any* bacterial flagella function *at all* (or possibly
without any function at all), not by design, but by a random mutational walk
across a vast functionless (or at least not exhibiting any flagellar
function) 'neutral' wasteland. Only when all the necessary changes exist,
by chance, in the final state (with full bacterial flagellar function) does
selection exert its effect. In essence, you are saying that evolution
claims that the flagellar 'function' poofs into existence by chance alone.
Only the final 'function' can be selected for.
This also is a form of teleological argument because all the intermediate
states are proposed to be without functional utility to the organism. And
the starting point also is implied to be without functional utility -- at
least none is mentioned. The argument is ahistorical in nature, since,
according to this model the structure/function is *necessarily*, because it
had to occur by sheer improbable chance alone, the end or terminal function
-- to modify this structure to a new function would presumably require it to
re-swim the absurdly vast sea of 'neutrality' until the changes, by chance
alone, hit upon another useful function. [The creationist model, of course,
assumes that the structure/function is the end or terminal function because
it is the structure that the designer willed into existence.] The one and
only end structure/function (which is, according to your assertion, an
isolated island of function in both models), is also the function/structure
you chose (which is really merely the current structure in the correct
evolutionary model -- see below, not the end structure), is always chosen to
be the most complex and least evidenced one the creationist can think of and
is the only structure that has, or is given, a design (utile) purpose in
your arguments. Ignorance and arguments from ignorance are never very far
away.
> Certainly the theory of evolution
> proposes that no particular goal was necessary or intended by the
> mindless workings of nature.
Your falsely dichotomous choices, of course, ignore the more standard
evolutionary mechanism described in 3) below; creationist arguments almost
always rely on false dichotomy and strawman evolution.
3) The flagella arose by a pathway that integrated subsystems that arose
for, and were selected for, different functions. It also involved proteins
that had (and still have) more than one function, with the possibility of
selection emphasizing one of these at the expense of the other by minor
changes in sequence. At no point in this pathway can there be any vast
'neutral' wasteland that needs to be crossed. All the crucial intermediate
steps *must* have functional utility in their own right.
In this mechanism, some of the underlying (and unstated) assumptions in the
first two mechanisms are essentially regarded as invalid. The first is the
assumption that the *current* function is *necessary* and teleologically
ordained; that the end function you chose the only function that the
structure is capable of performing (and thus that it must have been designed
directly for that function). Evolution specifically rejects the idea of the
*current* function being an *end* function or the *goal* toward which all
the intermediate stages were striving. It is *only* the current function.
The intermediates were also, at that point in time (and often still) also
*current* functions. The second is the idea of vast 'neutral' wastelands
that must be crossed either by an intelligent poofer or by chance alone.
> That is precisely the problem. If
> everything is a potential, then natural changes tend toward homogeny.
Not every sequence meets the rather stringent demands of an evolutionary
pathway. But some do. This produces the observed facts of evolution,
namely that most evolution involves modification of existing structure to
perform new function rather than the invention of 'new' structure from
scratch to perform new function at the morphological level. At the
molecular level, the same thing is observed. Both humans and arthropods
have homeobox-binding proteins that both do the same thing at one level of
analysis (bind sequences that have homology to the canonical homeobox
sequence) but at a different level does something slightly different
(identifying thoracic segments in insect blastula versus identifying
segments of the developing vertebral column) to, at a different level
performing quite different functions (specifying the development of insect
legs versus quite different structures in mammals). In short, there is
extensive recycling of fundamental functions (binding DNA sequences) to
generate different end results. This, and the ubiquity of gene families,
indicate that organisms are constrained to evolve using structures
(including genes and parts of genes) that they already have by *modifying*
those structures. That makes evolution quite conservative at the molecular
level.
> Obviously it is impossible to detail the entirety of the potential
> sequence space for a living organism in its environment. However, I
> think that it is possible to show that the neutral sequences within
> this potential space grow exponentially with increasing functional
> complexity. What does this mean? It means that on average, the
> neutral gaps between various functions of increasing complexity start
> to grow exponentially. This means that existing functions start to
> become surrounded, on EVERY side, by neutral sequences. At this
> point, it really doesn't matter which way evolution tries to go, it
> will be blocked by the surrounding ocean of neutral sequences. No
> teleological goal is needed since all goals, except for the most
> simple, are blocked.
Actually, I would argue the opposite. As the complexity of an interacting
network of related proteins increases, changes have effects (sometimes large
and sometimes small) on other functions. Consider them ripple effects. As
more functions are already performed and encompassed within the sequence
space that already exists in an organism, with some of them being
dispensible and all of them being subject to duplication and divergence,
there is more opportunity for there to be a protein which can easily be
modified to perform a different (but often related) function.
>
> I have used this example before, but it bares repeating: Try evolving
> a sentence or paragraph, one letter at a time with each change or
> "mutation" being beneficial in a given scenario. See how far you can
> get. It is a lot harder than one might think.
That is because the meaning of proteins, unlike words, are not as completely
dependent upon every letter being perfectly correct. Written language is
clearly more brittle and subject to catastrophic failure in meaning than
protein language is (as evidenced by the fact that even proteins with less
than 30% identity in sequence can have the same functional meaning with only
minor functional differences). Analogy is fine, as long as you understand
its limitations.
> Certain changes can be
> done that might change meaning in beneficial way, but very quickly
> neutral gaps are reached no matter which direction one tries to go.
> The same thing happens with random mutations and natural selection.
> Since the genetic real estate of a given organism or population is
> limited and the environment is also limited in resources and options,
> these limits severely limit the number of potential beneficial
> sequences that could be used by a given organism. Such limits put
> significant constraints upon the evolution of new functions since new
> beneficial functions of increasing complexity become extremely rare
> relative to all the neutral and detrimental sequences.
So how many such changes are needed? Take, for example, the pathways and
changes that led to the differences between the currently existing H.
sapiens and P. troglodytes (remember that, on the human side, this is not
due to humans evolving directly from the common ancestor to H. sapiens, but
through several *transitional* or *intermediate* species). If there were
large changes in the sequences of crucial genes needed to change a common
ancestor into either human or chimp, these would be easy to find using the
tools of molecular biology. Where are they? All the difference between the
sequences of chimp and humans can be accounted for by simple mutational
events (often point mutations, but some deletions and insertions as well),
with the selectively important ones being so few in number that they are
insignificant compared to the expected number that would be expected from
neutral drift alone.
Please notice that you have not presented a shred of evidence that there are
any differences in any evolutionary sequence that evolved through the
mechanism (a completely random walk) you propose is the one required by
'evolution'.
>
> Can this be absolutely proven? No, as nothing can be absolutely
> proven this side of eternity. One has to look at the weight of
> evidence. I think that the weight of evidence is clearly in favor of
> the idea that vast oceans of neutral sequences surround very tiny
> islands of function and that these oceans grow exponentially faster
> than the relative number of islands grow as the level of functional
> complexity increases.
What evidence? You have repeatedly *asserted* that there is evidence, but
have presented exactly nothing but empty assertions. I have explicitly
pointed out that there are clear implications that should be seen in the
nature of the genomes of organisms if you take your 'islands in an ocean'
ideas seriously. Specifically, proteins should not be present in families
as a common feature. They should not share sequence (and intron placement)
with proteins that perform different, but related function. The problem is
that the evidence argues against your idea that new proteins arise like
*random* islands out of a sea. The evidence supports the idea that new
proteins performing new functions arise by modification of existing proteins
(or, more often, modification of a duplicate of an existing protein). The
evidence supports the idea that new proteins arise like the next island of a
volcanic chain of islands, that is, clearly connected with and associated
with the other islands of the chain. Of course, like real island chains,
some of the older islands are now sunk below the sea and not visible from
above.
>
> You and other evolutionists, who are actually considering this
> problem, suggest that the neutral ocean is not nearly as big as I am
> proposing. You are suggesting that there are a lot more functional
> paths between these potential islands. You do not think that one path
> in particular can be detailed, since this would be "teleological",
It would only be teleological if the intermediate states were present solely
to ensure the future occurrence of the *end* function and one assumed that
there is no difference between *end* function and *current* function. In
evolution these are not the assumptions. The evolutionary assumption is
that the intermediate states are present and selected for (or not selected
against) because they are useful to the organism (wrt reproductive success
in a particular environment) *as they are*, not because they may or may not
be converted to some other function or structure. That is, they are not
there to act as intermediates to the final structure/function. They are
there because they have independent utility. That they *can* be modified to
a new function is not a necessity. It is a fortuitous circumstance. This
is quite different from creationist teleology, in which the end function
(more accurately, the current function) is the end point the 'designer'
intended.
> but
> you believe that there is very good evidence for the existence of
> common pathways none-the-less.
No. Because, as you point out in the cases where one can clearly observe
evolution in real time, evolution works not by starting at some anonymous
random sequence, but starts instead from a protein that *has* a useful
function and *modifies* that protein so that it now has a slightly different
functionality (e.g., does not bind an inhibitor as tightly or hydrolyzes a
slightly different bond better). There is no "common pathway". There is
the pathway that that particular modification took to reach a point that
makes it selectable for a particular functionality. It is impossible to
'predict' the easiest pathway to achieve a 'modified function' unless it is
repeatable (as in some of the simpler antibiotic resistances). Even then
there may well be alternative pathways to achieve a particular functional
effect, and in any one trial, a rare chance mutational event (compared to
the more common mutational event producing resistance) may occur first and
be the one that gets chosen purely for that reason. Evolution is a
teleologically blind process.
> Of course, this is a must for your
> position. Without these supposed paths, evolution is sunk and you
> know it. Your problem is that you cannot demonstrate these paths.
Actually you have demonstrated that in certain simple cases, such pathways
do exist. And, as I have pointed out, there are consequences, reflected in
the structure of current systems that one would expect to differ if that
system arose from a stepwise process (specifically, evidence that subsystems
have independendent functionality, that subunit parts of current systems
have similarity with other proteins, etc.) that would not exist if all the
parts of a current system arose with no detectable similarity to other
components in the organism (if all the parts were isolated islands of
proteins with no similarity to other proteins).
> Your position is not falsifiable. If you set up a test to find a path
> and you do not find it, all you have to say is, "gee, I guess this
> particular path does not exist, but that doesn't mean that there isn't
> another path somewhere else." This is a fine position since it is not
> falsifiable. No test could be set up that could absolutely disprove
> this position. Since no one knows all about the potential sequence
> space for any particular organism in any particular environment, it
> would take an eternity to demonstrate a lack of all potential
> pathways. So, since your position cannot be completely disproved this
> side of eternity, you can feel safe in your faith regardless of the
> mountains of evidence that remove one path after another. As long as
> a potential for some unknown path exists, you faith can take hold of
> the unknown that holds a potential answer to save your theory.
This is a regurgitated assertion that I have explicitly disagreed with by
pointing out that congruence of nature with the expectations of theory
explicitly supports the idea that *most* evolution is by descent with
modification. And specifically, the cases with the most evidence (recently
evolved features for example) show the most evidence of having done so by
descent with modification from pre-existing structures and sequences. Only
fools and creationists argue that cases without evidence (because they are
ancient features with long histories) prove their point.
> However, since you claim to be a man of science and not of blind
> faith, and since you cannot test for all pathways, there must be some
> testable way to support your position that these pathways are common
> enough to save your theory. What evidence do you have for this
> position?
The fact that the very introns of myoglobin and all hemoglobin globins,
including the duplicated pseudogenes, are essentially identically situated
is evidence (along with sequence similarity, of course) that, given the time
available, that they are all derived from a common ancestral globin
sequence, with the alpha and beta globins diverging later than the
hemoglobin globins from myoglobin. Such unnecessary similarity would be
expected if they arose by a process of duplication and divergence. That a
less complex form of hemoglobin (with only alpha globins, in hagfish) exists
says that a process of divergence could easily be responsible for the more
modern form of hemoglobin.
There are many such examples in the structure of genes in organisms.
In terms of complex processes like clotting, the fact that each of the steps
involved utilizes a self-digesting protease of a very specific kind (related
to other proteases) is another example of how multistep processes can arise
in a stepwise fashion. That is evidence consistent with a mechanism of
generating new genes that involves duplication and divergence.
There are many examples of such regulatory chains involving kinases of
kinases, phosphatases of phosphatases, etc.
In the case of the bacterial flagella, the fact that ontologically every
step in the process of building, in a stepwise fashion, the whip structure,
involves the *function* of protein export, that the final flagella has
protein export as a secondary function, that some non-motile flagella have
protein export as a primary function, that the 'motor' is a generic feature
which is simply hooking up to the 'whip', that the assembly is indeed
'stepwise' rather than 'all at once' (as if it were invented 'all at once'),
all are consistent with a stepwise model with each step having functional
utility (but not necessarily the motility function).
There are many examples of such complex systems that can be broken down into
simpler subsystems.
OTOH, all you have is your repeated *assertions without (actually against)
evidence* that most evolutionary events produce proteins that are dissimilar
from all other proteins because it has to pass through a sea of random
changes.
> Where is your "weight of evidence" for the existence of
> these common pathways toward not just one (teleological) but many
> potentially different functions of higher complexity?
>
>> the usual inability of creationists to see that evidence from nature
>> includes more than direct experimentation (specifically, it also includes
>> evidence that shows that nature worked through certain specific mechanisms
>> rather than others),
>
> All "evidences" must be interpreted. Such interpretations must be
> supported by direct experimentation that can falsify the
> interpretation. If the interpretation or hypothesis is not
> falsifiable, then no one can say that their interpretation is any
> better than anyone else's interpretation. All non-falsifiable
> interpretations become equal. You cannot say that someone who
> disagrees with your interpretation is "wrong" because you have no
> predictive value until you can test your hypothesis in a falsifiable
> way.
Actually, all that is necessary is to show that the explanation is, in
principle, possible and then to look for the evidence of the consequences of
that explanation. It is clear from direct experimentation that *under the
right circumstances*, specifically the existence of a precursor close enough
to reach a new function, that random mutation and selection can achieve
remarkable changes quite rapidly (instantaneously in geological terms) --
even across a gap of as large as 7-8 'neutral' steps. That mechanism,
descent with modification with intermediates having functional utility,
necessarily leaves a particular pattern in the genome of the organisms.
That pattern is seen. Your idea of islands of functionality separated by
vast seas of nonfunctionality would also produce specific patterns. Those
are not seen.
>
>> as well as other problems, and the usual overestimation
>> of the amount of change needed to produce the amount of evolution observed
>> in nature (most evolutionary change does not involve the 'invention' of any
>> new genes, but merely allelic variation of existing ones or their regulatory
>> regions, and via that, the modification of the quantitative traits).
>
> Why are not talking about what most point to as evidence of evolution
> in action. Certainly most examples of evolution are extremely simple
> to explain with the mindless processes of nature alone. The examples
> of allelic variation that have been demonstrated to occur in real time
> are extremely simple indeed. But, we are not talking quantity here,
> but quality. If the only question was, "Which type of changes occur
> most often?" then there would be no ball game here.
Allelic variation of genes that both organisms have accounts for the
difference between chimps and humans. Is that a large enough qualitative
difference for you?
> However, there
> really is no overestimate on the amount of change that is required to
> produce many functions of high complexity. A historically non-motile
> bacterium requires truly vast changes before any motility system could
> be realized (not just one specific teleological type of motility
> system such as a flagellar apparatus, but any type of motility
> system). This is not an overestimate.
Yes it is. There are other forms of bacterial motility, such as gliding
motility. So there is no single route to motility. Besides, I have just
made the point that a historically non-motile bacterium might well have a
protein export machinery around for different reasons entirely. And it
certainly would have 'motors' around that might get hooked up to the protein
export machinery for entirely different reasons other than motility. In
such an 'exaptated' bacteria, in fact, motility might be a minor (and not
particularly efficient) secondary function of the protein export machinery.
That is, the machinery may have two functions. But, you see, I have already
simplified the process by making different functional subunits. The way
nature solves the multibody problem is to have multiple two-body events.
The point is that they did not *have* to evolve lactase. And, in fact,
lactase didn't evolve independently in multiple organisms. The organisms in
which it *did* evolve do have a selective advantage in environments with a
lot of lactose, but the selective advantage they have does not appear
*until* some organism is able to utilize lactose. Until that time, no
organism is at a selective advantage or disadvantage.
> How does
> competition for survival provide the pathways across these neutral
> gaps so that the resources of new environments can be used in newly
> beneficial ways of increasing complexity?
That would be teleologic and Lamarckian thinking again. You are implying
that selection somehow *produces* the pathways. It doesn't. Selection only
discriminates among variants that are produced without respect to need. If
there never are variants that can cross a gap, there is no differential
selection. If there are such variants, the organisms with those variations
will be selectively favored in the appropriate environment. Period.
> Again, I'm not looking for
> specific teleological examples, but I am looking for specific examples
> of any function within a given *level* of complexity. For example, if
> you could show how any type of bacterial motility could evolve or if
> you could demonstrate the evolution of bacterial motility, that would
> be very convincing to me. Or, if the category of bacterial motility
> is still too teleological for you, then I would be satisfied with the
> demonstration of the evolution of any multi-protein function where all
> the parts are required to work at the same time. That is the *level*
> of functional complexity that I am looking for evolutionists to
> explain or demonstrate.
The evolution of hemoglobin from a tetrad of alpha globin to a tetrad of
both alpha and beta globin followed by duplication and divergence (and
developmentally timed regulation) to produce fetal and embryonic hemoglobins
as well as adult. In real science, the best test cases are the simplest
ones with the most evidence. Hemoglobin (except in hagfish) is a two
protein 'system' (or more if you include the beta-globin derivatives used
during development). It seems to me that all you are really searching for
is a system which has no evidence so you can proclaim your ignorance as
evidence that it is impossible for such a system to evolve.
Regardless of the length of the 'gap', the time involved (40 years) is
geologically insignificant. And, as you agree that it probably only the
limitations of population size in lab settings that prevents our seeing even
a 7-9 step process, I fail to see why you are upset with my characterization
that such gaps are rather easily crossed in nature.
>
>> So, it is quite clear that *in
>> principle* it is quite possible for selection to produce 'new functions'
>> even in Sean's world (since there do exist evolutionary changes that produce
>> 'new' functions that do not require his hypothesized many 'neutral' steps)
>> *and* that it is even possible to cross *reasonable* sized gaps in
>> functionality.
>
> New functions do evolve, but "reasonable" gaps are NOT crossed in the
> process. The gaps always involve the crossing of less than a handful
> of neutral mutations and usually require only one or two mutations.
> Even chloroquine resistance only requires 3 or 4 specific mutations,
> but even if 7 or 9 were required, this would not be a significant gap
> given the population size that exists in the wild. In determining
> what is or what is not a significant gap, you must look at not only
> the absolute gap involved, but the population size, the mutation rate,
> and the generation time. The problem here is that with every doubling
> of the neutral gap, the population would have to grow by a factor of
> two to keep up. In short order, growing neutral gaps outpace any
> population's ability to keep up with the exponentially growing random
> walk required to cross the gap.
So what evidence do you have that *most* evolutionary change *that has
occurred* involved gaps of significantly more than 7-9 changes before the
next protein has selectable activity? Your repeated assertion that that is
the case won't do.
>
>> Given this recognition that it is indeed possible to evolve 'new' functions
>> without having to cross his hypothetical large seas of multiple neutral
>> steps, Sean is left arguing that these observed cases do not represent the
>> normal cases. He instead tries to refocus our attention on the cases where
>> this does not happen and tries to convince us (by asserting without
>> presenting evidence) that the 'normal' situation is the one he posits: That
>> most new functions require his hypothetical ocean of completely useless
>> intermediate steps.
>
> Again, you are arguing from a position of quantity instead of quality.
Absolutely. If most evolutionary change shows evidence that it does not
involve crossing a hypothetical large sea (say by being part of a protein
family) and all you are left with are cases that have no evidence at all
(usually because the functions are ancient, and time removes evidence), you
have nothing.
> You are arguing that since you can demonstrate a huge number of
> examples of evolution in action where new functions are in fact
> evolved, that you really do not need to look at the level of function
> that these very common examples demonstrate. For you, absolute
> numbers are convincing.
And the fact that most of the evidence is consistent with the expectations
of descent with modification. And the cases you toss out are not cases
where there is evidence *against* descent with modification, even if all the
t's are not crossed. And systems where, from what evidence does exist, one
can easily predict certain kinds of reasonable intermediate stages with
functional utility.
> You don't need to know anything about the
> quality. All you want in quantity. Clearly, I do have very good
> "evidence" for the exponential decrease in examples of evolution as
> the level of functional complexity increases.
No. You have a numbers game without any evidence that the numbers are
meaningful in nature. You recognize that short gaps are crossable and large
gaps are not. Good. Everyone can agree on that. What you don't have is
evidence that there exist any systems in real organisms that actually did
cross such large gaps. Nor any evidence of systems that got poofed into
existence by some supernatural poofer. All you have is the statement that
"If there are any systems that require crossing large gaps, they likely
didn't evolve or appear via natural selection." BFD.
> When you start out with
> the lowest level of functional complexity, such as that required for
> de novo antibiotic resistance via one or two mutations, then it is
> very easy to find tons of examples. However, when you move up the
> ladder a little bit to functions that require the crossing of 3 or 4
> neutral steps, as with chloroquine resistance, the number of examples
> drops off dramatically. Then, when you move up to the de novo
> evolution of complete enzymes in real life organisms, such as lactase
> evolution in E. coli, the number of examples drops off even more
> dramatically.
That is highly dependent on the starting conditions, as you well know. If
the organism has certain *other* non-lactase enzymes, it is quite possible
to evolve lactase activity in real time in a laboratory.
> Then, when you move up to the de novo evolution of
> multi-protein functions, such as bacterial motility, the number of
> examples is ZERO. Its an interesting progression isn't it?
In real time in laboratory settings. That is to be expected. The question
is whether the mechanism, which *has* been observed in real time in simpler
cases and which is the mechanism proposed to account for multi-protein
functions over longer periods of time that cannot be directly examined in
real time or laboratory settings, namely a mechanism that does NOT involve
your purely hypothetical 'large gaps' is the one that explains such
multi-protein functions. To do so one must ask what evidence that could be
found in real organisms would distinguish a mechanism that produces
multi-protein functions by a step-wise process with *functional intermediate
steps* (the non-teleological process of evolution) from a mechanism that
produces multi-protein functions in one fell swoop from the mind of a
designer (the teleological creationist process) and from a mechanism that
produces multi-protein functions by crossing a vast sea of changes in a
completely random walk to find the lone island of functionality (your
teleological strawman version of evolution).
The answer comes about by asking what sorts of complexity would be common in
living organisms if multi-protein functions were the result of a step-wise
process that involved step-wise modification of pre-existing materials with
the requirement of function at each step compared to what would be common if
multi-protein functions were the result of a single-step (or multi-step with
no intermediate utility which effectively amounts to the same thing) process
that poofed the multi-protein complex into existence. As always, of course,
the best models are those with the most evidence not those with little
evidence.
One way to achieve a multi-protein function from a single protein
functionality is by duplication and specialization of an original
multi-functional protein. This can be achieved gradually in a step-wise
fashion and produce multi-protein functions which are irreducibly complex
from a complex that was redundantly complex. Hemoglobin in all but hagfish
is a good example. Hagfish hemoglobin is a tetrameric protein of which all
the parts are alpha globin, a single protein. Beta globin undoubtedly arose
via a duplication of the alpha globin gene (as evidenced by the retention of
such unnecessary features as the placement and size of introns) and
subsequent modification of one or both copies to specialize to slightly
different, but complementary functions. Such a mechanism means that there
never was a point where hemoglobin function disappeared or ceased to exist.
Immediately after the duplication, the two genes are redundantly complex.
But modification of one of the genes produced a product that still retained
the ability to form a tetramer with the alpha, but probably affected oxygen
binding and release in a positive way compared to the old homotetramer
(indeed the different beta globins that appear sequentially during
development do exactly that today -- affect the capacity of hemoglobin to
bind and release oxygen). Soon you have a mutual evolutionary change, where
changes in the alpha protein ensures that the alpha can no longer form
hemoglobin from homotetramers, but requires heterotetramers composed of two
each of alpha and beta. That is, the system is now irreducibly complex
because removal of one of the globins causes the collapse of the entire
hemoglobin function.
The consequence of such a mechanism is that current beta globin is NOT
reached by crossing a vast gap of functional wilderness and that it retains
the binding functions that allow it form tetramers with alpha as a matter of
history rather than random chance or instantaneous poofing. You would
expect, then, to see, quite often, evidence for such divergence and
specialization because the proteins would retain functional and structural
similarities --- they would form members of a gene family.
Another way to reach this multi-protein end is the evolution of "helper"
proteins into proteins that become "necessary" to the function. The
ribosomal proteins are a good example of this. The ribosomal RNAs, by
themselves and without any proteins at all, have been demonstrated to have
(quite weak) ribosomal function. The proteins of the ribosome, thus, are
not "necessary" for function but are clearly "necessary" for a certain level
of functioning. This makes the accidental binding of the ur-protein that
*quantitatively* improves a function and the subsequent adaptation of that
protein (or the protein of a duplicate) to better fulfill this particular
ribosomal function a quantitative transition rather than a qualitative
transition that requires transition across a hypothetical sea of no
functional change. In the case of ribosome, of course, I have pointed out
that the original RNA retains some small ribozymal functionality even
without the proteins. But that need not be the case. In the latter, of
course, the 'system' has become irreducibly complex, since you have no
function without both parts of the system. The 'helper' has become a
'necessary fixture' by a process that easily permits intermediate steps that
are useful in their own right.
There are many examples of such 'helper' or 'scaffolding' proteins in the
development of complex structures.
Entire systems or chains of enzymes (like those involved in all kinds of
signaling as well as clotting mechanisms) that self-interact can be thought
of as being evolved by such a helper mechanism.
Other complex structures arise because proteins tend to be sticky and even
minor changes can lead to them being sticky in different ways. Sometimes
this can lead to new functionalities by connecting two previously separate,
but independently functional, subsystems. In cases where such events
produce a desirable effect, selection can lead to the amplification of that
effect, sometimes at the cost of reducing the ability of the system to
perform its original function. But selection is *very good* at optimizing
conflicting functionalities to that level of both which most increases
overall reproductive success. Duplication, again, when or if it occurs, can
lead to specialization. At no point do you have loss of either function.
Most proteins can serve multiple functions. All enzymes are capable of
binding and sometimes utilizing other substrates than the one specified by
its name. Often, evolution merely involves emphasizing a previously
secondary function. In fact, there is a family of enzymes called
phosphoribosyl transferases that are involved in salvage of purines. In
some organisms the gene encodes a HGPRT which salvages both hypoxanthine and
guanine. Other organisms have a specialized HPRT and GPRT, although both
enzymes can work on the other purine (and other purines as well) to a
limited degree. In short, the transition between the different forms of PRT
does not require your hypothetical vast seas of no change in function. All
the PRTs already have the capacity to, at least in a minor degree, perform
the other functions. Now, of course, *if* you arbitrarily remove all the
purine PRTs and then ask whether or not one can evolve a specific PRT in
real time in a lab setting, it may not be possible in the available time
(it may, for example, require a rare chance recombination that puts a
purine-binding sequence onto a pyrimidine PRT). But remember that you are
*arbitrarily* setting up a situation in which there are no possible
immediate precursors. That is, the first step would need to be the
invention of some kind of useful precursor, not the end product.
But the point of all this is that the evolutionary mechanism does *indeed*
require intermediates that have utility in their own right. A mechanism
that requires this as the ordinary way of evolving systems will show signs
of this in that it will have many examples of proteins that show a lineage
and belong to families of enzymes. A mechanism that usually requires
proteins to evolve or get poofed into existence as islands of functionality
in a sea of non-functionality will not have proteins which show similarity
to other proteins. There should be very limited relatedness among proteins.
It will not show proteins that serve more than one function. It should not
have proteins that show trivial and unnecessary signs of being related. Of
course, one can always claim that the designer designed proteins with these
indicators of historical relatedness for purposes beyond our ken, but that
would render the creation hypothesis completely unfalsifiable. But the
evidence of nature clearly indicates that most systems arose by one of the
'real' evolutionary mechanisms rather than by your strawman 'evolution' that
requires huge functional gaps and complete unrelatedness. I cannot, of
course, disprove an unfalsifiable creationist argument that claims whatever
exists is how the designer designed it. I can falsify the notion that
organisms show many examples of 'islands' of function in a non-functional
sea with the islands being unrelated to other islands in the same chain but
scattered randomly in the ocean of non-functionality. Rather, in real
organisms, the 'islands' are 'islands' that clearly often fall into easily
recognizable 'island chains'.
>
>> This is a strawman argument and the biochemical
>> equivalent of the distinction between microevolution (evolution that can be
>> observed experimentally) and macroevolution (evolution that cannot be
>> directly observed and can be plausibly denied). Usually the latter is put
>> in terms of "we need to see a lizard give birth to a bird" or "where are all
>> the intermediates between amoeba and man?" or "if you start with a
>> completely random sequence of DNA, you need x gazzillion changes to get the
>> one (or small number of) sequence that has y function (teleologic function),
>> and none of the intermediates have y function".
>
> Of course, I'm trying to point out that the problem really isn't one
> that can be determined morphologically. The problem really is one of
> genetic gaps, not phenotypic gaps. There are in fact very significant
> gaps between functions that rely on single proteins alone. It only
> gets worse from here on out.
Where is your evidence, as opposed to assertion, that this is the common
case in real organisms?
>
>> Sean points out that if you remove all possibility of easy transition to a
>> new function by only looking at bacteria that lack ebg or other such genes,
>> then one cannot evolve lactase by *directly* selecting for lactase function
>> within the time constraints of human designed experimentation. That is, he
>> points out that evolution is not a mechanism which has the ability to
>> generate whatever function he chooses to generate, in whatever organism with
>> whatever genome he chooses (and he chooses genomes without any sequences
>> closely similar to lactase), in whatever time frame he thinks is sufficient
>> when the only thing being selected is the teleological or end result he
>> thinks exists.
>
> Not at all. These teleological examples only demonstrate that the
> average neutral gaps do in fact grow exponentially with increasing
> functional complexity. The functions do in fact become more and more
> rare relative to the total number of potential sequences in "sequence
> space".
It demonstrates no such thing about complexity. It demonstrates that, in
organisms without the requisite precursor proteins (which you artificially
removed), it is hard to evolve a particular function because there are many
intermediate steps that are not being selected for in their own right, but
that are necessary to get to the point where one has a selectable function.
I agree. *If* you remove all possibility of easy transition to a new
function, you often cannot evolve that function within the time and
population constraints of human experimenters by directly selecting for the
end or teleological function. But that merely means that the organism in
question is neither at a selective advantage or disadvantage relative to its
competition. It may or may not be able to retain the same overall
steady-state population level (and may even go extinct), but that is not
relevant. When, or *if*, a change occurs which permits utilization of the
resource occurs, then, and only then, will there be a phenotypic difference,
based on genetic variation, that selection will differentially affect.
And, in fact, most evolutionary changes do not involve changes in genes by
the invention of new functionalities. Most involve changes in alleles or
regulatory regions of genes that all the organisms within a large group
share. That is, new proteins/genes are relatively rare events. But many
organisms exhibit extensive redundancy in genes/proteins/functions.
> Given this fact, it is not up to you to demonstrate the
> commonality of functional paths that traverse this open ocean of
> neutrality as functional complexity increases. After all, these same
> bacteria that could not evolve the lactase function in a lactose rich
> environment would evolve antibiotic resistance to just about any
> antibiotic in short order - even if exposed to sublethal levels of an
> antibiotic. In other words, even if it was not absolutely "necessary"
> for life, these bacteria would still rapidly evolve antibiotic
> resistance to many different types of antibiotics, but they would not
> rapidly evolve the lactase function. Why?
Because you artificially removed the ebg protein.
> The reason for this
> difference in evolvability is not based on the level of selection
> pressure, but upon the level of functional complexity (the relative
> rarity of beneficial sequences in sequence space).
But only if you remove the ebg protein.
>
>> Note that Sean's argument is merely a restatement of the "you can't evolve a
>> wing because the intermediate stages of a wing is useless as an instrument
>> of flight" argument transferred to molecules.
>
> Yes it is. However, it is far easier for evolutionists to argue from
> morphology than from genetics. Where the morphological steps seem
> apparently small, the genetic steps involved are not necessarily so
> simple.
The same amount of genetic change, a point mutation, can have effects that
range from 'no effect' to 'catastrophic loss of function'. Moreover,
*because* organisms are filled with interacting proteins, one can often
modify other genes and have an effect on function. One of the ways one
looks for networks is to create a mutation and look for second mutations in
other genes that act as "enhancers" or "suppressors" of the original
mutation. There are lots and lots of ways to get genetic steps that produce
small or quantitative changes in phenotype. For example, the entire
category of "conditional" mutations (mutations with unchanged or not
significantly changed function under one set of conditions, say a
temperature between 23° and 37°C, but complete loss of function at 42°C)
represent such changes. Moreover, these often undergo duplication and
divergence in organisms to produce isozymes with different pH, temperature,
or other optima or which have slightly different substrate optima. It is
simply not true that mutation cannot result in minor selectable phenotypic
differences that can accumulate.
>
>> "You can't evolve a lactase
>> directly (if you start with certain conditions involving apparently random
>> sequences -- and *if*, of course, you arbitrarily exclude all those cases
>> where it has been empirically demonstrated that you can indeed evolve a
>> lactase directly ;-)
>
> Which is just one case. Again, what Hall's experiment demonstrates is
> the relative rarity of functional sequences as one moves up the ladder
> of functional complexity.
And, in nature, lactase did not get independently invented multiple times.
So, I agree, lactase activities in organisms are mostly the result of a
single event sometime in the past and subsequent transmission of that event
both horizontally (relatively common in bacteria) and vertically over time
in lineages where having lactase was useful and beneficial. The important
point is not that evolving lactase when you remove all related proteins is
difficult. It is that it is not impossible (since there do exist bacteria
with the appropriate precursors). And that it needed to happen only once.
After that point it is retained by vertical and horizontal transmission over
time; i.e., it evolves.
>
>> -- going *directly* toward the teleologically
>> determined end function Sean arbitrarily chooses) because, yawn!, the
>> half-way intermediates do not function as a useful (selectable) lactase.
>
> You really don't see the relevance here? I'm truly mystified.
Yes. I see you assuming that evolution is teleological in nature and that
somehow you think that if organisms evolve at all, that if they have a
perceived "need" for a function, they must be able to poof it across huge
gaps *everytime* or evolution is not true. Lamarck is dead, dead, dead.
Just because an organism has a "need" is no guarantee that it *will* evolve
a function. Nor is it a guarantee that it cannot.
>
>> Notice that Sean's argument also includes a restatement (in molecular terms)
>> of the idea that evolution can explain *micro*evolution (the evolution of
>> the differences between very closely related individual)
>
> Extremely closely related indeed! I mean, when statistical gaps as
> small as 20 or so differences in genetic functions effectively block
> the evolution of those functions by any reasonable sized population of
> life forms of any type, then I call those changes that can actually
> evolve VERY closely related or "micro" indeed. My definition of
> "macro"evolution is actually very "micro".
Such gaps, of course, would indeed probably block the *direct* evolution to
the teleological end function. I agree. My point is that evolution,
properly understood as opposed to your strawman, does not work by crossing
such gaps. It crosses smaller gaps to produce intermediate states that have
utility (not necessarily the teleological function you imagine) in and of
themselves. *If* that intermediate is closer to or has secondary activities
relevant to the end function and is not more than 20 events away from a
*selectable* utility, then evolution to that end *may* occur (dependent upon
environment).
>
>> but cannot explain
>> *macro*evolution, which is defined as a gap big enough that it cannot be
>> crossed in one step: "a cat giving birth to a dog" or differences between
>> very distantly related organisms, such as "amoeba to man".
>
> LOL - Not at all. The macro-evolution limiting boundary that I would
> draw need not look at such large morphologic differences as you note
> here, but on much much smaller differences in functional complexity -
> such as the difference between single protein functions that those
> functions that require multiple proteins all working together
> simultaneously. This is the "cat-dog difference" I'm talking about.
Again. Be specific rather than assert a meaninglessly vague idea. Do you
mean that you cannot envision how hemoglobin involving both an alpha and
beta globin could evolve?
>
>> In Sean's
>> argument this is the gap between some random sequence of DNA and his
>> teleologically determined final sequence. Again the assumption is that no
>> intermediate states can have any selective value or that the gap cannot be
>> crossed in the amount of time available to experiment. And, of course, it
>> is true that sometimes a gap cannot be crossed or crossed in the time
>> available.
>
> Again, what if these gaps turn existing functions into islands that
> are surrounded in all directions by neutral sequences?
Most *currently* existing functions are islands of *optimality* (determined
solely as effect on reproductive success) in all the functions that the
structures perform. If you arbitrarily choose one of the functions as "the
function" for which the system is designed, you will see many changes that
are effectively neutral, other changes that make the structure worse, in
widely varying quantitative effects, for the defined function, and others
that can sometimes make the structure better for the defined function (but
significantly enough worse in the other functions so that the overall
optimality of the system is impaired). But looking at it from the
perspective of evolution, it is quite possible for a *suboptimal* state in
one organism to be an *optimal* state in a different organism. And moving
from a suboptimal to optimal state is what selection does well.
> No
> teleological sequence target is needed, only target levels are needed.
> Hitting any target within a particular level of functional complexity
> is what I am talking about - not any one target in particular.
>
>> I agree entirely in one sense. Evolution cannot cross every possible gap
>> *directly* aiming for some teleological set goal (the terminal functionality
>> of Sean's arbitrary choice).
>
> Can evolution cross the gap between one *level* of function and the
> next higher *level* of function.
Sometimes. And sometimes it can lead to a switch in emphasis on functions.
All kinds of intermediate functionality are possible. Some may be
selectable for the teleological end function you envision. Some may be
selectable for other functions that are more locally relevant and reachable.
The point is that the fact that it is 'sometimes' and not 'never' means that
evolution is possible, but new functionality is relatively rare (rare enough
that most such functions are retained and spread via vertical and horizontal
genetic mechanisms rather than new invention, and that when new invention
occurs, it rarely produces the same result -- the wings of bats and birds
are not identical in structure). The requisite evolutionary mechanism
implies that most new functions involve modification of some pre-existing
structure (whether at the genetic or morphological level).
> That is the question. We are not
> talking specific targets here. Examples of specific targets being
> missed are used to demonstrate the relative rarity of such targets as
> complexity increases, but this is really not the main point or
> challenge. The challenge is to hit ANY target within such a level of
> increasing complexity (i.e., the level of multi-protein functions).
>
>> In fact, evolution, because of the mechanism
>> by which natural selection works, cannot proceed toward teleological goals
>> at all. Evolution's selection mechanism can only focus on reachable local
>> goals. If no bacteria in a particular environment can utilize lactose, then
>> no bacteria will use it and there is no selective advantage to any bacteria
>> on this basis.
>
> The fact is though, they could utilize the lactose if they only had
> only little relatively simple lactase protein. They would gain an
> advantage in this environment if they were able to evolve the lactase
> function just as these same bacteria would quickly evolve the
> antibiotic function in sublethal levels of many different antibiotics.
But such an advantage will only exist when and if such a protein arises.
The advantage will ensure that in such an environment, when and if a lactase
arises, it will be retained. It is, of course, *possible* for lactase to
evolve *in the organisms with the requisite precursor protein which does not
have lactase activity itself*. It is certainly not impossible for lactase
to evolve. Merely conditional upon the requisite precursor present for
other reasons.
>
>> If no bacteria in a particular environment can use nylon or
>> some other plastic polymer (and there are man-made plastic polymers that
>> could potentially be useful carbon sources but which are not used precisely
>> because no current bacteria can cleave a particular chemical bond), then no
>> bacteria has a selective advantage on that basis.
>
> Basically, what you are saying is that if evolution is impossible due
> to neutral gaps, then evolution will not occur. Well duh! That is
> what I've been saying all along.
I am also claiming out that the organisms and features that we do see
evolved via pathways that *were* possible, not via your hypothetical
impossible pathways. You are arguing against a strawman evolution.
>
>> When or if a bacteria
>> produces a variant able to cleave, say, the bond in polyvinyl chloride and
>> also deal adequately with the chlorine atoms, it will certainly have a
>> selective advantage over bacteria that cannot do this in certain
>> environments (those that contain significant amounts of polyvinyl polymers).
>
> In other words, if evolution can occur, then evolution will occur.
> Well duh again!
Absolutely. And the claim is that the observed features of organisms arose
via the evolutionary pathways that are possible not the hypothetical
pathways that are impossible.
>
>> There is no guarantee that such a variant will occur anytime soon. There is
>> also no guarantee that it won't happen.
>
> LOL - No guarantee and no testable predictions either. It's nice to
> believe in a non-falsifiable position - isn't it?
The test will be evident *when* such an event does happen, as in the case of
nylonase. If your argument were true, then nylonase, a new enzymatic
function, could only arise by a process that involves going from a random
sequence to the optimal function seen today via a process that involves a
long random walk of functional neutrality. If my argument is correct, then
the initial nylonase activity will occur via one or a few mutational steps
and that subsequent mutational steps will lead toward greater optimization
of nylonase functionality. I already know which explanation holds for
nylonase -- mine. Where do you have evidence that supports your idea that
new features arise either by crossing a vast sea of 'neutral' changes or
arise by some observable supernatural designer?
> "It could happen
> even if I have no clue how or when or where." You can always fall
> back on that one in order to maintain your unshakable faith in the
> powers of Darwinian evolution.
No. If such a *recent* new enzymatic activity were to occur, I would fully
expect to be able to trace exactly where the activity came from. For events
that are ancient, I might not be able to do so because the evidence would be
missing. But, interestingly enough, many times one can, even for relatively
ancient structures, trace a lineage to related proteins. OTOH, all you can
do is say "Where there is no evidence, I assert that the absence of evidence
is evidence that one must cross huge vast seas of nonfunctionality."
> Please . . . Even though there are no
> "guarantees" as you say, there certainly is very good evidence to
> support reasonable estimates about how long it would take on average
> given all known information about a given genome, population, mutation
> rates, reproduction rates, and current environment.
GIGO calculations are worthless.
> At least I can
> make a testable prediction based on this information.
Then what is the testable prediction? I have yet to see you make one. What
would organisms look like if your ideas about what is necessary for
'evolution' of a new function to arise were true that differs from the
expectations of my ideas about 'evolution'? I specifically stated that I
would expect to *often* be able to observe that new functions arise within
gene families and that functionalities rarely are isolate islands completely
different from other genes in the organism (or in other organisms from which
it could spread horizontally). What are your testable predictions? *If*
there are huge gaps that must be crossed, what would organisms and their
genomes look like?
> You can't even
> make a stab in the dark prediction, because as soon as your prediction
> for some sort of reasonable time frame fails, you can say, "Oh well, I
> guess evolution must have happened a different way."
>
>> But, of course, the key word in all this is *directly*. Evolution, properly
>> understood, does not often produce things *directly* from some random
>> starting sequence to some final teleological functionality under the "need"
>> for such functionality. In fact, it cannot do so (although Lamarck -- and
>> Sean -- would disagree).
>
> I don't know about Lamarck, but I never did say that the proposed
> process of evolution was teleological. What evolution does claim to
> be able to do is to produce vastly different functions of increasing
> *levels* of complexity if given enough time and competition in a
> non-lethal environment. I disagree with the suggested *levels* of
> functional complexity that evolution is supposed to be able to
> achieve. As I see it, the evidence suggests that only the very
> simplest of functions can be evolved in the limited time frame
> suggested by the theory of evolution (i.e., only 4 or 5 billion
> years).
Rather, you use a false idea of how evolution works to generate GIGO
calculations that produce the results you want.
>
>> Instead, there must usually be some intermediate
>> utility, but not *necessarily*, nor for any long or involved sequence of
>> changes (which we will define as more than 7-9 events, since it is quite
>> clear, from chloroquine resistance, that such gaps can be rather easily
>> crossed in human time-frames), *usually*, via intermediates with the
>> teleological end functional utility.
>
> Yeah yeah yeah . . . yadda yadda yadda. You keep saying this over and
> over and over again. But simply saying it over and over and over
> again doesn't make it true. Where is your evidence? You go on and on
> discussing how things are supposed to work. I get it already! I
> understand how evolution is supposed to work!
Yet your calculations completely ignore how evolution is supposed to work
and instead present a strawman. The evidence is that complex structures
often show evidence of having evolved by one of the mechanisms I already
presented. Duplication and divergence. Conversion of structural 'helpers'
or 'aides' into 'necessities'. Switching of parts to generate new
functionality. Chance production of activity (ala nylonase). Not once have
I pointed out evidence for evolution that works by crossing huge gaps of
completely neutral sequence space to a new function because evolution *does
not work that way*. That mechanism is a strawman of your own invention.
Claiming that evolution does not work via that absurd mechanism does not
disprove evolution. Claiming that that absurd mechanism is what evolution
does is what is absurd.
> Where is your evidence!
> Stop making these blanket statements of how things must have happened
> and start backing these statements up with something!
I have. I have pointed out hemoglobin as a simple mechanism of generating
greater complexity. I have pointed out the bacterial flagella's other
functionalities as reasonable intermediate states. I have pointed out the
ribosome as evidence of complexity generated by 'helpers' becoming more
'necessary' because they quantitatively affect a weak activity (similar to
suppressor and enhancer mutations today). In all these cases, examples of
gene family relationships exist and the ontological process of self-assembly
gives a reasonable phylogenetic pathway.
The above is meaninglessly vague.
>
>> Given this view, he cannot see how 'new'
>> functions can arise by selection, since it would require direct teleological
>> selection for that final function from an essentially unrelated sequence
>> without any affinity for or relationship to the final sequence.
>
> Again, you misrepresent my position as requiring teleological
> demonstrations, which I do not require - as detailed above.
Again, *all* creationist mechanisms are teleological in nature, based as
they are on the vision in the mind of the designer. So is your strawman
version of evolution. Both claim and, in fact, require that only the end or
terminal function or structure (which is really only the current
function/structure) has any meaning. For creationist mechanisms, teleology
is necessary because the end structure/function being discussed was the
direct intention of the designer. In your strawman evolution, the end
structure/function exists as an isolated island of function in a sea of
non-functionality, and thus is as much the only possible goal as is the
creationist poofed end position. In real evolutionary mechanisms, the
current structure/function is not the end structure or goal, but only the
current structure/function. And it arose via a pathway that largely
involved easily reachable intermediates that had utility in their own right.
>
>> That is, he is using his (what I regard as a strawman) idea of how 'new'
>> functions arise in order to then argue that they cannot arise that way.
>
> How would you say that new functions of increasing complexity arise?
Via steps which do not involve large gaps of functional inutility.
> Now, after you make your paper statements again, as you have done
> before, you need to be able to back your descriptions of how this
> process occurs with some testable evidence or repeatable demonstration
> of some kind. If you cannot do this, you certainly can believe
> whatever you want, but I don't see how you can hope to call your
> belief scientific.
The mechanisms I presented for generating multi-protein systems that perform
a function are evidence in that all the hypothesized and predicted possible
intermediate states, from simple duplications to isozymes that perform the
same function slightly differently to clearly related enzymes that perform
slightly different functions (HPRT and GPRT) to slightly more distantly
related enzymes (alpha and beta globin of hemoglobin), dispensible helper
proteins to indispensible helper proteins, enzymes and multi-protein with
similar structures but different functionalities (non-motile 'flagella' that
act as protein transport systems) exist in nature. I know of no evidence of
any system that formed by the mechanism you propose. You certainly have
failed to present any such evidence. All you have done is state that *if*
such a requirment (crossing a vast wasteland of selective neutrality and
functional irrelevance) existed often, then such systems would not evolve.
I agree with that. Such systems have not evolved. The systems that we see
did not evolve by the mechanism you claim is 'evolution'. They evolved by
the mechanism I claim represents 'evolution'. There is no evidence at all
to support the idea of a supernatural designer poofing them into existence.
The genomes of organisms represents my testable evidence and such organisms
allow repeatable observation of the predicted patterns of the observable and
demonstrated mechanisms of evolution.
>
>> And
>> then use the fact that they cannot arise that way to claim that "goddidit"
>> is a better explanation. One must always keep this attempted switcheroo,
>> the attempted focusing on (asserted but unsupported) claims that the failure
>> of natural selection to work under all and any conditions to produce a
>> teleologic end point somehow obviates the fact that natural selection does
>> work to produce new function when the clearly described requisite conditions
>> *are* present.
>
> And what would these "clearly described requisite conditions" be?
The existence of (or, in the absence of direct evidence that such functional
intermediates are reasonable, the potential for) a stepwise pathway allowing
the stepwise modification of a precursor (or precursors) to different
functionality and/or structure without huge gaps of non-functionality
requiring multiple chance events is the one most relevant here. It is the
same condition that holds wrt morphology, where one needs to look not at the
gap between amoeba (or even chimpanzee) and man and ask how man could
evolve, but rather at the difference between late H. erectus and primitive
H. sapiens as the relevant size of the gap that needs to be crossed.
But there also is the usual assumption of the existence of selectable
phenotypic variation and the requirement that some portion of that
selectable variation be genetically based. And the assumption of the
existence of a local environment that can select for relevant variations
along the stepwise pathway (but not necessarily selection for the current
function, which Sean falsely assumes is the terminal or teleological
function).
I am saying that the *absence* of similarity (or families of proteins) would
be consistent with your ideas about the existence of vast seas of
non-functionality. The *presence* of similarity (detectable families of
proteins) would be consistent with an explanation that such proteins do not
sail the vast seas you envision, but only go from island to island in the
same chain.
> There
> are many designed things that use similar or even identical parts in
> very different systems of function. The demonstration of similarities,
> even common similarities, of parts within different systems of
> function does not explain the differences that do exist. For example,
> all proteins use the same identical amino acids. Does this fact, in
> and of itself, mean that all proteins must have descended from a
> common ancestor?
As a matter of fact, it is clearly consistent with the idea of a common
ancestor. *And* the fact that there are exceptions to this generality
(there are some amino acids used by organisms that are non-canonical, such
as selenocysteine, and not in the code and others that are missing and whose
code has been reassigned, such as trp in mitochondrial genomes) is evidence
that this is a contingent fact of nature (the amino acids used are more
historical accident rather than historical necessity). The fact that such
exceptions to the rule are rare and also fall in a pattern consistent with
the standard evolutionary branching pattern. The reason for the rule is due
to selective constraint (which is, under the right conditions, able to be
bypassed), not to identical design.
> Just because all of the words in this thread us all
> the same letters or "parts" does not mean that this thread arose or
> even could have arisen via the mindless processes of Darwinian style
> evolution. If life were designed, as I think it was, by some
> intelligent mind, who is to say that this intelligence could not have
> used the same or similar parts for the performance of different
> functions?
Whatever exists is how the intelligence did it, then? What a nice
unfalsifiable assertion. Where are *your* testable ideas that would
demonstrate the *difference* between the expectations of a designer and the
expectations of either your strawman version of evolution or my more
standard version of evolution?
>
> You see, the theory of ID is not ruled out by appealing to
> similarities nor is the idea of common descent ruled in by appealing
> to similarities.
Your theory of ID, then, is as vacuous and empty of testable ideas as I
already know it to be.
> The determination of ID vs. evolution can only be
> determined based on the differences. Can the differences be explained
> by mindless naturalistic processes?
I know of no differences in genomes that cannot be explained by known
mechanisms of mutation, including, but not limited to duplication, point
mutation, frameshift, insertion, deletion, illegitimate and legitimate
recombination, and horizontal transfer. And certainly any of these
differences can (but need not) interact with the local environment in a way
that can affect reproductive success. The interaction between the genetic
component of phenotype and environment typically leads to optimizing the
genome for reproductive success in the local environment. The optimization
process can either increase, decrease, or leave unchanged the amount of
'complexity'. It can either modify or leave unchanged the current
functionalities/structures. In addition, there is additional change that is
simply a consequence of neutral drift. That change is unaffected by
selection and *will* occur in the future, as it has in the past.
Those are the only processes that I am assuming. You must be thinking of
some other process.
> If they can be explained by such
> processes, then ID cannot be supported. However, if mindless
> processes are limited to such an extent that certain differences
> cannot be explained except by comparison to or correlation with other
> intelligently designed creations, then ID is the only reasonable
> conclusion.
Nope. ID is an empty non-explanation. If the current explanations were
invalid, we could only say that we had no viable explanation.
>
> Another thing, phylogenetic trees that demonstrate differences between
> such functional proteins as cytochrome c sequences in various
> creatures, cannot necessarily be used to demonstrate or estimate
> evolutionary relationships.
They just happen to correlate so highly with morphological trees just by
chance, right?
> The reason for this is because if the
> differences were truly neutral then they would become scrambled very
> rapidly.
Obviously population genetics is not a strength of yours. For a selectively
neutral peptide (say fibrinogen peptide), the 100% point for neutral amino
acid exchange (equivalent to each amino acid in the fibrinogen peptide
undergoing selectively neutral change -- although one would actually have a
Poisson distribution of re-ratters) can be plotted to about 100 million
years. In times shorter than this, the amount of neutral exchange is less.
And, of course, for proteins that have functional constraint wrt sequence,
like cytochrome c, the rate of change is significantly *slower* than for
sequences that undergo neutral drift.
> The only way that the differences in cytochrome c in
> bacteria and fruit flies and fish and bats and horses and humans etc.,
> is if the differences were actually functional differences that were
> maintained by natural selection over the course of many generations.
The *differences* are largely in the parts of the protein that are NOT
functionally relevant, not in the parts that are functionally relevant.
There is selective constraint (slower change) in those parts of the protein
that functionally relevant. Your ideas are bass-ackwards. This merely is a
consequence of the conservative nature of selection for function. *When* a
change is beneficial or detrimental, selection, as a force can cause very
rapid change. Because this then means that sequences reach optimal current
function rapidly, most subsequent change is detrimental to optimum current
function (until the environment changes). *When* a change is neutral, drift
to fixation of a new variant is typically quite slow. But because of
evolutionary constraint, most observed change in proteins that have a
constant historical function (such as cytochrome c) and thus evolved early,
will be in the selectively neutral parts of the molecule. Think of it as a
pail with a continuing drip, drip, drip of water (nonselective change).
Eventually it would fill up completely if all the pail were selectively
neutral. But if you put a large hole two-thirds of the way up the pail, the
upper third can be considered the amino acids under severe selective
constraint for function, any drips that would fill up the upper third are
quickly removed. [Of course, like all analogies, this one has limitations,
since many of the amino acids under constraint can occasionally be
substituted, but often only for similar amino acids.]
> Such functional differences cannot then be used to estimate orders of
> divergence over variations in functional needs in particular life
> forms and environments. For further discussion of this point see:
>
> http://naturalselection.0catch.com/Files/geneticphylogeny.html
>
>> OTOH, if most protein functions in organisms arose via duplications and
>> divergence from proteins that serve related functions, one would expect to
>> be able to see, often, and especially for recently evolved new functions,
>> sequence evidence that indicates that the 'new' enzyme or function came from
>> a structurally related precursor. That is, proteins should exist in
>> families.
>
> Also, if similar internal functions were required by different systems
> of function, with only slight variations on functional needs or
> requirements, we would also expect to have such clustering of protein
> "families".
Such an argument is quite teleological in nature. Only the one structure
can perform the function. The fact is that we know that that isn't true.
The function of cell motility, for example, can be achieved, variously, by a
rotating flagella, a sliding back-and-forth flagella, a pump, molecules that
slide over one another to compress and decompress cells and can involve
molecules as different as pilins (in archea), flagellins (bacteria), actin
and myosin (eucaryotes), and tubulins (eucaryotes). There are examples of
independent invention of enzymatic activities. Those independent inventions
also cluster in the same evolutionary trees as morphology and sequence
similarity.
> Such clustering could just as easily be explained on the
> basis of function requirement, and not necessarily on evolutionary
> relationship.
That, functional constraint, can explain the commonality of airfoil shapes
in wings and streamlined shape in aquatic organisms. It does not explain
the observed *pattern* of differences in sequence in cytochrome c. Most of
the *differences* are functionally irrelevant. That there are fewer such
differences in organisms that are more recently divergence from a common
ancestor (but are more dissimilar in shape and functions, such as, say
chimps and humans who diverged around 6-10 million years ago) than there are
in organisms that are quite similar and shape and function (such as certain
African and South American frogs, who necessarily diverged over 40 million
years ago) tells us that it is history (time since divergence) and not
functional constraint that determines the amount of these selectively
neutral differences.
> Again, just because every protein uses the same 20 amino
> acids does not in itself give evidence of common ancestry of all of
> these different proteins. In the same way, just because a particular
> protein has similarities or is even identical to another protein
> elsewhere in another system of function does not mean that these two
> proteins must have arisen via a common evolutionary ancestor.
It certainly makes such a transition between similar structures easy and
does not require the invoking of your hypothetical vast sea of
non-functional neutrality between sequences.
> I use
> the same exact words in many different sentences all the time. This
> does not mean that these words evolved outside of ID. Very different
> cars also use very similar parts. This does not mean that these parts
> evolved via mindless processes from the same ancestor part.
I fully agree that words and car parts are necessarily the invention of an
intelligent designer (although both words and car parts change over time).
I *even* can tell you something about the nature of the intelligent designer
and the purposes for which he invented these objects that have no capacity
to reproduce independently of the designer nor do these objects have any
meaning outside a setting that contains the designer who constructed them
for his own purposes rather than theirs. Can you do the same for the
hypothetical designer of the cockroach and tapeworm?
> And, even
> if they did, this does not mean that the different cars evolved via
> mindless processes. Just because some simple parts can be shown to
> evolve into other simple parts does not mean that an extrapolation to
> include all parts and all functions in such an evolutionary process is
> warranted or reasonable.
>
>> So here we have a genetic 'test' of Sean's vision of what is
>> required for 'new' function (crossing large gaps) and what my vision of how
>> 'new' functions arise (by modification of related enzymes).
>
> This is hardly a test to separate my position from yours since both of
> our positions propose that such "families" of similar proteins are to
> be expected.
Your explanation most certainly does not lead to an expectation of "families
of similar proteins". It leads, specifically, to proteins which are quite
distinct and radically different from any possible protein it could have
originated from.
> There is absolutely no reason for you to propose that if
> my idea of limiting gaps were a true problem that we would not see
> such protein families. Upon what is this suggestion based? What
> makes you think this would be a requirement or even likely? - assuming
> of course the "correctness" of my position?
Because your position *demands* that, for most functions, there be huge and
*necessary* sequence differences between a protein with the proposed
'current function' and any possible source of that protein. It also
requires that there be no possibility of intermediate or partial
functionality at any intermediate structural state. Such a hypothesis
literally demands that functional proteins be quite different in sequence
from one another. Enzymes which perform the same function in different
organisms, OTOH, because, in your model, there is only a limited amount of
change without eliminating function, should be nearly identical to each
other. There is no expectation, in your model, that the differences that
exist in sequence should be highly correlated with evolutionary trees based
on the fossil record.
>
>> I would expect
>> that many genes would be found in gene families.
>
> So would I if life were actually the result of ID. It is called,
> "conservation of design." Why redesign the wheel for each new
> function that you want to create?
Do you remember that you were arguing that one must cross huge sequence gaps
to get new function and that that was your reason for supporting ID?
> It is only reasonable to use what
> works, with slight modifications, to do similar things as a part of
> different functions.
Do you remember that you were arguing that one must cross huge sequence gaps
to get new function and that that was your reason for supporting ID?
> Each of the 20 different amino acids still does
> the same job in the various different proteins that are formed. Brand
> new amino acids are not needed to perform very different functions.
> The same is true for larger systems of function. Brand new protein
> sequences are not needed to give rise to many different larger systems
> of function.
Do you remember that you were arguing that one must cross huge sequence gaps
to get new function and that that was your reason for supporting ID?
>
>> I would expect that genes
>> like the globins of hemoglobin should share similar sites for introns with
>> each other and with myoglobin.
>
> So would I. If I were the designer, I wouldn't think of making a
> completely different protein sequence to do a similar job just because
> it is in a different location or part of a different system of
> function. That would be illogical. These two different proteins do a
> similar job in different larger systems of function. Why then
> wouldn't one expect for them to be similar in structure and underlying
> code?
If I were an "intelligent" designer, I would not include type I introns at
all. And I certainly would not make superfluous changes in selectively
neutral sites that correlated with time since divergence and the branches of
the evolutionary tree. And I wouldn't 'forget' beta hemoglobin in the
hagfish. But your "intelligent" designer seems to be prone to such stupid
behavior, presumably because you need to match what he did with what is
observed even though such observations are NOT what your theory would
predict.
>
>> I would expect that many 'novel' genes would
>> appear to be 'chimeric' (due to fusion of different protein domains, of
>> which there is a limited number) events rather than via 'construction from
>> completely random sequences'.
>
> Likewise, if I were the designer, why would I think to make many
> different independent proteins or genetic sequences in widely spaced
> areas of the genome if the needed collective function were isolated to
> a small area? Why not just combine the sequences into one and make a
> single protein with multiple functions or "domains"? I have a
> pocketknife like that. It has multiple functional tools all stuck
> together in one place - very handy.
You missed the point.
>
>> I would expect enzymes and other proteins to
>> have secondary activities and to bind to other proteins, sometimes without
>> that interaction or secondary activity having biological meaning in the
>> current environmental setting.
>
> So would I. Many secondary activities can be realized by my car that
> were not intended or which do not have beneficial meaning in my
> current environment.
But why would you expect this when you expect that the way to new function
is through a vast wasteland of non-functionality?
>
>> I would expect this evidence to be clearer
>> for 'recently' evolved proteins than for the most ancient proteins.
>
> Certainly I would agree, unless there was an ancient function
> (designed or evolved) that was maintained the entire time by natural
> selection.
You again missed the point. It is precisely in ancient functions that I
would expect evidence for its origins to be least evident. I have many
sources of evidence to explain the reasons behind the existence of a recent
mass grave in Rwanda. I have many fewer sources of evidence to explain a
mass grave in the Iron Age in a pre-literate culture.
Essentially all you are doing is saying that whatever exists was designed to
exist. You have not justified *at all* why a theory of design *requires*
that genes show a pattern sequence changes consistent with the branching
evolutionary tree. You have not justified *at all* why a theory that thinks
that functions are rare islands in a sea of uniformly functionless
intermediates reached only by a random walk will exhibit a pattern that is
consistent with gene families if your assumption is that new functions
require structures that are so radically different from any other structures
that one cannot convert one into the other even in all the time that life
has existed. Your designer seems to be making completely arbitrary choices
that, just by chance, are the very same choices one must observe if descent
with modification were true.
>
>> 2) I would expect, if Sean's vision of how evolution works -- changes are
>> due to specific genes that have to have many, multiple changes to produce a
>> new phenotypic effect -- that humans and chimps would have certain genetic
>> sequences that code for proteins that are dramatically different from each
>> other.
>
> Not if humans and chimps were independently designed by the same
> designer or if the same common ancestor was very similar to both.
Explain the above. I clearly understand the last half, since the common
ancestor to both did indeed have many common features with both. But why
would a designer, whose existence you claim is supported by the hypothetical
requirement that new functions involve radically different proteins, then
decide to produce humans and chimps with so few differences that they would
be regarded as sister species in Drosophila? So are you saying that humans
and chimps are really just microevolutionary differences, no different than
different breeds of dog, that do not involve the invention of any new
functionalities?
>
>> I would expect that different dog breeds, likewise, should have
>> certain genes that are dramatically different from each other and from other
>> canids by many, many, sequence changes.
>
> I wouldn't expect this at all since most of the differences between
> various breeds of dogs are based on the Mendelian variation potential
> of a fairly static gene pool. Certain phenotypic differences, such as
> the very short legs of some breeds, are of course the result of new
> mutations that affect pre-existing alleles in a new way.
>
> Certainly some traits in certain breeds of dogs are the result of
> novel mutations.
But NOT new genes that have to transverse your hypothetical sea of
non-functionality.
So where are your examples of changes that involve your hypothetical
crossing of a vast sea to get the types of evolution that requires your
designer?
>
> The problem here is, using genetic recombination alone, you cannot get
> a cat to evolve into a dog. New functions are needed. How are these
> new functions gained? Some very simple functions are no problem, but
> this is not the issue. We are talking about functions of increasing
> complexity.
So what are the new 'unevolvable' functions involving large transitions
across vast seas of non-functionality that are required to evolve both a cat
and a dog from a common ancestor? And can you again relate how this is
reflected in the genome of humans and chimps? Is it possible that humans
and chimps evolved from a common ancestor but cats and dogs cannot?
>
> Dr. Walter Veith, zoologist, former evolutionist, and senior professor
> at the University of the Western Cape, says, "By selecting from the
> built-in natural variation of the gene pool, various breeds of dogs
> and domestic cattle were produced. Great changes in physiology and
> morphology are involved, and evolution is here certainly excluded."
> Darwin had no idea since he was not capable of understanding the
> genetics involved, so he can be excused for assuming some sort of
> evolutionary process here. However, for us in this modern age of
> increased enlightenment we can no longer use Darwin's finch beaks or
> other minor variations within a "kind" as examples of evolution in
> action. Why? Because in none of these examples has anything that is
> actually genetically new or unique evolved!
Neither, apparently does the evolution of humans and chimps from a common
ancestor. At least I can think of nothing in those genomes that is new or
unique, even though there is substantial changes in morphology and
physiology.
>
> http://naturalselection.0catch.com/Files/methinksitislikeaweasel.html
>
> http://www.amazingdiscoveries.org/evolution.html
>
>> Perhaps, just perhaps, much evolution does not, in fact, involve the
>> invention of new proteins at all.
>
> Oh really? So where did new proteins come from? Oh, I know, the
> sequential changes were so small along the evolutionary path that no
> one could say at any point that a "new" protein had evolved from the
> one before. Now of course, all these intermediate proteins have been
> lost so we have the appearance of "new" proteins. What a great story!
> Any evidence?
Gene families.
>
>> This would be a genetic test of the
>> expectation that protein sequence changes crossing large seas of inutility
>> are a necessary requirement for most evolutionary change.
>
> Again, quantity vs. quality. We are not talking "most", we are
> talking "type". How does your "most" explain the existence of the
> "type" of functions that I am talking about? These functions of
> increasing complexity do exist. How did they evolve?
The solution of the three body problem that nature typically employs is two
sequential two-body problems with an intermediate.
Sure. But I am interested in how the current proteins that do exist came to
exist, not in why the proteins that are not possible because of gaps don't
exist.
>
>> The duplication and divergence of
>> pre-existing genes is relatively common.
>
> Again, this has never been observed in real time. You are only able
> to ASSUME that gene duplication and divergence is relatively common if
> you take your theory of evolution as an a priori assumption of truth.
Duplications, both small and large, has been observed to be quite frequent
and its mechanisms are pretty well known. Most genomes, in fact, contain
redundancies and duplicates. They also contain pseudogenes in various
stages of randomization. I presume you would argue that all these
pseudogenes have a designed function of some sort? In terms of divergence
in duplicated sequences, that is, in fact, essentially inevitable given
neutral drift alone.
> Is it logical to argue that something is true based upon the assumed
> truth of what the position in question? Isn't this called "circular
> reasoning"?
No. Duplication and divergence makes certain specific predictions about what
one would expect in a genome which has been derived via such a mechanism.
All the possible intermediates in duplication and divergence are seen, from
simple duplicates to isozymes to genes like the developmental sequence of
beta globins (including pseudogenes). That is, the theory predicts certain
specific observations. Those observations are what is observed in nature.
The evidence is consistent with theory. Your turn.
>
>> The selection of chimeric genes is
>> relatively common. The retention of structure while changing function is
>> relatively common. Overlapping function and redundancy is relatively
>> common.
>
> Again, you assume what you are trying to defend here. The positive
> selection of chimeric genes is not observed all that "commonly" in
> real life. It is assumed to be common based only on evolutionary
> assumptions.
Chimeric genes are not produced by crossing long gaps of multiple events,
but are produced by single events. Like all mutation, the chimeric product
is under the scrutiny of the environment. I agree that positive selection
of a chimeric function is relatively rare compared to selective neutrality
or negative selection. That is like any mutation. But the point is that no
large gap of multiple events is required to produce such a chimeric protein.
>
>> In short, living organisms do not look like creatures which contain
>> functions that had to cross large gaps of inutility.
>
> Yes they do. You only deal with those functions and sequences that
> are already very similar but you carefully avoid the gaps between
> those sequences and functions that are not very similar.
I am indeed avoiding them. Because they don't play any role in evolution.
Evolution simply does not proceed by crossing such gaps. The idea that it
does is a strawman of no consequence.
> Even the
> similar sequences that you can detail as parts of different systems of
> function cannot be said to have arisen via gene duplication and
> selective divergence. If a gene duplicates and is not immediately
> selectable as advantageous, natural selection will select to get rid
> of that gene since it costs energy to maintain non-beneficial genetic
> real estate. Gene duplication really explains very little.
You are quite wrong. The energy cost is insignificant. Duplicates are
usually selectively neutral (there are exceptions). That means that they
only change by drift, which is a slow process. Indeed, most genomes contain
redundancies.
>
>> They look like
>> organisms that have considerable similarity wrt the proteins and functions
>> they perform.
>
> Not at all. Vast differences in structure and function exist within
> creatures as simple as single celled bacteria.
That is like saying that there are vast differences in structure and
function within eucaryotes (another superkingdom). Indeed there are.
> How are these
> differences explained?
Differences are due to neutral drift and selection (often combined with
other processes that produce new genes, like duplication and illegitimate
recombination) for new or secondary function in particular environments.
> You tend to dwell on similarities, most of
> which you cannot explain
Similarities are a consequence of common origins and selective constraint.
> or which do not help your position out much,
> and completely ignore the major differences that do exist and that
> never evolve in real time.
Real time is 3.5 billion years for some things. You may mean "evolve in the
time available for experimentation (i.e., the last 20 or 30 years wrt
sequence changes)".
>
>> 3) I would expect, if Sean is right, complex multi-protein systems to show
>> no evidence of subsystem utility nor the ability to be generated in a
>> step-wise fashion, either ontologically or phylogenetically.
>
> First off, you cannot or at least have not shown that such systems can
> be "generated in a step-wise fashion". This sort of demonstration has
> simply never been done.
OTOH, one can indeed observe the requisite intermediate functions of
subunits in nature. There exist non-motile bacteria that use the secondary
protein export capacity of flagella. There exist bacteria that have
modified the protein export sub-part to export proteins. Each step in the
ontogeny or construction of the whip subunit involves a subsystem with
protein export capacity and a lengthing of the exporting tube away from the
exporting bacteria. The motor system exists for other functions as well.
That is, it is not a giant stretch to see intermediate stages that have
function (but not the teleological motility function).
> Also, if a multi-amino acid protein shows
> evidence of subsystem utility, why wouldn't a multi-protein system
> show evidence of subsystem utility? Again, it is conservation of
> design.
Remember that your argument for design is NOT the similarity or subsystem
utility of subparts, it is the inability to produce them without having the
teleologic function able to select for them.
>
>> OTOH, if Sean
>> is wrong, I would expect an ontological process that would indicate that the
>> final 'teleological in hindsight' product was actually composed of amplified
>> recursive systems or composed of subsystems that are related to functions
>> that the subsystem can have independently of the teleological 'end function'
>> that Sean posits. That is, my claim is that the solution that nature uses
>> for the three-body problem is to produce two two-body events.
>
> This is a fine theory, but where is your evidence?
My god, man, what do you think the *fact* that subunits of flagella have
independent activity as protein export is but evidence of subsystems that
have function independent of the teleological 'end function' of motility?
> I'm saying that
> any collection of items, parts, or systems can be categorized
> according to shared similarities, but this does not necessarily mean
> common descent or any sort of actual relationship. Certainly I would
> expect that if the evolutionary scenario where true that such
> intermediate steps would be quite evident in hindsight.
Not always. Particular so for ancient systems.
> However, just
> because something can be categorized along some sort of continuum does
> not mean that this continuum is by necessity an evolutionary
> relationship or any other sort of particular relationship. There must
> be other evidence and some sort of detailed mechanism.
The fact that each step in the formation of the bacterial flagellar whip is
a protein export function is not a detailed mechanism? As opposed to saying
some unspecified something at some unspecified time did an unspecified
something and whatever exists poofed into existence?
> Also, arguing
> from morphology is always easier than arguing from code or genetics
> since what seems like a short step morphologically can be quite a leap
> genetically.
And vice versa.
Are you claiming that the bacterial flagella does not self-assemble but
needs some outside intelligent manufacturer? In fact, the bacterial
flagella does self-assemble and does so in order because of the nature of
the proteins. No outside agitator or manufacturer is needed. The
eucaryotic flagella and tubulins also self-assembles (tubulin does so
reversibly in test tubes). The ribosome also self-assembles (in test tubes,
even and it also assembles in a specific order). The lambda phage capsids
self-assemble viruses (in test tubes, even and it also assembles in a
specific order).
> Also, it should be
> noted yet again that not even one of the proposed evolutionary steps
> in flagellar evolution have been demonstrated to be crossed in real
> time, much less any complete motility system.
Real time, wrt evolution, is not the 20-30 years since sequencing was
possible. That is off by anywhere from a few to many orders of magnitude
(like 8). You should immediately cease calling it 'real' time. Use 'human
time frames' or 'geological time frames' if you wish.
>
>> He does that because such a
>> strawman version of how evolution works is necessary for his claim that
>> evolution must work randomly through large completly useless gaps to be
>> accepted in the face of evidence that the genetic structure of organisms
>> belies his strawman model.
>
> You continually misrepresent my position in order to make it appear
> like I am building a straw man. It is actually you who are building
> the straw man to represent my position because you know that I am
> actually correct in my understanding and description of the Darwinian
> process. It is a lot easier for you to attack me if you misrepresent
> me. Next time, please, try and be more honest in your representations
> of my views. I know you understand what they are, so I find it
> difficult to think that you just don't understand what you are doing.
> I think you are deliberately trying to confuse the issue here.
If I am misrepresenting you, either I do not understand your position or you
have presented it badly. I most certainly do not think you are correct in
your understanding and description of evolution and how it happens. I am
trying to be as honest as I can be in representing your views. And I am
trying to clarify, not confuse the issues. If that effort is
misrepresentation, you need to explain how it is. From where I sit, it
isn't misrepresentation. Indeed, from where I sit, you are the one doing
the misrepresenting.
>
>> I could go on, but why bother. It is clear that Sean is asserting a
>> strawman version both of what is required of evolutionary change and of what
>> actually exists in nature in order to claim that, because his strawman
>> vision cannot occur by known evolutionary mechanisms, that evolution is
>> false. That is what creationists do.
>
> Nice try. You build a straw man to represent my position and then you
> claim that I built it. Good one . . . but pretty much transparent for
> anyone familiar with my posts.
I have presented my alternative to your strawman "large functionless gap"
model of evolution and pointed out why that vision is irrelevant (because
evolution did not and cannot work that way).
>
> Sean
>
Sean Pitman
snip
> We observe new mutations and new alleles all the time.
Yes we do, and they are all extremely simple as far as function is
concerned (i.e., antibiotic resistance - which is based on the
interference of pre-established molecular interaction and other
functions that are based on the potential of a single protein - such a
various single protein enzymes). No function that required multiple
proteins working together simultaneously has ever been demonstrated to
evolve de novo.
> In your own model of
> "all variation present from the start"
That's not my model at all. New variations do arise via mindless
evolutionary mechanisms, but these variations are universally simple.
There are significant constraints on what evolution can do.
Statistically, the evolution of all that we see around us is an
impossibility given only 4 or 5 billion years to work with.
> you have to generate many new alleles by
> recombination.
You have to generate these new alleles however you can, but the fact
of the matter is that you haven't done it or show how it might even be
possible on the level of complexity that is required to keep your pet
theory alive.
> How can you tell your recombined new alleles from alleles that
> happened due to mutation?
By demonstrating the evolution of new functions that were not there
before that are above the most simple levels of function that you keep
on trying to use to support yourself. What do you have? So far you
are very good at blowing smoke, but not much else of substance.
> The answer is that you can't, and you can't even
> begin to generate the genetic diversity that we see in humans let alone all the
> other species that have much more genetic variation than humans do.
Certainly I can. Humans are extremely similar to each other. The
diversity that we do see is not something that requires high levels of
new functions or alleles. The functional differences that do exist
between individuals, families and races of humans are no more than can
be explained with the same mechanisms that explain such things as
antibiotic resistance. You like to talk about MHC differences, but
these differences are not so much about function but about antigen
specificities. Single point mutations can rapidly change antigens so
that very specific antibodies would not be able to recognize them.
This have very little to do with any sort of pre-established
functional change however. No higher levels of function are evolved
here and such minimal changes can be realized in extremely short order
considering that each human child has sustained between 100 and 300
new mutations by the time it is born.
snip
> >Certainly new alleles can be made and added to the gene pool, but the
> >new functions that result are always of a very low complexity. As one
> >moves up the ladder of complexity, fewer and fewer example of the
> >evolution of novel functions can be found. I believe that the reason
> >for this phenomenon is that functions that are part of increasing
> >levels of complexity are surrounded by an exponentially expanding
> >ocean of neutral sequences in sequence space.
>
> This is bogus. Design an experiment that we can do you your lifetime to
> demonstrate that you could be correct.
This is like asking me to design an experiment to show that cows could
never jump over the moon. You cannot completely prove a negative.
That does not mean however that such a negative prediction is not a
true prediction. There is plenty of evidence to back up this
assertion. I have presented several points of evidence in this
thread. You haven't been able to it as of yet, as least no in a way
that I could understand. I have suggested various positive
experiments that would in fact disprove my position conclusively, such
as a demonstration of the evolution of a functional system that
required multiple proteins working together at the same time. You
have yet to provide such an experiment. Also, you have yet to detail
a falsifiable hypothesis or a genetic test/experiment that would
disprove your position. I have asked for such a falsifiable
experiment over and over again in this thread and all I get in
response are statements to the effect that no such experiments are
required from your position as your position is as clear as the nose
on my face. Well, that simply isn't so if you wish to claim to be on
the side of science. You must have something, some experimental test
that could in fact invalidate your position, if you wish your genetic
theory of evolution to be a scientific theory.
> You admit that we readily observe the
> "simple" things, but how long would it take to observe the complex things and
> how much would it cost in time and money.
I am betting you would run out of both time and money to before you
observed even a simple multi-protein system of function evolve in any
life form.
> If you can design such an experiment
> and want to carry it out for a few million years you can try and get someone to
> do it and fund it.
There you go again. You take comfort in the fact that your position
is not falsifiable. No one can disprove you absolutely because to do
so requires an eternity. Well my friend, that is a position that is
based on blind faith. If your position cannot be falsified this side
of eternity, then you are talking religion, not science.
> Demonstrate that such limits exist in the evolution of an ape like creature
> into a human. Where are these gaps and how did you determine that they exist?
> These mutations occurred over a period of at least 5 million years. Where are
> the impossible mutations?
As I have said before, the genomes of both humans and apes are so
complex that we simply do not know enough about either one to make any
such conclusive statements about relationship or common ancestry.
However, we do know much more about other organisms such as bacteria,
fruit flies, and the like. Based on the genetics and various levels
of function found in these more simple creatures, we can get a much
better idea about what the mindless process of evolution can and
cannot do. Evolution can do many very simple things, but as soon as
one steps up a few rungs on the ladder of complexity, evolution stalls
out. You cannot prove that I'm wrong either, even though this is in
fact a falsifiable statement. All you would have to do is show that
multi-protein systems of function can evolve de novo. No particular
teleological kind of system is required. Any such multi-protein
system will do. You see, it is the *level* of functional complexity
that is in question here, not any one function in particular. So,
what do you have? I'm waiting . . .
> Snip:
> I'm not going to bother with most of the rest, and AOL can't paste the whole
> piece so I'll have to quote the last bit.
>
> [Sean ends.]
> Sean
>
> P.S. Also, the finding of nested hierarchies does not necessarily
> support the idea of common descent via the mindless processes of
> evolution over the idea of ID based on the functional needs of
> different creatures in different environments.
>
> [Ron]: This is an example of Sean trying to put the clothes that we have
> demonstrated that our emperor is wearing on his emperor without justification.
> He never gets around to telling us how the clothes fit and what they look like
> on his emperor. It is really weird, on the one hand he claims that our emperor
> is naked, but he wants to borrow clothes from our emperor.
But I do explain how your supposed "clothes" can be easily explained
from my position. Nested hierarchies do not necessitate common
descent over common design with variations on certain themes being
functional variations according to differing needs of different life
forms in different environments. Explain to me how this cannot be.
Certainly if evolution were true, one would expect such nested
hierarchies to develop over time. However, if ID were true, one would
also expect for such nested patterns to be present since even human
designers employ conservation of design and variation of common design
themes depending upon different environments or particular needs.
Because of this potentiality where both theories could equally explain
the same observation, this observation cannot be used to conclusively
support one position over the other position.
So, you are still left with the task of coming up with some
falsifiable test and an actual way in which you could be proven wrong.
What result to what test in particular would prove your ideas about
genetic evolution wrong?
> [Sean continues]: Certainly, if these
> differences in similar proteins (like cytochrome c - for example) were
> not based on differences in the functional needs of different
> creatures (making the differences neutral), then random mutations
> would quickly destroy the nested differences that we find in different
> creatures. Evolutionary "clocks" that are based on such differences
> only work over the course of relatively short periods of time
> (thousands and not millions of generations).
>
> [Ron]: The tragedy is that these things were all worked out before Denton
> wrote his first bogus book in the mid 1980's and if Sean were to read a real
> science text on the subject he would realize that this argument is about as
> bogus as they can possibly get.
You can say that such things were worked out and that such arguments
as this are "bogus", but talk is cheep. Where is your evidence?
Also, it is misleading for you to compare my position with Denton's
position since Denton was clearly wrong in his views and I have said
so in this forum many times. I even say so on my website dealing with
the topic of genetic phylogeny. My position is nothing at all like
Denton's position, and you know it. But, I guess even you are not
above stooping to such deliberately deceptive levels.
You were all gung-ho about the obvious differences between Neandertals
and modern humans, but your arguments based on the work of those like
Krings et al., really didn't hold much water since they were
statistically inconclusive. I'm sure you will deny your many blunders
in the Neandertal thread, but you continually made exaggerated
statements that did your position more harm than good. I read many of
your views on this topic as well as the views of many others, to
include entire scientific articles on the topic (not just the
abstracts like you). As it turns out, I'm not the only one who thinks
that such phylogenetic tree building has a lot more to do with voodoo
than with science. These trees are so subjective that, beyond very
close relationships, common establishment of common descent is
certainly far from conclusive.
> The signal is expected to degrade because genes are finite. This is exactly
> what we observe.
The problem is that the signal degrades far faster than previously
realized so that the useful time frame is within tens of thousand, not
hundreds of thousands much less millions of years.
A "few million years" might also be a problem for the resolution of
mitochondrial D-loop sequences. Consider that the sequences used (two
of them) to estimate the time of the most recent common ancestor
(MRCA) between modern humans, Neandertals, and chimpanzees where each
less than 400 base pairs in length (333bp and 340bp respectively). The
mutation rate used by Krings et. al. was based on the a priori
assumption that modern humans split off from chimps some "4-5 million
years" ago. Based on this perhaps plausible, but indirect assumption,
a substitution rate of 0.94 x 10e-7 substitutions per site per year
per lineage, was determined. Using this rate, the MRCA between humans
and Neandertals was calculated to have lived about 465,000 years ago.
The MRCA of modern humans was calculated to have lived around 163,000
years ago. And, the MRCA of chimps and bonobos was calculated to have
lived around 2,844,000 years ago.
Krings' figures are all fine and good except if we happen to come
across a more direct measurement of mtDNA mutation rates. Consider the
following work by Thomas Parsons published in the journal Nature
Genetics:
"The rate and pattern of sequence substitutions in the mitochondrial
DNA (mtDNA) control region (CR) is of central importance to studies of
human evolution and to forensic identity testing. Here, we report a
direct measurement of the intergenerational substitution rate in the
human CR. We compared DNA sequences of two CR hypervariable segments
from close maternal relatives, from 134 independent mtDNA lineages
spanning 327 generational events. Ten substitutions were observed,
resulting in an empirical rate of 1/33 generations, or 2.5/site/Myr.
This is roughly twenty-fold higher than estimates derived from
phylogenetic analyses. This disparity cannot be accounted for simply
by substitutions at mutational hot spots, suggesting additional
factors that produce the discrepancy between very near-term and
long-term apparent rates of sequence divergence. The data also
indicate that extremely rapid segregation of CR sequence variants
between generations is common in humans, with a very small mtDNA
bottleneck. These results have implications for forensic applications
and studies of human evolution . . . The observed substitution rate
reported here is very high compared to rates inferred from
evolutionary studies. A wide range of CR substitution rates have been
derived from phylogenetic studies, spanning roughly
0.025-0.26/site/Myr, including confidence intervals. A study yielding
one of the faster estimates gave the substitution rate of the CR
hypervariable regions as 0.118 +- 0.031/site/Myr. Assuming a
generation time of 20 years, this corresponds to ~1/600 generations
and an age for the mtDNA MRCA of 133,000 y.a. Thus, our observation of
the substitution rate, 2.5/site/Myr, is roughly 20-fold higher than
would be predicted from phylogenetic analyses. Using our empirical
rate to calibrate the mtDNA molecular clock would result in an age of
the mtDNA MRCA of only ~6,500 y.a., clearly incompatible with the
known age of modern humans. Even acknowledging that the MRCA of mtDNA
may be younger than the MRCA of modern humans, it remains implausible
to explain the known geographic distribution of mtDNA sequence
variation by human migration that occurred only in the last ~6,500
years."
So, it seems as though more direct real-time measurements of mtDNA
mutation rates show a 20-fold higher mutation rate than that which was
used by Krings et al. What does this mean, besides the obvious? The
sequences studied by Krings totaled 673 base pairs in length.
According to the rate determined by Parsons, every single one of these
base pairs would have changed more than twice in one million years and
at least once in 400,000 years. Half of the base pairs would have
mutated at least once in 200,000 years. And yet, humans are separated
by only about 95 or so substitution differences from chimps? What is
wrong with this picture? Each substitution difference (in a sequence
some 673 base pairs in length) takes an average of 600 years to
achieve. Taking into account that each lineage would build up
substitution differences separately, in 600 years there would be
around two substitution difference between two lineages. This seems to
indicate that the common ancestor of humans and chimps lived some
30,000 years ago (not 4 to 8 million years ago as Krings et al.,
suggest - based on indirect methods). Modern humans, being separated
from each other by an average of only 10 substitutions (according to
Krings), appear to have a common ancestor living some 3,000 years ago.
Modern Humans and Neandertals are separated by an average of only 35
substitutions. This seems to indicate a common ancestor living only
some 10,000 years ago.
Parsons, Thomas J. A high observed substitution rate in the human
mitochondrial DNA control region, Nature Genetics vol. 15, April 1997,
pp. 363-367
Krings, M., Geisert, H., Schmitz, R., Krainitzki, H., and Pääbo, S.
DNA sequence of mitochondrial hypervariable region II from the
Neandertal type specimen. Evolution, Proc. Natl. Acad. Sci. USA, Vol.
96, pp. 5581-5585, May, 1999.
Krings M., Capelli C., Tschentscher F., Geisert H., Meyer S., von
Haeseler A. et al. (2000): A view of Neandertal genetic diversity.
Nature Genetics, 26:144-6.
http://www.pnas.org/cgi/content/full/96/10/5581
> People have spent a lot of time to tell us that once around
> 10% of the sites have been mutated the error of second hits at already mutated
> positions becomes significant and you have to have more sequence to overcome
> this error and get a reasonable answer.
Exactly . . .
> The laughable thing is that we observe
> this degredation in the signal and it matches theory.
If only . . . but it doesn't match the theory at all. The theory
theorizes far too much time than the actual evidence of mutation rates
will support.
> If multiple mutations
> were not happening randomly why would we observe this signal degredation?
I have no problem with signal degradation. That is my whole point.
What is your point?
> Why
> is it that a gene like hemoglobin is pretty much out the window in accuracy
> past around 200 million years.
Not 200 million years. Giving all the benefits of the doubt,
hemoglobin sequence analysis would be pretty much worthless well
before 100,000 years.
> It is pretty accurate in estimates involving
> mammals and their phylogenetic associations, but it becomes very inaccurate for
> things like fish where the radiations occurred over 300 million years ago.
I think that you are far too optimistic my friend.
> Why
> doesn't Sean's idea of similar lifestyles meaning more similar genetics not
> work for the different groups of fish?
Oh, it does work rather well. The more similar the fish and their
particular habitats, the more similar their sequencing of various
functional proteins such as cytochrome c, hemoglobin etc. If such
similarities and differences were not function based, fish, having
evolved way before mammals and humans evolved, would be very widely
divergent with possible if not probable overlaps with mammals and even
humans. Remember, modern fish are on the ends of the wheel spokes
just like humans and apes are. If their sequence differences were not
based on differences in functional needs, they would be neutral
differences. Such neutral differences would have become scrambled
randomly beyond any recognition or phylogenetic interpretation far
before now.
> Not only that but hemoglobin works just
> fine for within specific groups of fish like teleosts (guppies to marliin)
> because they evolved relatively recently, but predictably, not so well between
> the major groups of different types of fish that evolved hundreds of millions
> of years before the teleost radiation. So why would guppies have more similar
> DNA to a marlin than it would to a gar or ceolacanth?
Very recent divergence could theoretically be the result of common
descent. But, such a divergence would have had to happen very
recently indeed (a few thousand years ago at best) in order for such
neutral differences to mean anything. Also, fish such as modern
coelacanths would still have been mutating over the course of many
millions of years. They could be anywhere along the spectrum of
potential sequence space. So, at best, such sequence analysis doesn't
tell you much beyond the most recent of potential divergences.
> This has all be worked out and if Sean knew the data he would know that it is
> all consistent with biological evolution, but not with his stop gap "me too"
> models.
Actually, it is very consistent with my model as well, and much less
consistent with your model. And, I'm not the only one who thinks this
way.
In 1998 biologist Carl Woese, an early pioneer in constructing
rRNA-based phylogenetic trees, lamented the problem by writing: "No
consistent organismal phylogeny has emerged from the many individual
protein phylogenies so far produced. Phylogenetic incongruities can be
seen everywhere in the universal tree, from its root to the major
branchings within and among the various taxa to the makeup of the
primary groupings themselves."
Woese, Carl. 1998. The Universal Ancestor. Proceedings of the National
Academy of Sciences USA 95:6854-6859.
> [Sean continues]: More discussion of this concept at:
>
> http://naturalselection.0catch.com/Files/geneticphylogeny.html
>
> [Ron]: Yes, go to this web site and read the first home page bull pucky about
> the Emperor and no clothes. You will find the rest of the web site
> demonstrates that the scientific emperor has lots of clothes on, but Pitman
> doesn't like the style. He would drool over anything as good that he could
> hang on his emperor, but he doesn't have anything as good. What is really
> ridiculous is that he takes some of the scientific clothes and claims that they
> would fit his emperor, but he never gets around to seeing if they really fit
> (like the genetic similarity argument above). It is like, so what if you have
> these clothes, my emperor could wear the same clothes. Pitman's problem is
> that he can't demonstrate that his emperor has these clothes on, and science
> observes these clothes on their emperor. Such is the dishonest creationist
> mind set.
Again, saying stuff like this is far different from explaining how I
am wrong. You can say, "You are wrong" and "Your ideas are a bunch of
BS" all day long. But, that is just talk until you are able to explain
where I went wrong. Explain, exactly, how your phylogenetic "clothes"
bit exclusively on your emperor and not on mine. I am the first one
to admit that if the theory of evolution were true, we would certainly
expect to see such phylogenetic clusterings as we currently see (based
on differences in function). However, the actual evidence fits much
more easily with my position of recent intelligent creation of
distinct genotypic "kinds" or gene pools. You have to manipulate the
data too much and actually force it to fit with your position - and
still the fit really doesn't work all too well for you. No. I'm
afraid that you will have to come up with something that can actually
be tested in a falsifiable way before your position can gain any sort
of true scientific credibility.
> Pitman claims that honest creationist arguments exist, but he never gets around
> to presenting any.
This is your opinion for sure. But, what do you call my arguments in
this thread? They are honest. I really do think that I have
something, just as you think that you have something that is true. I
truly believe the "crap" that I'm presenting here. These are my
honest questions and I am presenting real evidence from the research
of evolutionists no less. There is also a lot of independent research
by creationist scientists that is very interesting - in many different
fields of science. I have given names and references to the works of
these scientists many times. I have also presented their ideas in
this forum many times. Just because you don't agree does not mean
that their ideas and work are not honest or relevant. I don't agree
with the conclusions of many evolutionary scientists, but that doesn't
mean that I think that they are dishonest or that their work is not
valuable.
> He has claimed several times that such arguments exist, but
> he has yet to present one that he has confirmed to be honest.
This is complete nonsense. I have presented many ideas, papers, and
discussions from those that I know to be honest and very intelligent
men and women. They may in fact be wrong or misguided, but I know
that they are honest and sincere in their work and ideas. I list many
of these on my website and know many of them personally. A few
examples of creationists whose work and ideas I have presented here
are:
Arthur V. Chadwick, Ph.D., University of Miami (with honors),
Sedimentology, Basinal Geology and Postdoctoral, Geology, University
of California
Walter J. Veith, B.Sc. (Hons), M.Sc. (cum laude), Ph.D., is a (full)
Professor at the University of the Western Cape (Republic of South
Africa) where he holds the chair of Zoology.
http://naturalselection.0catch.com/Files/methinksitislikeaweasel.html
http://www.amazingdiscoveries.org/walter.html
Anthony J. Zuccarelli, Ph.D., in biophysics from California Institute
of Technology. He is professor of microbiology and biochemistry at
Loma Linda University School of Medicine.
Bruce Wilcox, Ph.D., received his doctorate from the University of
Utah. He is Professor of Biochemistry in the School of Medicine at
Loma Linda University.
Leondard Brand, Ph.D., Cornell University, 1970 Professor of biology
and paleontology
http://naturalselection.0catch.com/Files/geologiccolumn.html
http://www.llu.edu/llu/grad/natsci/brand/leo.html
Of course, I have presented such names and references to the ideas of
these scientists and others in this forum, but you blow the same smoke
and make the same nonsense claims that these men really aren't
scientists or that they are so biased as to be absolutely crazy.
Well, I have to disagree with you until you can do more than a bunch
of hand waving and smoke blowing.
> Remember that
> when you read his web site. Pitman acknowledges that the creationist arguments
> are mostly bogus,
Many creationist arguments are bogus. However, just as many
evolutionist arguments are just as bogus and more so. It is just
amazing what some people will claim as "evidence" to support their
respective positions. Of course, you claim to be shocked at what I
think to be good evidence, but I am just as shocked by what you claim
to be so convincing. In any case, there are smart and honest
scientists on both sides of this issue. Biases, ignorance and agendas
are just as prevalent on both sides as well. Given these facts, we
must each consider the evidence for ourselves. You suggest that I get
my head out of creationist literature and start reading some works
from evolutionist scientists. I have been doing this for some time.
I actually read entire books and entire papers on evolution. You seem
to read mostly abstracts, not taking the time to look into much of
anything in more than a superficial way. I would suggest to you
though that you start trying to challenge what you believe. Actually
try to come up with something that could disprove your position in a
truly testable way. Also, try and read more than just the abstracts
of papers that you claim support your assertions in this way or that
way when they really do no such thing once you actually read the paper
itself.
> he just hasn't determined that the ones on his web site are
> bogus enough for him not to continue using them. He knows that once he checks
> them out they all have problems, but his answer is to not check them out.
No one has an infinite amount of time on this earth to learn and do
all that one might want wish. I still have much to learn and
anticipate growing in knowledge and understanding all along until I
die. To say that I do not "check out" the potential problems that you
and many others have presented to me is simply untrue, and you know
it. You know that I have done a great deal of reading on this topic,
to include many of your outlandish and crude posts as well as many of
the references that you have listed. If I wished to stick my head in
the sand and not consider potential problems or the opinions of those
who strongly disagree with me, I would be here talking to those such
as yourself, who are not often very pleasant or adult, much less
professional in their use of language and debating techniques.
> The real damning thing is that when pressed to present an honest creationist
> argument, he has never put forward something from his own web site.
Anyone who has ever gone through my website and who has followed my
posts in this forum in an even superficial way would know that you are
completely wrong here. Just about everything that I present here is
on my website. There are even links to these very threads on my
website for those who are interested in views opposite to mine. The
fact is that you know this is true and so it is you who are being
deliberately dishonest here. But hey, if that's the best you can come
up with . . .
> Ron Okimoto
Sean
zosdad
of subtle issues that the occasional more sophisticated
antievolutionist will raise.
And it must have taken all day to write...
Howard Hershey <hers...@indiana.edu> wrote in message news:<BB28B9E7.DC3D%hers...@indiana.edu>...
R. P. Johnson
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>...
>But I do explain how your supposed "clothes" can be easily explained
>from my position. Nested hierarchies do not necessitate common
>descent over common design with variations on certain themes being
>functional variations according to differing needs of different life
>forms in different environments. Explain to me how this cannot be.
>Certainly if evolution were true, one would expect such nested
>hierarchies to develop over time. However, if ID were true, one would
>also expect for such nested patterns to be present since even human
>designers employ conservation of design and variation of common design
>themes depending upon different environments or particular needs.
Untrue. Human designs show considerable cribbing from unrelated fields.
For instance, my car, which is clearly a product of the automotive
industry, has features taken from the music industry, the computer
industry, the furniture industry, the plastics industry, and probably many
others I can't think of now. The analogy in the living world would be
robins with tits or dolphins with gills. We don't see anything like that.
Your Intelligent Designer, Whoever He is, operates in a manner different
than the only designer we *know* exists.
>Because of this potentiality where both theories could equally explain
>the same observation, this observation cannot be used to conclusively
>support one position over the other position.
>
>So, you are still left with the task of coming up with some
>falsifiable test and an actual way in which you could be proven wrong.
> What result to what test in particular would prove your ideas about
>genetic evolution wrong?
See above.
--
R. P. Johnson rpjo...@mindspring.com
Von Smith
> I nominate this post by Howard Hershey as it addresses a large number
> of subtle issues that the occasional more sophisticated
> antievolutionist will raise.
>
> And it must have taken all day to write...
>
> Howard Hershey <hers...@indiana.edu> wrote in message news:<BB28B9E7.DC3D%hers...@indiana.edu>...
<the biggest snippage ever>
Seconded. The sad thing is, Dr. Pitman so stubbornly refuses to
acknowledge the point that Howard can write three POTM-quality posts
in as many weeks on essentially the same material, with no discernible
effect.
Von Smith
> poke...@aol.com (Pokemoto) wrote in message news:<20030628160031...@mb-m07.aol.com>...
>
> snip
> > We observe new mutations and new alleles all the time.
>
> Yes we do, and they are all extremely simple as far as function is
> concerned (i.e., antibiotic resistance - which is based on the
> interference of pre-established molecular interaction and other
> functions that are based on the potential of a single protein - such a
> various single protein enzymes). No function that required multiple
> proteins working together simultaneously has ever been demonstrated to
> evolve de novo.
>
I suppose that depends on what you mean by "de novo". If you mean
that all the components appeared individually from non-coding DNA, I'm
sure you are correct, but that is a fairly rare occurence even for the
evolution of single proteins, let alone multi-protein functions.
Fortunately, no one except you proposes such a thing as a normal
evolutionary mechanism.
However, functions requiring multiple proteins do seem to have
evolved. There is, of course, the pentachlorophenol cascade, which
AIUI evolved by adding a duplicate protein to an existing cascade,
followed by a mutation to the duplicate, and subsequent mutations
optimizing the new cascade for the new substrate.
"Molecular analysis of pentachlorophenol degradation", Orser CS, Lamae
CC, Biodegradation 5:277 Dec 1994
There's also the 2,4-dinitrotoluene pathway, which appears to involve
at least three novel enzyme activities:
Johnson GR, Jain RK, Spain JC. "Origins of the 2,4-dinitrotoluene
pathway."
J Bacteriol. 2002 Aug;184(15):4219-32.
ABSTRACT:
"The degradation of synthetic compounds requires bacteria to recruit
and adapt enzymes from pathways for naturally occurring compounds.
Previous work defined the steps in 2,4-dinitrotoluene (2,4-DNT)
metabolism through the ring fission reaction. The results presented
here characterize subsequent steps in the pathway that yield the
central metabolic intermediates pyruvate and propionyl coenzyme A
(CoA). The genes encoding the degradative pathway were identified
within a 27-kb region of DNA cloned from Burkholderia cepacia R34, a
strain that grows using 2,4-DNT as a sole carbon, energy, and nitrogen
source. Genes for the lower pathway in 2,4-DNT degradation were found
downstream from dntD, the gene encoding the extradiol ring fission
enzyme of the pathway. The region includes genes encoding a
CoA-dependent methylmalonate semialdehyde dehydrogenase (dntE), a
putative NADH-dependent dehydrogenase (ORF13), and a bifunctional
isomerase/hydrolase (dntG). Results from analysis of the gene
sequence, reverse transcriptase PCR, and enzyme assays indicated that
dntD dntE ORF13 dntG composes an operon that encodes the lower
pathway. Additional genes that were uncovered encode the 2,4-DNT
dioxygenase (dntAaAbAcAd), methylnitrocatechol monooxygenase (dntB), a
putative LysR-type transcriptional (ORF12) regulator, an intradiol
ring cleavage enzyme (ORF3), a maleylacetate reductase (ORF10), a
complete ABC transport complex (ORF5 to ORF8), a putative
methyl-accepting chemoreceptor protein (ORF11), and remnants from two
transposable elements. Some of the additional gene products might play
as-yet-undefined roles in 2,4-DNT degradation; others appear to remain
from recruitment of the neighboring genes. The presence of the
transposon remnants and vestigial genes suggests that the pathway for
2,4-DNT degradation evolved relatively recently because the extraneous
elements have not been eliminated from the region."
end quote
How is this not an example of recent evolution of a novel
multi-protein function?
Lenny Flank
<snip>
> You see, the theory of ID
<snip>
Er, what theory of ID would that be. What does this theory state.
What, according to this theory of ID, does the designer(s) do. What
mechanisms, according to this theory of ID, do the designer(s) use.
Where, according to this theory of ID, can we see any of these
mechanisms in action.
By the way, Dr, when your patients become sick, do you suggest that
they give up their secularist materialist naturalist biases, and begin
to search for non-material or non-naturalistic causes for their
illnesses--- such as, oh, evil spirits or witchcraft or black magic or
curses or The Evil Eye? Do you suggest non-secularist non-materialist
non-naturalist cures for their non-materialist non-natural illnesses
-- such as, oh, dancing around a campfire, chanting, shaking gourds
and rattles, or praying really really hard? Or do you just use
naturalistic materialistic antibiotics to cure their naturalistic
materialistic illnesses by killing their naturalistic materialistic
germs?
It seems to me that medicine is every bit as atheistic and
secularistic and naturalistic and materialistic as is evolutionary
biology, Dr . . . . Are you just a secular materialist naturalist
atheist at heart too, Dr?
===============================================
"There are no loose threads in the web of life"
Creation "Science" Debunked Website:
http://www.geocities.com/lflank
"DebunkCreation" email list at Yahoogroups:
http://groups.yahoo.com/group/DebunkCreation/join
Pokemoto
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>
>
>poke...@aol.com (Pokemoto) wrote in message
>news:<20030628160031...@mb-m07.aol.com>...
>
>snip
>> We observe new mutations and new alleles all the time.
>
>Yes we do, and they are all extremely simple as far as function is
>concerned (i.e., antibiotic resistance - which is based on the
>interference of pre-established molecular interaction and other
>functions that are based on the potential of a single protein - such a
>various single protein enzymes). No function that required multiple
>proteins working together simultaneously has ever been demonstrated to
>evolve de novo.
Since you admit that we don't expect to see more than that in someones lifetime
what is your beef. Where are your observations for your model? We have
evidence for ours, but you do not have a single thing as good as what you claim
isn't good enough. What does that say about your model if ours isn't any good?
>
>> In your own model of
>> "all variation present from the start"
>
>That's not my model at all.
You have stated that the variation that we observe in the current species was
in the originally created kinds. You have repeatedly used the dog example and
claimed that all the variation that we observe in domestic dogs is derived from
the original wolf kind that you expect to have been on the ark. Since they are
carnivores you would expect only a single pair to be responsible for all of
this variation.
New variations do arise via mindless
>evolutionary mechanisms, but these variations are universally simple.
>There are significant constraints on what evolution can do.
You have yet to demonstrate that these constraints exist. You need some
evidence, but you don't seem to understand what that is. Observation of
mutations and seeing new functions evolve is evidence. Very direct evidence.
You don't have to depend on these, but you have to acknowledge that these are
so much better than what you have backing up your model that it is simply
pathetic to consider your model as being scientifically valid.
>Statistically, the evolution of all that we see around us is an
>impossibility given only 4 or 5 billion years to work with.
If you could demonstrate that this is true you would truely become famous.
Where are your calculations and how have you backed them up? Since no one has
ever demonstrated that this is true what chance do you think that you have in
doing this?
>
>> you have to generate many new alleles by
>> recombination.
>
>You have to generate these new alleles however you can, but the fact
>of the matter is that you haven't done it or show how it might even be
>possible on the level of complexity that is required to keep your pet
>theory alive.
We have what we have. It is so much better than what you have that it is
laughable. Present one piece of evidence for your model that is better than
what you claim isn't good enough to keep our theory alive, and then tell us why
you still consider your model to be as viable as our scientific theory.
>
>> How can you tell your recombined new alleles from alleles that
>> happened due to mutation?
>
>By demonstrating the evolution of new functions that were not there
>before that are above the most simple levels of function that you keep
>on trying to use to support yourself. What do you have? So far you
>are very good at blowing smoke, but not much else of substance.
We have all of this evidence. We evolve new function from antibody sequences.
We observe the evolution of new function from existing proteins that did
different things. We can get enzymatic function from random sequences. You
acknowledge that we can do all of this, but it isn't enough for you. So why
isn't it valid to ask what do you have that is better? If our evidence isn't
good enough show us what kind of evidence you accept for your model.
>
>> The answer is that you can't, and you can't even
>> begin to generate the genetic diversity that we see in humans let alone all
>the
>> other species that have much more genetic variation than humans do.
>
>Certainly I can. Humans are extremely similar to each other. The
>diversity that we do see is not something that requires high levels of
>new functions or alleles. The functional differences that do exist
>between individuals, families and races of humans are no more than can
>be explained with the same mechanisms that explain such things as
>antibiotic resistance. You like to talk about MHC differences, but
>these differences are not so much about function but about antigen
>specificities. Single point mutations can rapidly change antigens so
>that very specific antibodies would not be able to recognize them.
>This have very little to do with any sort of pre-established
>functional change however. No higher levels of function are evolved
>here and such minimal changes can be realized in extremely short order
>considering that each human child has sustained between 100 and 300
>new mutations by the time it is born.
>
Do it, generate this diversity. Humans would be your easiest case so it is
your best chance. Remember the dog example. Just think about how hard it
would be to demonstrate that you can generate the diversity in dog kind when it
probably has over 5 times the genetic diversity found in humans in just the
North American population and it would have more if we hadn't driven them to
extinction in the US and only left them in Canada and Mexico. What about the
Wolf variation in Europe and Asia?
What about cat kind? Are Lions and Tigers the same kind? Just the lions in
Africa probably have much more genetic diversity than humans do and then you
had the European and Asian lions, but if you combine lions and tigers and then
claim only a single pair on the ark, you are in even bigger trouble. You don't
just have to account for humans. We acknowledge that humans went through a
recent bottle neck, but even then it is you that is blowing smoke. Account for
the MHC diversity. Remember to take into consideration that we share some of
these alleles with chimps and keep those around while generating all the
others. MHC are involved in antigen presentation and recognition by the
antibodies. The diversity is not generated like it is in antibodies.
>snip
>> >Certainly new alleles can be made and added to the gene pool, but the
>> >new functions that result are always of a very low complexity. As one
>> >moves up the ladder of complexity, fewer and fewer example of the
>> >evolution of novel functions can be found. I believe that the reason
>> >for this phenomenon is that functions that are part of increasing
>> >levels of complexity are surrounded by an exponentially expanding
>> >ocean of neutral sequences in sequence space.
>>
>> This is bogus. Design an experiment that we can do you your lifetime to
>> demonstrate that you could be correct.
>
>This is like asking me to design an experiment to show that cows could
>never jump over the moon. You cannot completely prove a negative.
>That does not mean however that such a negative prediction is not a
>true prediction. There is plenty of evidence to back up this
>assertion.
Knock, Knock, wake up. I threw this back in your face to make this point. I'm
glad you agree that your form of argument is bogus.
I have presented several points of evidence in this
>thread. You haven't been able to it as of yet, as least no in a way
>that I could understand. I have suggested various positive
>experiments that would in fact disprove my position conclusively, such
>as a demonstration of the evolution of a functional system that
>required multiple proteins working together at the same time. You
>have yet to provide such an experiment. Also, you have yet to detail
>a falsifiable hypothesis or a genetic test/experiment that would
>disprove your position. I have asked for such a falsifiable
>experiment over and over again in this thread and all I get in
>response are statements to the effect that no such experiments are
>required from your position as your position is as clear as the nose
>on my face. Well, that simply isn't so if you wish to claim to be on
>the side of science. You must have something, some experimental test
>that could in fact invalidate your position, if you wish your genetic
>theory of evolution to be a scientific theory.
ebg lactase function is a hexamer. This is your own example. The normal beta
gal is a tetramer.
A single amino acid substitution in the hemoglobin molecule causes a complex
interaction inside the blood cell that inhibits malaria parasite reproduction.
Something that we do not fully understand. The hemogolbin mutation doesn't do
this by itself, but the mutation is needed for the effect.
Whatever we put up it will not be enough. What do you have that is better?
What is good enough for you to support your model?
>
>> You admit that we readily observe the
>> "simple" things, but how long would it take to observe the complex things
>and
>> how much would it cost in time and money.
>
>I am betting you would run out of both time and money to before you
>observed even a simple multi-protein system of function evolve in any
>life form.
That is the point and why noone has ever gotten funding to do such a thing and
why you don't see any results in this area.
>
>> If you can design such an experiment
>> and want to carry it out for a few million years you can try and get
>someone to
>> do it and fund it.
>
>There you go again. You take comfort in the fact that your position
>is not falsifiable.
We have evidence supporting our position. It isn't our problem that you can't
demonstrate your point with equal evidence.
No one can disprove you absolutely because to do
>so requires an eternity. Well my friend, that is a position that is
>based on blind faith. If your position cannot be falsified this side
>of eternity, then you are talking religion, not science.
You admit that we have evidence. You just don't like it, but you don't have
anything as good. You ask for evidence that we can't produce because the
events you ask for are about as rare in the history of life as hens teeth.
Just count them up. How many times in the history of life did something like
you want to see evolve actually evolve? The flagellum evolved just once in the
history of life. Blood clotting for the major metazoans evolved just once. In
the 3 billion year history of life how many such events would you expect to
observe in 100 years? In a million years? We have the actual data that tells
us how rare these events are. What do you have?
>
>> Demonstrate that such limits exist in the evolution of an ape like creature
>> into a human. Where are these gaps and how did you determine that they
>exist?
>> These mutations occurred over a period of at least 5 million years. Where
>are
>> the impossible mutations?
>
>As I have said before, the genomes of both humans and apes are so
>complex that we simply do not know enough about either one to make any
>such conclusive statements about relationship or common ancestry.
>However, we do know much more about other organisms such as bacteria,
>fruit flies, and the like. Based on the genetics and various levels
>of function found in these more simple creatures, we can get a much
>better idea about what the mindless process of evolution can and
>cannot do. Evolution can do many very simple things, but as soon as
>one steps up a few rungs on the ladder of complexity, evolution stalls
>out.
It isn't just a few steps up the complexity. You know that we already observe
the changes up a few steps in complexity. What you want is full blown system
evolution in less than a geologic eyeblink. What a joke.
You cannot prove that I'm wrong either, even though this is in
>fact a falsifiable statement. All you would have to do is show that
>multi-protein systems of function can evolve de novo. No particular
>teleological kind of system is required. Any such multi-protein
>system will do. You see, it is the *level* of functional complexity
>that is in question here, not any one function in particular. So,
>what do you have? I'm waiting . . .
How many proteins would it take in such a system to be complex enough for you?
Give a specific number and a reason for this number. Whatever we present it is
never enough.
No the explanation is not equal. You admit that common descent would create
this pattern. It would be expected to create this pattern because it is
descent with modification. You claim that ID can explain this, but you never
get around to saying how the ID mechanism really explains the data. You just
claim that parts could be reused, but this only explains some gross similarity.
The fact is that the similarity is nested. I know that you refuse to
understand what nesting is and how it makes your ID explanation worthless, but
you should try. Humans also do mixing and matching and this seems to be as
common as reusing something. So why aren't lifeforms mixed up. Why is it that
most of what we observe in nature is what we expect from common descent and not
mixing? Why do ID advocates like Dembski and Behe claim that common descent is
likely a fact of nature? Can it have anything to do with the fact that it is
only through common descent that the designer could have generated what we
observe in nature?
ID also could have done it some other way. Designed life could have no
relationship between "kinds." Why is there such a relationship and why is it
nested?
>
>So, you are still left with the task of coming up with some
>falsifiable test and an actual way in which you could be proven wrong.
> What result to what test in particular would prove your ideas about
>genetic evolution wrong?
I've gone over this before in other posts. The test have been done and
biological evolution passed. We can't redo the tests and get a different
answer. The genetic evidence could have indicated individual created kinds,
but it did not. The molecular evidence could have had no evidence of
similarity or nesting, but it showed similarity and nesting. What more do you
want? Just because you can't think of anymore tests doesn't mean that we
didn't test biological evolution. I hate to tell you this, but scientific
theories have to pass their tests or they fail and are replaced by better ones.
>
>> [Sean continues]: Certainly, if these
>> differences in similar proteins (like cytochrome c - for example) were
>> not based on differences in the functional needs of different
>> creatures (making the differences neutral), then random mutations
>> would quickly destroy the nested differences that we find in different
>> creatures. Evolutionary "clocks" that are based on such differences
>> only work over the course of relatively short periods of time
>> (thousands and not millions of generations).
>>
>> [Ron]: The tragedy is that these things were all worked out before Denton
>> wrote his first bogus book in the mid 1980's and if Sean were to read a
>real
>> science text on the subject he would realize that this argument is about as
>> bogus as they can possibly get.
>
>You can say that such things were worked out and that such arguments
>as this are "bogus", but talk is cheep. Where is your evidence?
>Also, it is misleading for you to compare my position with Denton's
>position since Denton was clearly wrong in his views and I have said
>so in this forum many times. I even say so on my website dealing with
>the topic of genetic phylogeny. My position is nothing at all like
>Denton's position, and you know it. But, I guess even you are not
>above stooping to such deliberately deceptive levels.
I used the Denton example because he has made a complete turn around, and he
should have never written the bogus arguments in his book. He knows that now,
but you do not. He blew it over 15 years ago and there should be no excuse for
you blowing it today. I did not say that your argument was the same as
Denton's main argument. I can't recall if he made this stupid of an argument.
You may think on that before you continue. He made some really stupid
mistakes, but claiming that we don't see the expected degeneration in signal
wasn't one of them that I recall. How can you claim that this signal
degeneration is a problem for us when we observe it in the molecules that we
use for our analysis and we have developed methods to compensate for it? This
argument is a crock, and you are really stupid for pursuing it. The signal
degeneration is not only observed, but it creates problems that we have to deal
with in evaluation of the data. You are really an idiot for trying to make
some claim in your favor about this topic.
>
>You were all gung-ho about the obvious differences between Neandertals
>and modern humans, but your arguments based on the work of those like
>Krings et al., really didn't hold much water since they were
>statistically inconclusive. I'm sure you will deny your many blunders
>in the Neandertal thread, but you continually made exaggerated
>statements that did your position more harm than good. I read many of
>your views on this topic as well as the views of many others, to
>include entire scientific articles on the topic (not just the
>abstracts like you). As it turns out, I'm not the only one who thinks
>that such phylogenetic tree building has a lot more to do with voodoo
>than with science. These trees are so subjective that, beyond very
>close relationships, common establishment of common descent is
>certainly far from conclusive.
What was the most likely conclusion from every study involving the Neandertals?
I want to see if you are honest enough to admit the most likely conclusion of
each of the papers even those critical of Krings. Is the most likely
conclusion that Krings and the others are most likely correct? What is the
most likely phylogenetic tree in all studies?
>
>> The signal is expected to degrade because genes are finite. This is
>exactly
>> what we observe.
>
>The problem is that the signal degrades far faster than previously
>realized so that the useful time frame is within tens of thousand, not
>hundreds of thousands much less millions of years.
What was your point about signal degeneration?
>
>A "few million years" might also be a problem for the resolution of
>mitochondrial D-loop sequences. Consider that the sequences used (two
>of them) to estimate the time of the most recent common ancestor
>(MRCA) between modern humans, Neandertals, and chimpanzees where each
>less than 400 base pairs in length (333bp and 340bp respectively). The
>mutation rate used by Krings et. al. was based on the a priori
>assumption that modern humans split off from chimps some "4-5 million
>years" ago. Based on this perhaps plausible, but indirect assumption,
>a substitution rate of 0.94 x 10e-7 substitutions per site per year
>per lineage, was determined. Using this rate, the MRCA between humans
>and Neandertals was calculated to have lived about 465,000 years ago.
>The MRCA of modern humans was calculated to have lived around 163,000
>years ago. And, the MRCA of chimps and bonobos was calculated to have
>lived around 2,844,000 years ago.
The signal degrades in the hypervariable region of the mitochondrial DNA much
faster than for just about any other sequence known. That is why we use it for
within species evaluations. The chimp outgroup isn't a good one for the hyper
variable region (5 million years is too distant and a lot of the sites have
probably been hit more than twice), but it is the only one that we have left.
If we had a Homo erectus that would be much better. The researchers are stuck
using what they have.
I have told you before, but you may not have seen the posts. I can't even
remember what thread it is in. I think it is in the one for the emperors new
clothes. Your mitochondrial argument is bogus. It is based on the
misrepresentation of the Cann et al paper and the Parsons paper. It ranks as
one of the most dishonest slock pieces I have seen. In the case of the Cann
and Wilson paper you try and claim that this paper was shown to be false in its
conclusions, while you heap praises on the Parsons paper. The exact opposite
is true. The Cann and Wilson paper was vindicated by later studies. The
Parsons paper was never verified. Not a single researcher got close to
Parsons' estimate. If it had been verified the Krings papers would have had to
use those numbers in calculating their divergence estimates. Have you ever
thought about that?
Cold fusion was published in a decent journal, but it wasn't verified either.
You even claim that the Cann paper was wrong, so why didn't you check out the
Parsons' paper? You are either a rube that got sucked into some other
creationists scam or you haven't given the literature a fair hearing and you
know that you are probably wrong, but would rather lie to people about it. If
you don't want to be fooled into doing this sort of stupid thing again you can
do a Citation Index search of the Cann and Parsons papers and see what science
really concludes about these papers. Your web page dishonestly misrepresents
these papers. What are you going to do about it?
This is getting too long and I'll have to continue.
Ron Okimoto
Pokemoto
>Parsons, Thomas J. A high observed substitution rate in the human
>mitochondrial DNA control region, Nature Genetics vol. 15, April 1997,
>pp. 363-367
>
>Krings, M., Geisert, H., Schmitz, R., Krainitzki, H., and Pääbo, S.
>DNA sequence of mitochondrial hypervariable region II from the
>Neandertal type specimen. Evolution, Proc. Natl. Acad. Sci. USA, Vol.
>96, pp. 5581-5585, May, 1999.
>
>Krings M., Capelli C., Tschentscher F., Geisert H., Meyer S., von
>Haeseler A. et al. (2000): A view of Neandertal genetic diversity.
>Nature Genetics, 26:144-6.
>
>http://www.pnas.org/cgi/content/full/96/10/5581
>
>
>> People have spent a lot of time to tell us that once around
>> 10% of the sites have been mutated the error of second hits at already
>mutated
>> positions becomes significant and you have to have more sequence to
>overcome
>> this error and get a reasonable answer.
>
>Exactly . . .
So what is your beef about degeneration of signal? Since we observe it and we
expect to observe it, what was your problem? I told you it was a stupid
argument.
>
>> The laughable thing is that we observe
>> this degredation in the signal and it matches theory.
>
>If only . . . but it doesn't match the theory at all. The theory
>theorizes far too much time than the actual evidence of mutation rates
>will support.
Demonstrate that this could be true.
>
>> If multiple mutations
>> were not happening randomly why would we observe this signal degredation?
>
>I have no problem with signal degradation. That is my whole point.
>What is your point?
So you've given up and are trying to shift the goal posts.
>
>> Why
>> is it that a gene like hemoglobin is pretty much out the window in accuracy
>> past around 200 million years.
>
>Not 200 million years. Giving all the benefits of the doubt,
>hemoglobin sequence analysis would be pretty much worthless well
>before 100,000 years.
Why would the hemoglobin sequence evolve as fast as the hypervariable region of
the mitochondrial DNA?
Don't you know that nuclear genes evolve much more slowly than mitochondrial
sequences? Don't you know that the hyper variable region is called the hyper
variable region because it is the fastest evolving sequence in the
mitochondrial DNA. Don't you know that it has already been established that
third positions of the codons that are pretty much free to change are saturated
in a few million years (for mitochondrial sequence, but 10s of millions for
nuclear genes), but first and second condon postions that result in amino acid
substitutions hold phylogenetic information much longer? You claim to have
read a book on evolution. What book was it and did it cover molecular
evolution?
>
>> It is pretty accurate in estimates involving
>> mammals and their phylogenetic associations, but it becomes very inaccurate
>for
>> things like fish where the radiations occurred over 300 million years ago.
>
>I think that you are far too optimistic my friend.
Creationist are fond of citing the study linking birds to alligators and
turtles using the hemoglobin sequence. It isn't very accurate for this, but
there is still enough of a signal left for the researchers to claim that it was
likely that birds were more closely related to alligators than to lizards and
this divergence is out around 300 million years. You ought to keep up with
your own bogus creationist literature. Why would a warm blooded bird have a
hemoglobin sequence more similar to a cold blooded reptile than another warm
blooded animal like a mammal? Why would the molecular phylogeny match the
morphological phylogeny linking alligators and turtles with birds?
>
>> Why
>> doesn't Sean's idea of similar lifestyles meaning more similar genetics not
>> work for the different groups of fish?
>
>Oh, it does work rather well. The more similar the fish and their
>particular habitats, the more similar their sequencing of various
>functional proteins such as cytochrome c, hemoglobin etc. If such
>similarities and differences were not function based, fish, having
>evolved way before mammals and humans evolved, would be very widely
>divergent with possible if not probable overlaps with mammals and even
>humans. Remember, modern fish are on the ends of the wheel spokes
>just like humans and apes are. If their sequence differences were not
>based on differences in functional needs, they would be neutral
>differences. Such neutral differences would have become scrambled
>randomly beyond any recognition or phylogenetic interpretation far
>before now.
Demonstrate that it is linked to environment and lifestyle rather than common
descent. Why don't fresh water fish have more similar molecules than some
fresh water fish have with salt water fish. Some predator fish have with
vegetarians. Why don't deep see teleosts have more similar genes to a deep sea
coelacanth than they do to other teleosts? You can't seem to back up your
assertions.
>
>> Not only that but hemoglobin works just
>> fine for within specific groups of fish like teleosts (guppies to marliin)
>> because they evolved relatively recently, but predictably, not so well
>between
>> the major groups of different types of fish that evolved hundreds of
>millions
>> of years before the teleost radiation. So why would guppies have more
>similar
>> DNA to a marlin than it would to a gar or ceolacanth?
>
>Very recent divergence could theoretically be the result of common
>descent. But, such a divergence would have had to happen very
>recently indeed (a few thousand years ago at best) in order for such
>neutral differences to mean anything. Also, fish such as modern
>coelacanths would still have been mutating over the course of many
>millions of years. They could be anywhere along the spectrum of
>potential sequence space. So, at best, such sequence analysis doesn't
>tell you much beyond the most recent of potential divergences.
They cannot be anywhere in the spectrum of diversity because they are
constrained by common descent. They can converge on similar sequences, but
they have to undo all the previous evolution of their lineage to do it. It is
possible but not very likely. You calculate how likely this is, and tell us if
we should have observed such an overlap in the few thousand species that we
have tested. Remember that the sequence space for existing cyt c sequences was
was estimated to be 10^45. What is the probability of convergence?
Are you claiming that the teleost species can be accounted for by recent
evolution? How long would it take a guppy to evolve into a marlin or a giant
tuna?
>
>> This has all be worked out and if Sean knew the data he would know that it
>is
>> all consistent with biological evolution, but not with his stop gap "me
>too"
>> models.
>
>Actually, it is very consistent with my model as well, and much less
>consistent with your model. And, I'm not the only one who thinks this
>way.
>
>In 1998 biologist Carl Woese, an early pioneer in constructing
>rRNA-based phylogenetic trees, lamented the problem by writing: "No
>consistent organismal phylogeny has emerged from the many individual
>protein phylogenies so far produced. Phylogenetic incongruities can be
>seen everywhere in the universal tree, from its root to the major
>branchings within and among the various taxa to the makeup of the
>primary groupings themselves."
>
>Woese, Carl. 1998. The Universal Ancestor. Proceedings of the National
>Academy of Sciences USA 95:6854-6859.
This is a dishonest misrepresentation of the Woese quote. He is talking about
the base of the tree of life and the major groups eukaryotes, eubacteria and
archebacteria. There was apparently a lot of horizontal mixing of genetics
between the exiting lifeforms when these three groups were evolving billions of
years ago, but this quote doesn't apply to humans, mammals, vertebrates or
anything that evolved within the last billion years. Why would you even try
and pull something as stupid as trying to use this quote in this way? Does the
Woese quote apply to fish or the relationships of known vertebrates? You
should be ashamed of yourself.
>
>
>> [Sean continues]: More discussion of this concept at:
>>
>> http://naturalselection.0catch.com/Files/geneticphylogeny.html
>>
>> [Ron]: Yes, go to this web site and read the first home page bull pucky
>about
>> the Emperor and no clothes. You will find the rest of the web site
>> demonstrates that the scientific emperor has lots of clothes on, but Pitman
>> doesn't like the style. He would drool over anything as good that he could
>> hang on his emperor, but he doesn't have anything as good. What is really
>> ridiculous is that he takes some of the scientific clothes and claims that
>they
>> would fit his emperor, but he never gets around to seeing if they really
>fit
>> (like the genetic similarity argument above). It is like, so what if you
>have
>> these clothes, my emperor could wear the same clothes. Pitman's problem is
>> that he can't demonstrate that his emperor has these clothes on, and
>science
>> observes these clothes on their emperor. Such is the dishonest creationist
>> mind set.
>
>Again, saying stuff like this is far different from explaining how I
>am wrong. You can say, "You are wrong" and "Your ideas are a bunch of
>BS" all day long. But, that is just talk until you are able to explain
>where I went wrong. Explain, exactly, how your phylogenetic "clothes"
>bit exclusively on your emperor and not on mine.
You have to create birds before land animals. The genetic relationships
between birds and terrestrial animals falsifies this. Your designer could not
have created birds before other terrestrial vertebrates. The nesting of the
gene sequences tells us that amphibians came first and then reptiles and then
birds and mammals. The Bible has flying creatures created first and you can't
defend this using the current genetic templates. If this part of the Bible is
in error what other parts are in error and how do you determine this?
I am the first one
>to admit that if the theory of evolution were true, we would certainly
>expect to see such phylogenetic clusterings as we currently see (based
>on differences in function). However, the actual evidence fits much
>more easily with my position of recent intelligent creation of
>distinct genotypic "kinds" or gene pools.
No it doesn't. Explain marsupial moles and eutherian moles. Why do they
inhabit similar environments and have similar morphologies and yet still have
the nesting in marsupials and eutherians.
You have to manipulate the
>data too much and actually force it to fit with your position - and
>still the fit really doesn't work all too well for you. No. I'm
>afraid that you will have to come up with something that can actually
>be tested in a falsifiable way before your position can gain any sort
>of true scientific credibility.
This is laughable, who is trying to force the data to fit their model. Explain
how birds could have been created before other terrestrial animals.
>
>> Pitman claims that honest creationist arguments exist, but he never gets
>around
>> to presenting any.
>
>This is your opinion for sure. But, what do you call my arguments in
>this thread? They are honest. I really do think that I have
>something, just as you think that you have something that is true. I
>truly believe the "crap" that I'm presenting here.
Just because you truely believe the "crap" doesn't make it less "crap" or even
honest. The guy that fooled you into believing this crap may have been just as
much a fool as you, but someone had to know better. When arguments get refuted
and still are handed down as being valid this is dishonest.
These are my
>honest questions and I am presenting real evidence from the research
>of evolutionists no less. There is also a lot of independent research
>by creationist scientists that is very interesting - in many different
>fields of science. I have given names and references to the works of
>these scientists many times. I have also presented their ideas in
>this forum many times. Just because you don't agree does not mean
>that their ideas and work are not honest or relevant. I don't agree
>with the conclusions of many evolutionary scientists, but that doesn't
>mean that I think that they are dishonest or that their work is not
>valuable.
Just because you don't know that the argument is dishonest doesn't make it
honest or valid. We have been through this before. Stupid honest arguments
are still stupid. You know that everything that you have been able to confirm
to an acceptable degree has turned out to be bogus. Yet you still use
creationist sources. How honest is this? Why don't you state this the very
first thing on your web page? Just present one honest argument that you have
found to be valid.
>
>> He has claimed several times that such arguments exist, but
>> he has yet to present one that he has confirmed to be honest.
>
>This is complete nonsense. I have presented many ideas, papers, and
>discussions from those that I know to be honest and very intelligent
>men and women. They may in fact be wrong or misguided, but I know
>that they are honest and sincere in their work and ideas. I list many
>of these on my website and know many of them personally. A few
>examples of creationists whose work and ideas I have presented here
>are:
We don't care about people that are honestly wrong. We want your arguments
that are honestly correct.
>
>Arthur V. Chadwick, Ph.D., University of Miami (with honors),
>Sedimentology, Basinal Geology and Postdoctoral, Geology, University
>of California
>
>Walter J. Veith, B.Sc. (Hons), M.Sc. (cum laude), Ph.D., is a (full)
>Professor at the University of the Western Cape (Republic of South
>Africa) where he holds the chair of Zoology.
>http://naturalselection.0catch.com/Files/methinksitislikeaweasel.html
>http://www.amazingdiscoveries.org/walter.html
>
>Anthony J. Zuccarelli, Ph.D., in biophysics from California Institute
>of Technology. He is professor of microbiology and biochemistry at
>Loma Linda University School of Medicine.
>
>Bruce Wilcox, Ph.D., received his doctorate from the University of
>Utah. He is Professor of Biochemistry in the School of Medicine at
>Loma Linda University.
>
>Leondard Brand, Ph.D., Cornell University, 1970 Professor of biology
>and paleontology
>http://naturalselection.0catch.com/Files/geologiccolumn.html
>http://www.llu.edu/llu/grad/natsci/brand/leo.html
State what creationist arguments that these people have demonstrated to be
valid and honest. Just giving names is not giving honest arguments. Read the
Talk.origins archive material on the Arkansas balanced treatment law and Judge
Overtons decision. If you seach the site using "Overton" you will find links
to articles on the partial transcripts of the testamony of "honest creation
scientists." They all admitted that they didn't have any evidence backing up
the arguments that they put forward, but they believed that they could still
put forward such arguments. They were honest, but it just told everyone that
their arguments were dishonest if they didn't tell anyone the truth about
whether they could really back up their assertions. They knew for a fact that
they couldn't back up their arguments and had to admit this in court under
oath. These guys were honest enough to tell the truth about what they had
backing up their arguments, but were their arguments honest or valid?
>
>Of course, I have presented such names and references to the ideas of
>these scientists and others in this forum, but you blow the same smoke
>and make the same nonsense claims that these men really aren't
>scientists or that they are so biased as to be absolutely crazy.
>Well, I have to disagree with you until you can do more than a bunch
>of hand waving and smoke blowing.
I never claimed that these guys could not be scientists, just that they had no
honest creationist arguments. If you don't know the difference, I can't help
you. Present their honest creationist arguments.
>
>> Remember that
>> when you read his web site. Pitman acknowledges that the creationist
>arguments
>> are mostly bogus,
>
>Many creationist arguments are bogus. However, just as many
>evolutionist arguments are just as bogus and more so. It is just
>amazing what some people will claim as "evidence" to support their
>respective positions. Of course, you claim to be shocked at what I
>think to be good evidence, but I am just as shocked by what you claim
>to be so convincing. In any case, there are smart and honest
>scientists on both sides of this issue. Biases, ignorance and agendas
>are just as prevalent on both sides as well.
Demonstrate that this is true. Present two or three of your best arguments for
your belief and then compare it to our arguments. How far down the line of our
arguments before you get to something as bad as what you have to use? Pretty
far down the line isn't it.
Given these facts, we
>must each consider the evidence for ourselves. You suggest that I get
>my head out of creationist literature and start reading some works
>from evolutionist scientists. I have been doing this for some time.
>I actually read entire books and entire papers on evolution. You seem
>to read mostly abstracts, not taking the time to look into much of
>anything in more than a superficial way.
I've used the abstract to the Hall work because I have no interest in this work
and you never present any reason for me to do more than that. Why should I
spend the time to look into the Hall work when you don't give any reason that I
should? Your own quotes are enough to tell me that you are full of baloney.
It is up to you to defend Hall's work because you are the one putting it
forward. If I can counter just by looking at abstracts you have to counter
with real data and experimental protocols, but you never do this. If you had
presented experimental protocols that I thought were suspect I would have
looked up the papers, but the only protocols that you ever presented about the
color change assay supported my assertions.
I would suggest to you
>though that you start trying to challenge what you believe. Actually
>try to come up with something that could disprove your position in a
>truly testable way.
The genetic evidence could have done this, but it did not. Morphological data
could have done this, but it did not. The fossil evidence could have done
this, but it did not. We could observe species popping out of the vacuum, but
we observe new species evolving from existing species. We have never observed
a creation event from nothing. If we did observe this to happen biological
evolution by natural mechanisms would be thrown into question. We can't change
the way things are. The fact is that the evidence supports biological
evolution. It has been tested and it passed. No one expects any data to show
up that would disprove the theory at this time because there is so much
evidence in its favor that practically no one expect data to come up that would
change the current explanation. This isn't a problem for us it is a problem
for you.
Also, try and read more than just the abstracts
>of papers that you claim support your assertions in this way or that
>way when they really do no such thing once you actually read the paper
>itself.
I am very well versed in my field, but I have no interest in Hall's work. My
thesis was on molecular evolution. That is why I know that your molecular
arguments are bogus. I've worked with mitochondrial DNA for a very long time.
You should learn more about mitochondrial DNA, so that you won't be accused of
being dishonest in your use of the Cann and Parsons papers. A Citation Index
search will confirm that I am correct and you are bogus.
>
>> he just hasn't determined that the ones on his web site are
>> bogus enough for him not to continue using them. He knows that once he
>checks
>> them out they all have problems, but his answer is to not check them out.
>
>No one has an infinite amount of time on this earth to learn and do
>all that one might want wish. I still have much to learn and
>anticipate growing in knowledge and understanding all along until I
>die. To say that I do not "check out" the potential problems that you
>and many others have presented to me is simply untrue, and you know
>it. You know that I have done a great deal of reading on this topic,
>to include many of your outlandish and crude posts
State one thing that is crude about my posts. When something is bullshit I
call it bullshit. When something is dishonest I call it dishonest.
Demonstrate that I've been wrong in these evaluations.
as well as many of
>the references that you have listed. If I wished to stick my head in
>the sand and not consider potential problems or the opinions of those
>who strongly disagree with me, I would be here talking to those such
>as yourself, who are not often very pleasant or adult, much less
>professional in their use of language and debating techniques.
Demonstrate that you can learn something. Apply the nested data to your model.
Don't claim that it can fit, really try and make it fit. You can't do it.
Check out the Cann and Parsons papers that you use for your bogus mitochondrial
argument on your web page. Do this for all your web topics, and what do you
expect to find?
>
>> The real damning thing is that when pressed to present an honest
>creationist
>> argument, he has never put forward something from his own web site.
>
>Anyone who has ever gone through my website and who has followed my
>posts in this forum in an even superficial way would know that you are
>completely wrong here. Just about everything that I present here is
>on my website. There are even links to these very threads on my
>website for those who are interested in views opposite to mine. The
>fact is that you know this is true and so it is you who are being
>deliberately dishonest here. But hey, if that's the best you can come
>up with . . .
When asked to present an honest creationist argument you have never present
your own work. I stand by that statement. You now claim that your arguments
are honest because you really believe them even if they are "crap", but what
kind of honest arguments are those? They have zero value to science or to the
honest evaluation of biological evolution. Stupid arguments have no value.
Wrong arguments are just deceptive. Using garbage that you should have known
better like the mitochondrial argument is just bogus and dishonest.
Ron Okimoto
Stuart
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03062...@posting.google.com>...
>
>
> <snip>
> > You see, the theory of ID
> <snip>
>
>
>
> Er, what theory of ID would that be. What does this theory state.
> What, according to this theory of ID, does the designer(s) do.
Well, as far as I can tell, they get frightfully stoned.
Stuart
Howard Hershey
seanpi...@naturalselection.0catch.com wrote on 6/25/03 7:20 PM:
> Howard Hershey <hers...@indiana.edu> wrote in message
> news:<BB1DD0E6.C783%hers...@indiana.edu>...
I wrote a very long reply to this, which somehow got into a malfunctioning
transporter and all those electrons disappeared into the aether. So this
time, I will greatly shorten my response and just make a few points.
>
>> This is a summary of the argument that Sean is making, as I see it, and why
>> I think the core features of his argument is based on a strawman version of
>> nature, which includes a whopping dose of teleological thinking (the
>> assumption that a current function was an intended and necessary end goal),
>
> As I have said multiple times before, I do not make this
> "teleological" assumption at all.
This merely shows that you have not even thought through your own argument.
You have proposed a creationist argument to explain a function, and
creationist arguments are *always* teleological in nature.
Specifically, the creationist argument is that structure x was designed by
intelligent agent z in order to perform the function y; that is the
creationist explanation for the existence of structure x. That is a
teleological explanation which necessarily is ahistorical, for if structure
x arose through a historical process, the necessity of a designer
disappears. This argument implies that structure x was specifically
developed for the end or ultimate (hence teleological) purpose of performing
function y and that the reason x has the structure it does is that, in the
eyes of the designer, such a structure performs the end or goal function to
the designer's satisfaction.
Your false strawman version of how you think evolution works, via a
completely random walk of structure across a large chain of intermediates
that have either no function at all or no selectable difference in function
from the original preceding structure (your argument is unclear on that
point). That is, you posit an evolutionary explanation which winds up with
a structure which is as isolated and unique (set as it is as an island of
functionality (for function x) in a sea of indistinguishable variants that
have NO selectable function x whatsoever). This isolated structure, which
is the rare or sole structure able to perform function y, is the end or goal
of your (strawman) 'evolutionary' explanation. It is an end or terminal
goal because it is as difficult to change it or modify it to any other
functionality as it was to generate its current functionality. To change
function would require re-crossing a vast void of functionless intermediates
(if there were intermediates with different or modified functionality to
which the structure could move, the reverse pathway would also be
available). In other words, you are positing the same teleological
relationship between structure and function (that the end or terminal goal
you posited in the creationist alternative was *the* only structure and
*the* only function which was aimed for). You merely asserted (falsely)
that evolution reaches that function and structure by a completely random
walk with no selection or intermediate or alternative functionality.
Evolution (the real theory, not your strawman) is agressively
non-teleological. Not only does every intermediate in the pathway have to
be functional and (generally) useful in its own right (although it can be
and often is redundantly useful), but the *current* function and structure
is not considered a terminal or end structure. It is merely the *current*
function to which the structure is put to use. This allows that structure
to then be modified to different uses even in current organisms. For
example, there are bacteria whose flagella are not used for motility but are
still used (and useful) for protein export.
The explanation you ignore is the non-teleological one, where intermediate
steps do have utility in their own right (but not necessarily the utility
you consider to have been the teleological goal of your strawman
evolution/creation) and the *current* structure is considered to be merely
the structure that best optimizes reproductive success in a local condition
by emphasizing a particular function.
[snip]
>
> You and other evolutionists, who are actually considering this
> problem, suggest that the neutral ocean is not nearly as big as I am
> proposing. You are suggesting that there are a lot more functional
> paths between these potential islands.
Actually, we are proposing that most of the observed evidence doesn't
support your idea of functions being derived by proteins that isolate
islands of functionality, but rather that most functions occur by
modification of pre-existing proteins forming island chains closely
associated with each other (related by descent) rather than islands that are
isolated in a void.
> You do not think that one path
> in particular can be detailed, since this would be "teleological",
Actually, evolution proposes that one path *did* occur, but we cannot always
tell which of several possible pathways did. And, with the evidence that is
available, it certainly seems reasonable to think that the evolution of
bacterial flagella for example, likely arose by modification of a protein
export device. Teleology comes in when one assumes that flagella was *the*
end goal of the process, as you do. It wasn't. And flagellar motility is
not an end goal even today. It is a structure that performs a function that
has *current* utility to some kinds of bacteria in some conditions. Period.
> but
> you believe that there is very good evidence for the existence of
> common pathways none-the-less.
Evidence of step-wise pathways with intermediates that have independent
functional utility (not necessarily the end function) that can be selected
for (not necessarily selected for the end function) in some conditions.
> Of course, this is a must for your
> position. Without these supposed paths, evolution is sunk and you
> know it. Your problem is that you cannot demonstrate these paths.
Except, of course, when we can. As in the cases you describe. And when,
because history leaves traces, we can notice that, say, sub-systems of the
bacterial flagella have independent functionality beyond that of motility.
And when the ontogeny of formation of structures like bacterial flagella
show that each step in the formation of flagella also has independent
utility. And when we observe that the proteins that perform current
function also are closely related to proteins that perform other closely
related functions rather than far distant in sequence (as necessitated by
your vast sea of random changes). And when we observe that mutational
events (particularly point mutations) can have variant effects ranging from
no difference wrt to the original, to mild or conditional difference wrt
substrates or environmental optimi, to more dramatic differences, to
loss-of-function, we have the possiblity of intermediate or gradations in
functionalities that can be selected for in particular environments.
> Your position is not falsifiable.
History does not always provide evidence for any particular case. But the
point is that the mechanism that has been *observed* to work to result in
new or modified functions and structures in organisms, both by direct
experimentation and by observation in nature and by the predicted
consequences of the mechanism is not supernatural poofing. Nor is it the
long completely random process you use as a strawman. It is evolutionary
mechanism with pathways involving intermediate states of independent
utility.
[major snip]
>> So, it is quite clear that *in
>> principle* it is quite possible for selection to produce 'new functions'
>> even in Sean's world (since there do exist evolutionary changes that produce
>> 'new' functions that do not require his hypothesized many 'neutral' steps)
>> *and* that it is even possible to cross *reasonable* sized gaps in
>> functionality.
>
> New functions do evolve, but "reasonable" gaps are NOT crossed in the
> process. The gaps always involve the crossing of less than a handful
> of neutral mutations and usually require only one or two mutations.
> Even chloroquine resistance only requires 3 or 4 specific mutations,
> but even if 7 or 9 were required, this would not be a significant gap
> given the population size that exists in the wild. In determining
> what is or what is not a significant gap, you must look at not only
> the absolute gap involved, but the population size, the mutation rate,
> and the generation time. The problem here is that with every doubling
> of the neutral gap, the population would have to grow by a factor of
> two to keep up. In short order, growing neutral gaps outpace any
> population's ability to keep up with the exponentially growing random
> walk required to cross the gap.
Note that up to this point, Sean has been arguing that evolution is false
because of the necessity to cross huge 'neutral' gaps to reach a new
function.
>
>> Given this recognition that it is indeed possible to evolve 'new' functions
>> without having to cross his hypothetical large seas of multiple neutral
>> steps, Sean is left arguing that these observed cases do not represent the
>> normal cases. He instead tries to refocus our attention on the cases where
>> this does not happen and tries to convince us (by asserting without
>> presenting evidence) that the 'normal' situation is the one he posits: That
>> most new functions require his hypothetical ocean of completely useless
>> intermediate steps.
>
> Again, you are arguing from a position of quantity instead of quality.
> You are arguing that since you can demonstrate a huge number of
> examples of evolution in action where new functions are in fact
> evolved,
You mean my ability to demonstrate a huge number of examples of evolution in
action, as opposed to your inability to provide the number of neutral steps
that were involved in the appearance of any single real feature of life --
as opposed to GIGOing up hypothetical numbers until you reach a point where
the GO says evolution can't happen.
> that you really do not need to look at the level of function
> that these very common examples demonstrate. For you, absolute
> numbers are convincing. You don't need to know anything about the
> quality. All you want in quantity.
Very funny for someone arguing (without providing any numbers) that the
reason that evolution cannot be true is because of the *number* of neutral
steps that must be crossed.
> Clearly, I do have very good
> "evidence" for the exponential decrease in examples of evolution as
> the level of functional complexity increases.
Well, duh.
> When you start out with
> the lowest level of functional complexity, such as that required for
> de novo antibiotic resistance via one or two mutations, then it is
> very easy to find tons of examples. However, when you move up the
> ladder a little bit to functions that require the crossing of 3 or 4
> neutral steps, as with chloroquine resistance, the number of examples
> drops off dramatically. Then, when you move up to the de novo
> evolution of complete enzymes in real life organisms, such as lactase
> evolution in E. coli, the number of examples drops off even more
> dramatically. Then, when you move up to the de novo evolution of
> multi-protein functions, such as bacterial motility, the number of
> examples is ZERO. Its an interesting progression isn't it?
And one that is entirely expected (in human time frames) if one does indeed
have to have intermediate utility in its own right for the steps. But there
are examples of two step processes of selection. For example, selection for
antibiotic resistance followed by selection for optimal growth in media
containing antibiotic to the point where the bacteria are now at a selective
disadvantage in media without the antibiotic. There are other examples,
both experimentally and in nature, where what was once a toxin has now
become a necessary metabolite. These are necessarily two (or more) step
processes, often involving an initial selection followed by "suppressor" or
"enhancer" mutations in other genes that produce an IC system.
>
[snip]
>
>> Sean points out that if you remove all possibility of easy transition to a
>> new function by only looking at bacteria that lack ebg or other such genes,
>> then one cannot evolve lactase by *directly* selecting for lactase function
>> within the time constraints of human designed experimentation. That is, he
>> points out that evolution is not a mechanism which has the ability to
>> generate whatever function he chooses to generate, in whatever organism with
>> whatever genome he chooses (and he chooses genomes without any sequences
>> closely similar to lactase), in whatever time frame he thinks is sufficient
>> when the only thing being selected is the teleological or end result he
>> thinks exists.
>
> Not at all. These teleological examples only demonstrate that the
> average neutral gaps do in fact grow exponentially with increasing
> functional complexity.
No. All it shows is that the *future* evolution of features in an organism
is constrained by its past history and current genome. You did not show
that it was *impossible* to evolve lactase from another protein, you showed
that doing so required an organism to have had a past history that left it
with an enzyme that was dispensible or redundant and that could be easily
(no more than a few steps) converted to lactase. When lactase first evolved
in the past, it was undoubtedly from an organism that had such properties.
Just as flagella undoubtedly did not arise in a poof of smoke in some random
organism, but rather arose in an organism that already had a motor
(functioning for other reasons, perhaps including motility) and a whip
(functioning for protein transport) by a mutation that hooked the two
sub-systems together in a way that was useful to that organism (not
necessarily immediately for motility).
[big snip]
>> In Sean's
>> argument this is the gap between some random sequence of DNA and his
>> teleologically determined final sequence. Again the assumption is that no
>> intermediate states can have any selective value or that the gap cannot be
>> crossed in the amount of time available to experiment. And, of course, it
>> is true that sometimes a gap cannot be crossed or crossed in the time
>> available.
>
> Again, what if these gaps turn existing functions into islands that
> are surrounded in all directions by neutral sequences? No
> teleological sequence target is needed, only target levels are needed.
> Hitting any target within a particular level of functional complexity
> is what I am talking about - not any one target in particular.
>
>> I agree entirely in one sense. Evolution cannot cross every possible gap
>> *directly* aiming for some teleological set goal (the terminal functionality
>> of Sean's arbitrary choice).
>
> Can evolution cross the gap between one *level* of function and the
> next higher *level* of function. That is the question. We are not
> talking specific targets here. Examples of specific targets being
> missed are used to demonstrate the relative rarity of such targets as
> complexity increases, but this is really not the main point or
> challenge. The challenge is to hit ANY target within such a level of
> increasing complexity (i.e., the level of multi-protein functions).
I have no clue what you mean by higher *level* of function.
>
[snip]
>
> Basically, what you are saying is that if evolution is impossible due
> to neutral gaps, then evolution will not occur. Well duh! That is
> what I've been saying all along.
No. If a *particular* pathway is impossible because of the number of gaps
*that* particular pathway will not be used to evolve the system. As the
example of lactase shows, not all pathways are impossible.
>
>> When or if a bacteria
>> produces a variant able to cleave, say, the bond in polyvinyl chloride and
>> also deal adequately with the chlorine atoms, it will certainly have a
>> selective advantage over bacteria that cannot do this in certain
>> environments (those that contain significant amounts of polyvinyl polymers).
>
> In other words, if evolution can occur, then evolution will occur.
> Well duh again!
And, I would argue, evolution (all of evolution) *has* occured and *will*
occur because such pathways *do* exist. And when a structure that performs
a function is observed in some present organism, it most likely arose via
such a *possible* pathway rather than via your strawman *impossible*
pathway. You have to present an argument against the *possible* pathways of
evolution, not against the pathways that we both agree are *impossible* and
*didn't* happen. You and I can both agree that there is no tooth fairy. I
can claim that all examples of the tooth fairy taking teeth are due to human
activity (and the occasional accident). You cannot argue against my claim
that humans are responsible by saying that since I agree that the tooth
fairy don't take teeth, that therefore it is impossible for teeth to be
taken.
>
[snip]
>
> I don't know about Lamarck, but I never did say that the proposed
> process of evolution was teleological. What evolution does claim to
> be able to do is to produce vastly different functions of increasing
> *levels* of complexity if given enough time and competition in a
> non-lethal environment. I disagree with the suggested *levels* of
> functional complexity that evolution is supposed to be able to
> achieve. As I see it, the evidence suggests that only the very
> simplest of functions can be evolved in the limited time frame
> suggested by the theory of evolution (i.e., only 4 or 5 billion
> years).
I have no idea what you mean by *levels* of complexity.
>
[snip]
>
>> His argument is that most 'new' functions in organisms
>> involve multiple changes through a wasteland of *no utility at all* until
>> the final moment when it all falls into place and we have selection for the
>> final teleological function.
>
> Not entirely true. You are misstating my position. My position is
> not so much concerned with quantity as it is with the quality of the
> evolved functions. Most new functions of a very low level of
> functional complexity are separated by a very small "wasteland."
> However, this wasteland grows dramatically with just a few steps up
> the ladder of functional complexity until it becomes true that "most
> new functions" at such higher levels of complexity "involve multiple
> changes through a wasteland of no utility at all until the final
> moment when it all falls into place and we have selection for . . . "
> something, anything, of benefit at that level of functional
> complexity.
I have no idea what you mean by "ladder of functional complexity". You are
still talking about selection for a teleological goal and denying the
possibility of intermediate utility useful in its own right to generate your
increasingly hypothetical large gaps, AFAICT.
>
>> Given this view, he cannot see how 'new'
>> functions can arise by selection, since it would require direct teleological
>> selection for that final function from an essentially unrelated sequence
>> without any affinity for or relationship to the final sequence.
>
> Again, you misrepresent my position as requiring teleological
> demonstrations, which I do not require - as detailed above.
All creationist explanation is teleological in nature -- see above.
>
>> That is, he is using his (what I regard as a strawman) idea of how 'new'
>> functions arise in order to then argue that they cannot arise that way.
>
> How would you say that new functions of increasing complexity arise?
Via intermediates that had utility to the organism that contained them. And
stepwise through such intermediate steps.
[snip]
>
> And what would these "clearly described requisite conditions" be?
The existence of multiple steps to the current state with utility at each
step. And variation and selection. And redundant complexity. And the
chance vagaries of an historical nature that generate organisms with the
requisite genome that can take advantage of variation and selection.
From this point on, Sean clearly abandons his argument that the
(hypothetical) huge gaps in structure required to generate new functions is
what prevents evolution from happening. And starts claiming that his
designer actually creates new functions by minimally modifying structures!
And he does this without even noticing that closely related gene families is
not what an argument based on huge gaps in structure required to generate
new function would predict. Well, as has been said, "A foolish consistency
is the hobgoblin of small minds." To which, I would add, "So is a foolish
inconsistency."
This merely points out that "goddidit" can explain and, to use the term
erroneously, "predict" anything (it also explains the common sites of the
ERVs in chimps and humans, I am sure). Evolution (but not the strawman
version Sean presents) does require similarities and families and would be
falsified if all new functions involved entirely new proteins that had no
relationship to any other protein.
Bzzzt. You lose. Neutral change in sequence is actually quite slow. If
you choose a protein sequence like the fibrinogen peptide (the part that is
cleaved off to activate fibrinogen), it can be experimentally demonstrated
that the sequence is essentially all neutral. If you plot the rate of
change in fibrinogen peptide over time since divergence, 100% exchange
(which would actually result in less than 100% exchange because some sites
will have re-ratted) takes about 100 million years. This is quite close to
what you would expect if you calculate it theoretically. The theoretical
rate of neutral change is essentially, u, or the average rate of mutation at
a particular site.
> The only way that the differences in cytochrome c in
> bacteria and fruit flies and fish and bats and horses and humans etc.,
> is if the differences were actually functional differences that were
> maintained by natural selection over the course of many generations.
Bzzt. You lose. Because cytochrome c has sites that are necessary for
function, selection for that function results in *less* change than occurs
due to chance alone. In general, small proteins whose function involves a
large percent of the protein (as in histone) evolve much more slowly than
large proteins whose active sites are typically only a small percentage of
the total sequence (such as hemoglobin). Both, because of evolutionary
constraint, evolve slower than they would if all the amino acids were
selectively neutral, like fibrinogen peptide. Most of the differences that
do occur in cytochrome c involve the amino acid sites that are more
selectively neutral, not the functional ones. The sites that are slowly
evolving tend to be selectively important to function.
> Such functional differences cannot then be used to estimate orders of
> divergence over variations in functional needs in particular life
> forms and environments. For further discussion of this point see:
>
> http://naturalselection.0catch.com/Files/geneticphylogeny.html
>
>> OTOH, if most protein functions in organisms arose via duplications and
>> divergence from proteins that serve related functions, one would expect to
>> be able to see, often, and especially for recently evolved new functions,
>> sequence evidence that indicates that the 'new' enzyme or function came from
>> a structurally related precursor. That is, proteins should exist in
>> families.
Again, Sean abandons the idea that evolution is falsified because new
function requries crossing these vast functionless gaps.
Your position, that "goddidit", can be asserted to be consistent with
anything that exists. The position that function requires crossing large
gaps of structural differences is inconsistent with the existence of
"families". So I am really arguing against your strawman version of
evolution, since that is the only one of your false dichotomy that lends
itself to a scientific argument.
So, unlike your strawman version of evolution, ID looks like the
expectations of the real version of evolution? That is fine, but it doesn't
exactly point out any testable differences between ID and the *real* theory
of evolution, does it?
>
[snip]
>
>> Perhaps, just perhaps, much evolution does not, in fact, involve the
>> invention of new proteins at all.
>
> Oh really? So where did new proteins come from? Oh, I know, the
> sequential changes were so small along the evolutionary path that no
> one could say at any point that a "new" protein had evolved from the
> one before. Now of course, all these intermediate proteins have been
> lost so we have the appearance of "new" proteins. What a great story!
> Any evidence?
New proteins as opposed to alternate or modified alleles or the anagenetic
process described by you, proteins encoded by different genes, arise via
duplication and divergence, via chimera formation, via insertion.
>
[snip]
>> The duplication and divergence of
>> pre-existing genes is relatively common.
>
> Again, this has never been observed in real time.
Methotrexate resistance in cells in culture. Resistance of insects to
certain pesticides.
> You are only able
> to ASSUME that gene duplication and divergence is relatively common if
> you take your theory of evolution as an a priori assumption of truth.
Gene duplication is certainly common enough and is experimentally observed.
What do you think happens to the duplicates? Do you think that they all
remain unchanged and never mutate? The duplicated genes certainly do
diverge, given the existence of pseudogenes, unless you think that
pseudogenes are part of god's efficient design, just as ERVs are and the
thousands of copies of Alu are.
> Is it logical to argue that something is true based upon the assumed
> truth of what the position in question? Isn't this called "circular
> reasoning"?
>
>> The selection of chimeric genes is
>> relatively common. The retention of structure while changing function is
>> relatively common. Overlapping function and redundancy is relatively
>> common.
>
> Again, you assume what you are trying to defend here. The positive
> selection of chimeric genes is not observed all that "commonly" in
> real life. It is assumed to be common based only on evolutionary
> assumptions.
Selection does not have to be positive to be selection. Are you going to
claim that positive selection *never* occurs?
>
>> In short, living organisms do not look like creatures which contain
>> functions that had to cross large gaps of inutility.
>
> Yes they do. You only deal with those functions and sequences that
> are already very similar but you carefully avoid the gaps between
> those sequences and functions that are not very similar.
Such as, in cases where finding a gap would not be expected by sheer time
and the possibility of loss since divergence? Say, two species of closely
related (recently diverged) organisms (say chimps and humans), one of which
has a new gene which has undergone your hypothetical crossing the large gap?
Any real, rather than more GIGO hypothetical, examples?
> Even the
> similar sequences that you can detail as parts of different systems of
> function cannot be said to have arisen via gene duplication and
> selective divergence. If a gene duplicates and is not immediately
> selectable as advantageous, natural selection will select to get rid
> of that gene since it costs energy to maintain non-beneficial genetic
> real estate. Gene duplication really explains very little.
Given the amount of non-coding DNA already carried by most organisms, the
added energy cost is irrelevant. While it is certainly true that a
selectively neutral duplicate (rather than one that has immediate selectable
utility) can eventually be lost, remember that neutral drift produces, on
average, 1 amino change per 100 (1% change) per million years. That is
hardly rapid change. And, of course, that 1% change need not result in
loss-of-function.
>
>> They look like
>> organisms that have considerable similarity wrt the proteins and functions
>> they perform.
>
> Not at all. Vast differences in structure and function exist within
> creatures as simple as single celled bacteria.
This is like saying that there are vast differences in structure and
function within eucaryotes!
> How are these
> differences explained? You tend to dwell on similarities, most of
> which you cannot explain or which do not help your position out much,
> and completely ignore the major differences that do exist and that
> never evolve in real time.
>
>> 3) I would expect, if Sean is right, complex multi-protein systems to show
>> no evidence of subsystem utility nor the ability to be generated in a
>> step-wise fashion, either ontologically or phylogenetically.
>
> First off, you cannot or at least have not shown that such systems can
> be "generated in a step-wise fashion". This sort of demonstration has
> simply never been done.
I can certainly state that sub-systems of the procaryotic flagella, in
specific the whip, has functional utility independent of its ability to
function in motility.
> Also, if a multi-amino acid protein shows
> evidence of subsystem utility, why wouldn't a multi-protein system
> show evidence of subsystem utility? Again, it is conservation of
> design.
Arguing out of both forks of your tongue, again, eh. If two proteins are
similar, it is common design. If they are different, that also is evidence
that "goddidit". What is your falsifiable theory, again?
>
>> OTOH, if Sean
>> is wrong, I would expect an ontological process that would indicate that the
>> final 'teleological in hindsight' product was actually composed of amplified
>> recursive systems or composed of subsystems that are related to functions
>> that the subsystem can have independently of the teleological 'end function'
>> that Sean posits. That is, my claim is that the solution that nature uses
>> for the three-body problem is to produce two two-body events.
>
> This is a fine theory, but where is your evidence? I'm saying that
> any collection of items, parts, or systems can be categorized
> according to shared similarities, but this does not necessarily mean
> common descent or any sort of actual relationship.
"Goddidit" can certainly explain anything, can't it?
> Certainly I would
> expect that if the evolutionary scenario where true that such
> intermediate steps would be quite evident in hindsight.
No more so than any other historical event. If I come across a field in
Utah that has arrows, skeletons with arrow points in the skull or midribs,
battle gear, etc., I can clearly say that there was a battle on that field
(and from the material evidence, can probably estimate the time frame +/- a
certain number of years), but the further back that time frame is
(especially if it is pre-Columbian and pre-written language), the less
likely I will be able to say what led up to the battle. That doesn't mean
that there was no cause for the battle; only that I have no evidence of the
cause. That is why the crucial tests are those that demonstrate recent
changes rather than changes that occurred in deep time and have proceded in
lineages for hundreds of millions of years. Historical information does get
lost with time.
> However, just
> because something can be categorized along some sort of continuum does
> not mean that this continuum is by necessity an evolutionary
> relationship or any other sort of particular relationship. There must
> be other evidence and some sort of detailed mechanism. Also, arguing
> from morphology is always easier than arguing from code or genetics
> since what seems like a short step morphologically can be quite a leap
> genetically.
And vice versa. And everything inbetween.
>
[snip]
> Obviously many parts have many different functions within
> living things. The problem is that these various parts, that could in
> fact be arranged to perform many different joint functions, such as
> bacterial motility, simply do not know how to self-assemble themselves
> properly. Even if all the required parts for a functional flagellum
> are being made within a given cell, this does not mean that the
> flagellum will self-assemble.
Yes it does. Not only do bacterial flagella self-assemble, so to ribosomes,
eucaryotic flagella, phage lambda (the capsid and genome), tobacco mosaic
virus, etc., etc. All of a cell's organelles and structures self-assemble.
There is no outside agent that assembles them.
> The order of the parts is also
> important. Putting them together in the proper sequences is vital to
> the motility function. The fact is that all the parts are not present
> in any given cell
Bacteria are unicellular. Do you think that bacteria share the parts with
other cells? The fact is that the bacterial flagella *self-assembles*.
> and even if they were, they would not necessarily
> self-assemble to produce the motility function. Also, it should be
> noted yet again that not even one of the proposed evolutionary steps
> in flagellar evolution have been demonstrated to be crossed in real
> time, much less any complete motility system.
Actually, since my proposal is that the ontogeny of the step-wise
self-assembly (and it does self-assemble in a step-wise fashion) of the whip
is a good reflection of what I expect was the phylogenetic pathway (mostly
with protein export as the selectable function), each of the steps in
assembly looks like a phylogenetic step.
>
>> He does that because such a
>> strawman version of how evolution works is necessary for his claim that
>> evolution must work randomly through large completly useless gaps to be
>> accepted in the face of evidence that the genetic structure of organisms
>> belies his strawman model.
>
> You continually misrepresent my position in order to make it appear
> like I am building a straw man.
I am sorry that you think I am misrepresenting your position. That is
either because of my ignorance of what you say or your inability to clearly
explain (or perhaps, to understand) your position.
> It is actually you who are building
> the straw man to represent my position because you know that I am
> actually correct in my understanding and description of the Darwinian
> process.
No. I have clearly and explicitly rejected your understanding and
description of the Darwinian process. I regard your understanding as
fatally flawed and a description of a process that is non-Darwinian (as it
explicitly rejects the requisite do-able steps and selection for current
function).
> It is a lot easier for you to attack me if you misrepresent
> me. Next time, please, try and be more honest in your representations
> of my views. I know you understand what they are, so I find it
> difficult to think that you just don't understand what you are doing.
> I think you are deliberately trying to confuse the issue here.
If I am misrepresenting you, it is not due to my being dishonest in what I
say. Actually, you are all over the map in your position. If things are
the same or similar, that is what 'design' expects. If they are different,
that falsifies evolution, and also what 'design' expects. Heads I win.
Tails you lose. But that is what "goddidit" explanations always do.
Whatever we see, "goddidit".
Sean Pitman
< snip >
I don't have the time right now to respond in detail, but I will
respond to the following paragraph for now.
> When asked to present an honest creationist argument you have never present
> your own work. I stand by that statement.
What would you call a person's own work? I present my own ideas in
this forum at great length all the time. I really do not see how you
can possibly say that I never present my own ideas or "work"? Are
you off your rocker?!
> You now claim that your arguments
> are honest because you really believe them even if they are "crap", but what
> kind of honest arguments are those?
This is the best that anyone can say about their own honest opinions.
No one has absolute knowledge concerning the "truths" of the external
world. All of us are subjective human beings who are capable of
making erroneous "crappy" conclusions. God forbid, but you yourself
could actually be mistaken in your views! Like me, you are in fact
capable of believing in something that really is nothing more than
crap. We must all consider this possibility. We must all
individually weigh the evidence that we have available to us for
ourselves.
The scientific method is a very good "crap detector", but it never
fully removes the potential crap from our understanding of anything.
You think that you are correct in your views and that your views are
not crap based on the interpretation of the evidence as you see it and
interpret it using your reasoning capabilities and your own methods of
sorting out information. I think the same thing about my position.
You believe that you are better at determining truth and crap than I
am. Well, I think that I am better at it than you are.
No one with any sort of established opinion on a topic approaches a
discussion thinking that they are wrong or that their position is
"crap". Everyone thinks that they are right. Everyone thinks that
the evidence best supports his or her own position. One may disagree
with another and say that the other's position is "crap", but
certainly they cannot say that this position is not honest. Honesty
has nothing to do with the correctness of a position, but with motive
or sincere belief. Obviously, it is possible to be honestly wrong.
At the very least, you should give me this benefit of the doubt. I
give you this benefit of the doubt. I think that you are honestly
wrong in your views. Of course, you also think that I am wrong, but
somehow you think that my "wrongness" equates to "dishonesty". You
really cannot know or say this since you cannot know my true internal
motives. Certainly I have not been above admitting error in this
forum when I have been convinced of it. I have even admitted when you
have made a point that actually disproves this or that position of
mine (such as in the case where you showed that Hall was wrong to say
that fixation was required to cross neutral gaps). Obviously then, I
am not above saying that I make mistakes rather commonly and I am not
above admitting a mistake when I understand it as a mistake. It seems
to me then that I have actually provided some evidence of my honest
effort to discuss this issue sincerely.
Really then, it is impossible for me to be more than I am. If I
honestly believe something to be true, I cannot present it as "crap"
but as the truth as I see it. Likewise, you cannot understand that
the theory of evolution is crap until you honestly recognize it as
crap. It may in reality be a crappy theory, but until your eyes are
opened to this truth, you will be blind to the crap and cannot present
any more honest argument than one that is really crappy. The same
thing holds true for me if in reality evolution is the truth. If
evolution is true, then my position really is based on a very crappy
understanding of reality, but I cannot help myself until my eyes are
opened to this reality. Therefore, you can argue that I am wrong and
that you are right, but how can you argue that my arguments are
dishonest? - that they are anything more than misguided?
> They have zero value to science or to the
> honest evaluation of biological evolution.
And, who is to decided this? Upon what basis do you make this
statement? This is a statement of opinion, but not fact. You cannot
fully know that my evaluation is not an honest evaluation of
biological evolution from my perspective. You have a different
perspective. From your perspective you make the subjective conclusion
that my evaluation is "wrong". But really, you cannot say that my
evaluation is not an honest evaluation from my perspective. I mean -
Are you God?
> Stupid arguments have no value.
That is true, but who is to judge what is stupid and what isn't? You?
Are you all-wise? Do you know all truth? Are you above all error or
crappy conclusions? Are you God?
You can only judge for yourself and your judgment is subjective -
prone to error. Because of this, everyone must make up his or her own
minds as to what is "stupid" and what isn't.
> Wrong arguments are just deceptive.
Yes they are, but who is to determine which arguments are right and
which ones are wrong? Can you tell us what is right and what is wrong
without making any mistakes? So far, you haven't done such a good job
when it comes to perfection - in my subjective opinion at least . . .
> Using garbage that you should have known
> better like the mitochondrial argument is just bogus and dishonest.
My problem, you see, is that I do not recognize that the mitochondrial
argument is "bogus" at all. It makes a whole lot of sense to me in my
current, albeit limited, view of the external world. This may mystify
you, but no more so that how you have often mystified me with your
outlandish statements concerning the accuracy of phylogenetic tree
building and the definite intermediate relationship of Neandertals
between humans and chimps . . . etc. I am continually mystified by
the arguments that you use. Occasionally you come up with something
that actually makes sense to me, but mostly you do not seem to deal
with the evidence, but spend much of your time throwing mud, making
personal attacks, and presenting just-so stories as fact. And, the
clincher, you have yet to present a falsifiable test of your position
on genetic evolution. When challenged I have actually presented
various tests that would disprove my position, but none of you guys
have ever presented such a test that could disprove your position when
it comes to your theories on genetic evolution.
And again, who is to determine what is garbage and what isn't?
Certainly we each do this judging for ourselves. But, when it comes
to judging the internal ideas and/or motives of others, we should hold
back a bit. Even when it comes to something that we believe another
person "should have known" we cannot easily pass judgment on motive.
For example, it completely mystifies me that you cannot see what seems
so obvious to me. In my view, the facts are so clear and obvious that
it seems very strange to me that this whole issue of evolution would
have to be argued with anyone of even average intelligence much less a
person educated in the biological sciences. Given the information
that you have had access too, you should know better than you do.
But, just because I think that you should know better does not mean
that you do know better or that you are being dishonest in your
erroneous views. You see, even though I cannot imagine how you could
let yourself be so mislead, I think that you actually believe the crap
that you are spouting off. Certainly your honesty doesn't make your
views any less crappy, but it does make you less crappy. Perhaps you
should extend this same sort of courtesy or benefit of the doubt to
me?
> Ron Okimoto
Sean
Don McIntosh
> poke...@aol.com (Pokemoto) wrote in message news:<20030704003634...@mb-m07.aol.com>...
> < snip >
>
> I don't have the time right now to respond in detail, but I will
> respond to the following paragraph for now.
Aha! No time to debate for the rest of your life, eh? Then everything
you've said so far must be false. You see, if you're not willing to
abandon all other relationships, responsibilities, interests and
pursuits, and debate one topic with one person *ad infinitum*, it
proves your own psychological insecurity and the untenability of your
position. Least that's what I've been told...
> > When asked to present an honest creationist argument you have never present
> > your own work. I stand by that statement.
>
> What would you call a person's own work? I present my own ideas in
> this forum at great length all the time. I really do not see how you
> can possibly say that I never present my own ideas or "work"? Are
> you off your rocker?!
It's really easy: "You never present your own ideas or work." Now of
course it's up to you to multiply your efforts in order to disprove
the baseless accusation that you haven't actually written any of these
posts yourself. Morton's Demon is no respecter of persons.
> > You now claim that your arguments
> > are honest because you really believe them even if they are "crap", but what
> > kind of honest arguments are those?
>
> This is the best that anyone can say about their own honest opinions.
> No one has absolute knowledge concerning the "truths" of the external
> world. All of us are subjective human beings who are capable of
> making erroneous "crappy" conclusions. God forbid, but you yourself
> could actually be mistaken in your views! Like me, you are in fact
> capable of believing in something that really is nothing more than
> crap. We must all consider this possibility. We must all
> individually weigh the evidence that we have available to us for
> ourselves.
Amazing that an intolerant dogmatic fundy with blind faith would have
to explain this...
> The scientific method is a very good "crap detector", but it never
> fully removes the potential crap from our understanding of anything.
> You think that you are correct in your views and that your views are
> not crap based on the interpretation of the evidence as you see it and
> interpret it using your reasoning capabilities and your own methods of
> sorting out information. I think the same thing about my position.
> You believe that you are better at determining truth and crap than I
> am. Well, I think that I am better at it than you are.
> No one with any sort of established opinion on a topic approaches a
> discussion thinking that they are wrong or that their position is
> "crap". Everyone thinks that they are right. Everyone thinks that
> the evidence best supports his or her own position. One may disagree
> with another and say that the other's position is "crap", but
> certainly they cannot say that this position is not honest.
Well stated, though so obvious it shouldn't have to be stated in the
first place.
> Honesty
> has nothing to do with the correctness of a position, but with motive
> or sincere belief. Obviously, it is possible to be honestly wrong.
> At the very least, you should give me this benefit of the doubt. I
> give you this benefit of the doubt. I think that you are honestly
> wrong in your views. Of course, you also think that I am wrong, but
> somehow you think that my "wrongness" equates to "dishonesty". You
> really cannot know or say this since you cannot know my true internal
> motives.
Indeed, you'd almost think the ad hominem fallacy was...a fallacy.
Perhaps the idea is that the Genetic version of it is based on real
genetics, so it's a "scientific" sort of slander. ;-)
Sure I can, as long as I assert quite groundlessly that you *know*
biological "evolution" (however that conveniently elastic term happens
to be used at the moment) to be a fact of science. ;-)
> I mean -
> Are you God?
>
> > Stupid arguments have no value.
>
> That is true, but who is to judge what is stupid and what isn't? You?
> Are you all-wise? Do you know all truth? Are you above all error or
> crappy conclusions? Are you God?
>
> You can only judge for yourself and your judgment is subjective -
> prone to error. Because of this, everyone must make up his or her own
> minds as to what is "stupid" and what isn't.
>
> > Wrong arguments are just deceptive.
Then honest disagreements cannot take place? Sean's right. This is
absurd.
> Yes they are, but who is to determine which arguments are right and
> which ones are wrong? Can you tell us what is right and what is wrong
> without making any mistakes? So far, you haven't done such a good job
> when it comes to perfection - in my subjective opinion at least . . .
I'm sorry, but that was a little too subtle. Besides, the idea that
people aren't perfect, let alone perfectly objective, has no support
from the scientific community. Can't you at least back that up with a
solid reference from a peer-reviewed science journal so everyone can
turn around and accuse you of quote-mining?
> > Using garbage that you should have known
> > better like the mitochondrial argument is just bogus and dishonest.
>
> My problem, you see, is that I do not recognize that the mitochondrial
> argument is "bogus" at all. It makes a whole lot of sense to me in my
> current, albeit limited, view of the external world. This may mystify
> you, but no more so that how you have often mystified me with your
> outlandish statements concerning the accuracy of phylogenetic tree
> building and the definite intermediate relationship of Neandertals
> between humans and chimps . . . etc. I am continually mystified by
> the arguments that you use. Occasionally you come up with something
> that actually makes sense to me, but mostly you do not seem to deal
> with the evidence, but spend much of your time throwing mud, making
> personal attacks, and presenting just-so stories as fact.
Just remember that by definition you're a mud-slinging,
fallacy-committing, myth-believing creationist yourself...so you have
it coming because the ends justify the means. Besides, uhhh,
well...you started it.
> And, the
> clincher, you have yet to present a falsifiable test of your position
> on genetic evolution. When challenged I have actually presented
> various tests that would disprove my position, but none of you guys
> have ever presented such a test that could disprove your position when
> it comes to your theories on genetic evolution.
You don't understand evolution, and you don't understand
falsification. *Everything* is evidence for evolution; therefore it
*cannot* be falsified. That's what makes it such a uniquely powerful
scientific theory. ;-)
> And again, who is to determine what is garbage and what isn't?
> Certainly we each do this judging for ourselves. But, when it comes
> to judging the internal ideas and/or motives of others, we should hold
> back a bit. Even when it comes to something that we believe another
> person "should have known" we cannot easily pass judgment on motive.
> For example, it completely mystifies me that you cannot see what seems
> so obvious to me. In my view, the facts are so clear and obvious that
> it seems very strange to me that this whole issue of evolution would
> have to be argued with anyone of even average intelligence much less a
> person educated in the biological sciences. Given the information
> that you have had access too, you should know better than you do.
> But, just because I think that you should know better does not mean
> that you do know better or that you are being dishonest in your
> erroneous views. You see, even though I cannot imagine how you could
> let yourself be so mislead, I think that you actually believe the crap
> that you are spouting off. Certainly your honesty doesn't make your
> views any less crappy, but it does make you less crappy. Perhaps you
> should extend this same sort of courtesy or benefit of the doubt to
> me?
One can only hope.
> > Ron Okimoto
>
> Sean
Ron Okimoto
> < snip >
>
> I don't have the time right now to respond in detail, but I will
> respond to the following paragraph for now.
>
> > When asked to present an honest creationist argument you have never present
> > your own work. I stand by that statement.
>
> What would you call a person's own work? I present my own ideas in
> this forum at great length all the time. I really do not see how you
> can possibly say that I never present my own ideas or "work"? Are
> you off your rocker?!
When asked to present a single honest creationist argument, you have
never presented your own work and you still avoid stating one of your
arguments that you have found to be honest and valid. I stand by that
statement and this waffling only makes you look bad. If you have an
honest argument present it.
>
> > You now claim that your arguments
> > are honest because you really believe them even if they are "crap", but what
> > kind of honest arguments are those?
>
> This is the best that anyone can say about their own honest opinions.
> No one has absolute knowledge concerning the "truths" of the external
> world. All of us are subjective human beings who are capable of
> making erroneous "crappy" conclusions. God forbid, but you yourself
> could actually be mistaken in your views!
I've been wrong many times and I admit it. I make it a point to admit
each of my mistakes when they are pointed out to me.
Like me, you are in fact
> capable of believing in something that really is nothing more than
> crap. We must all consider this possibility. We must all
> individually weigh the evidence that we have available to us for
> ourselves.
>
> The scientific method is a very good "crap detector", but it never
> fully removes the potential crap from our understanding of anything.
> You think that you are correct in your views and that your views are
> not crap based on the interpretation of the evidence as you see it and
> interpret it using your reasoning capabilities and your own methods of
> sorting out information. I think the same thing about my position.
> You believe that you are better at determining truth and crap than I
> am. Well, I think that I am better at it than you are.
All you have to do to demonstrate that you are better at it than me is
to present the evidence that you have backing up your argument and we
can compare it to the evidence that you don't think is any good and
determine who is the better crap detector. You avoid doing this
because like all creationist with half a brain you know for a fact
that your evidence doesn't count for very much and it would be
embarrassing for people to see what you think is good enough to
support your view, while denigrating the evidence that science has put
forward. How honest is it to waffle and try to deny this plain and
simple fact. If you don't think that it is a fact, present your best
evidence for evaluation.
>
> No one with any sort of established opinion on a topic approaches a
> discussion thinking that they are wrong or that their position is
> "crap". Everyone thinks that they are right. Everyone thinks that
> the evidence best supports his or her own position. One may disagree
> with another and say that the other's position is "crap", but
> certainly they cannot say that this position is not honest. Honesty
> has nothing to do with the correctness of a position, but with motive
> or sincere belief. Obviously, it is possible to be honestly wrong.
> At the very least, you should give me this benefit of the doubt. I
> give you this benefit of the doubt. I think that you are honestly
> wrong in your views. Of course, you also think that I am wrong, but
> somehow you think that my "wrongness" equates to "dishonesty".
Look at yourself. Can you possibly say that what you are doing is
honest? You deliberatly avoid weighing the evidence. You would
rather stick with your opinion whether the evidence supports it or
not. This is dishonest. An honest person would evaluate the problem
and not hide his head in the sand and hope that no one notices. A lot
of people know the data better than you do. They have weighed the
evidence and it overwhelmingly goes against your view. Your YEC views
are so far removed from what the evidence tells us that it wouldn't
hurt you very much if you were a flat earther or a geocentric
fundamentalist Christian. You know some of the evidence that we have
and even the stuff that you complain about is so much better than
anything that you could put forward that it is laughable, and you
avoid the data that gives solid conclusions and would rather pick at
the difficult stuff that is less conclusive. How is this an honest
opinion?
You
> really cannot know or say this since you cannot know my true internal
> motives. Certainly I have not been above admitting error in this
> forum when I have been convinced of it. I have even admitted when you
> have made a point that actually disproves this or that position of
> mine (such as in the case where you showed that Hall was wrong to say
> that fixation was required to cross neutral gaps). Obviously then, I
> am not above saying that I make mistakes rather commonly and I am not
> above admitting a mistake when I understand it as a mistake. It seems
> to me then that I have actually provided some evidence of my honest
> effort to discuss this issue sincerely.
I do not know your internal motives, but your actions are just what I
stated. You refuse to weigh the evidence. You never put your
evidence up for evaluation, you only nit pick at things that other
dishonest creationist have raked up for you to pick at. You haven't
really gone to the mitochondrial literature to evaluate your opinion.
If you had you wouldn't hold that opinion any more. Nearly all
eukaryotes have mitochondria. We can trace the mitochondria to a
possible symbiotic association between a eukaryote and something
related to todays purple sulfer eubacteria. How do we know that this
symbiont wasn't a archae? We can trace the vertebrate lineage via the
mitochondrial genome, and for the lineage of fish, frog, reptiles,
birds and mammals, what do you think this data tells us? Your model
doesn't fit this data unless you claim that the Bible was wrong in the
order of creation.
Why haven't you tried to weigh the evidence instead of nit picking at
peripheral issues?
We have a living example of Lobefin fish. According to the main
hypothesis about the evolution of land vertebrates we should be most
closely related to lobefins. When we compare land vertebrate DNA to
coelacanth and a fish like a carp or salmon we find that we are more
closely related to the coelacanth just like the morphologists
predicted. Remember that this is nested similarity and not gross
similarity. Why your designer would design in this nested similarity
down through the vertebrates and cordates and even things like sea
urchins. We start having a problem with metazoans around the Cambrian
explosion. The hypothesis is that there was a rapid radiation of
different body plans over a relatively short period of time over 500
million years ago. Because of the degeneration of signal that we
expect to get the phylogenetic information about this event is full of
noise. We are trying to sort out a signal representing 10s of
millions of years between divergence events through an order of
magnitude greater time of signal degeneration. It is going to take a
lot of sequence data to accurately sort things out, but the rough
picture is that it is about what the taxonomist thought. If you look
at the old morphological trees the sequences trees taken as a whole
support that tree. What is your explanation for this data?
>
> Really then, it is impossible for me to be more than I am. If I
> honestly believe something to be true, I cannot present it as "crap"
> but as the truth as I see it.
This isn't true. Scientist nearly always present what they think is
the relative value of their data. They try and make the strongest
case, but they also state the obvious limitations. This is a given
for most scientific papers. You will be hard pressed to find a paper
that doesn't hedge their bets. The data has to be very solid for the
reviewers to let the authors get away with something like that. For
some short brief notes you don't have the space to do it, but for a
standard length paper you don't miss seeing it very often.
Look at how you start off your web page. Is this an honest way to
begin? Why begin with a known lie? Our emperor has plenty of
clothes, your emperor is naked. You even try to borrow clothes from
our emperor, but you never take it to your emperor and try it on to
see if the clothes really fit. Don't you think that it would be the
honest thing to state at the beginning of your web page that you have
yet to find a valid, honest creationist argument and that the readers
of your slock, should be forwarned, that whatever you have been able
to confirm has turned out to go against the creationist interpretation
of the data? You know for a fact that you have run into this time
after time. When does it become dishonest to continue to use
creationist material without a disclaimer? After the first three
dishonest arguments? The first four? 10? Shouldn't you confirm at
least one honest argument after the first couple of failures before
you try and foist these arguments on someone else?
Likewise, you cannot understand that
> the theory of evolution is crap until you honestly recognize it as
> crap. It may in reality be a crappy theory, but until your eyes are
> opened to this truth, you will be blind to the crap and cannot present
> any more honest argument than one that is really crappy. The same
> thing holds true for me if in reality evolution is the truth. If
> evolution is true, then my position really is based on a very crappy
> understanding of reality, but I cannot help myself until my eyes are
> opened to this reality. Therefore, you can argue that I am wrong and
> that you are right, but how can you argue that my arguments are
> dishonest? - that they are anything more than misguided?
Present your evidence and we will see whose eyes can be opened and
whose eyes are always closed to reality. Scientists know that they
can be fooled because if you are working on anything of value you
really don't know what the answer is. You learn to weigh evidence and
make the best conclusions from the data that you can. You have never
learned to do this.
>
> > They have zero value to science or to the
> > honest evaluation of biological evolution.
>
> And, who is to decided this? Upon what basis do you make this
> statement? This is a statement of opinion, but not fact. You cannot
> fully know that my evaluation is not an honest evaluation of
> biological evolution from my perspective. You have a different
> perspective. From your perspective you make the subjective conclusion
> that my evaluation is "wrong". But really, you cannot say that my
> evaluation is not an honest evaluation from my perspective. I mean -
> Are you God?
Reality decides this. They do have zero value to science because
science can't evaluate them.
>
> > Stupid arguments have no value.
>
> That is true, but who is to judge what is stupid and what isn't? You?
> Are you all-wise? Do you know all truth? Are you above all error or
> crappy conclusions? Are you God?
No, I'm not God, but you decide this by weighing the evidence.
Creationist never do this because they know that they will lose. They
know for a fact that their evidence doesn't count for much in the real
world where results matter. You admit to knowing this fact too, since
you avoid presenting this evidence every time it is asked for. How
honest is that?
>
> You can only judge for yourself and your judgment is subjective -
> prone to error. Because of this, everyone must make up his or her own
> minds as to what is "stupid" and what isn't.
>
> > Wrong arguments are just deceptive.
>
> Yes they are, but who is to determine which arguments are right and
> which ones are wrong? Can you tell us what is right and what is wrong
> without making any mistakes? So far, you haven't done such a good job
> when it comes to perfection - in my subjective opinion at least . . .
To demonstrate how wrong you are using the tools of science you have
to present your data and compare it to the data that you don't think
is good enough. You never let us do that. We are left trying to
clean up the smudges that you leave behind you. You make assertions,
repeatedly, and can't back them up, like your "Sea of neutral
mutations." All we can point out is that you present no evidence that
this assertion is valid in the way that you are trying to use it.
Where is your evidence. You can't just make assertions without
backing them up. ID does this all the time, and when they had to put
forward one single assertion about ID that they could teach, they
couldn't put one forward because they knew that they have as much
backing up their ID assertions as you have. This is nothing of
significance, and they know for a fact that they can't teach it. How
honest is the ID propaganda?
>
> > Using garbage that you should have known
> > better like the mitochondrial argument is just bogus and dishonest.
>
> My problem, you see, is that I do not recognize that the mitochondrial
> argument is "bogus" at all.
All you have to do is check out the literature directly. A citation
index search will provide all the papers your creationist sources
failed to mention to you.
It makes a whole lot of sense to me in my
> current, albeit limited, view of the external world. This may mystify
> you, but no more so that how you have often mystified me with your
> outlandish statements concerning the accuracy of phylogenetic tree
> building and the definite intermediate relationship of Neandertals
> between humans and chimps . . . etc.
What was the most likely phylogenetic tree found in all papers, even
those critical of the Neandertal claims? Do you know what the tree
tells you? Do you know how to interpret the data?
I am continually mystified by
> the arguments that you use. Occasionally you come up with something
> that actually makes sense to me, but mostly you do not seem to deal
> with the evidence, but spend much of your time throwing mud, making
> personal attacks, and presenting just-so stories as fact. And, the
> clincher, you have yet to present a falsifiable test of your position
> on genetic evolution. When challenged I have actually presented
> various tests that would disprove my position, but none of you guys
> have ever presented such a test that could disprove your position when
> it comes to your theories on genetic evolution.
You are mystified because you do not understand the data that you are
using. That isn't my problem, it is obviously yours.
You lie about this topic, admit it? This whole piece is just waffling
to avoid the fact that you are doing something that is dishonest and
you know it. Why don't you know that your mitochondrial argument is
bogus? You cite later papers like the Neandertal papers so you should
have known that something was wrong with the Parsons' paper, but you
just didn't bother to check. This is just another bogus creationist
argument that you got your faced rubbed into because you failed to
learn anything from your previous bad dealing with creationist
literature. If I were you, the first thing that I would do would be
to check out the conclusions and data before repeating them. Why
don't you do this?
>
> And again, who is to determine what is garbage and what isn't?
The source that you got your mitochondrial argument from was garbage.
That is how you tell. By checking it out and finding out that it
looks like garbage and smells like garbage and is just the same old
garbage. Your problem is that you have never found anything that
wasn't garbage in creationist literature, so you don't know what the
alternative looks like.
> Certainly we each do this judging for ourselves. But, when it comes
> to judging the internal ideas and/or motives of others, we should hold
> back a bit. Even when it comes to something that we believe another
> person "should have known" we cannot easily pass judgment on motive.
Well now you know and you don't have that excuse any more. Present
one creationist argument that you have found to be valid and honest.
I would just say honest, but most people expect honest arguments to
have some validity, but you do not.
> For example, it completely mystifies me that you cannot see what seems
> so obvious to me. In my view, the facts are so clear and obvious that
> it seems very strange to me that this whole issue of evolution would
> have to be argued with anyone of even average intelligence much less a
> person educated in the biological sciences.
You never present the evidence that would lead us to believe that your
assertions are clear and obvious. You only bad mouth our evidence,
but our evidence actually exists.
Given the information
> that you have had access too, you should know better than you do.
> But, just because I think that you should know better does not mean
> that you do know better or that you are being dishonest in your
> erroneous views. You see, even though I cannot imagine how you could
> let yourself be so mislead, I think that you actually believe the crap
> that you are spouting off. Certainly your honesty doesn't make your
> views any less crappy, but it does make you less crappy. Perhaps you
> should extend this same sort of courtesy or benefit of the doubt to
> me?
OK so now you know better. Get the bogus emperor's clothes off your
web page and remove the slock mitochondrial argument. If our emperor
is naked, what kind of clothes is your emperor wearing? Check out
your other Creationist arguments before using them or foisting them
off onto unsuspecting rubes. Tell them up front what value that you
have found these arguements to contain. Have you ever been able to
confirm a single one as being valid or if it is valid is it even worth
mentioning? Shouldn't you state this at the beginning of your web
page? Why don't you see the ID proponents stating that there is
nothing about ID that they are willing to present as being teachable
at this time? Don't you think that a lack of such a statement is
dishonest when they know for a fact that, that is how it is? How is
what you are doing any different?
I am probalby harder on you than other creationist posters, but you
have actually read some of these papers, and you should know better.
If you don't understand what you are reading, why do you think that
you can use the arguments that you are using? Shouldn't you be asking
for clarification rather than making incorrect claims from the data?
From my point of view you are no better than the creationist slock
miesters that have led you astray. You have the ability to know
better, but you would rather look the other way. I admit that I am
probably too quick to call you dishonest, but you haven't done
anything to change my mind. Where are your honest creationist
arguments, and where is your evidence for your view so that we can
tell who probably believes in crap? Doesn't the fact that you avoid
doing these things an indication of your honesty? Why have you spent
so much verbage presenting anything except an example of an honest
creationist argument? Is this tactic an honest one?
It is only my opinion, but the only way a YEC can claim that their
belief is the most likely to be correct is through ignorance. You
made the mistake of looking at the subject and you can't claim
ignorance any longer. That is why I claim that only the ignorant guys
that regurgipost like Simple-Divas can maintain an "honestly"
incorrect interpretation. The guys that have looked into the matter
and have had to weigh the evidence can't say that any longer. You
shouldn't have eaten the forbidden fruit. There is no going back.
You know that this is a fact or you wouldn't avoid posting the
requested material.
You can have faith that even if your version isn't the best one that
it is the correct one, but you have to acknowledge that it isn't the
best one. It isn't even close. From a scientific perspective the
theistic evolutionists have the most supportable scenario then come
other forms of Old Earth creationism, then comes the Young earth
scenarios, with YEC flat-earthers coming up dead last. It should tell
you something when the most literal interpreters of the Bible are the
farthest out of whack with reality, but it still could be that
everyone else is wrong. I wouldn't bet the farm on it.
Ron Okimoto
>
> > Ron Okimoto
>
> Sean
Sean Pitman
Simply hilarious and so well put! I really enjoyed reading your
comments, but I doubt that too many other members of this forum, much
less Ron, will "get it". However, I'm glad that there are a least a
few people with some common sense left in this world. Some things
should simply be obvious. The fact that I have to spend so much time
explaining the obvious really is a challenge. It is much harder to
explain the obvious than the obscure. It's just like former president
Clinton asking for the definition of common sense words like "sex" and
"is". It seems to me that those with the most tenuous positions start
having the most obvious lapses of common sense. But, at least such
lapses are good for a little comedy. Thanks again . . .
Sean
Ron Okimoto
It may be hilarious to you, but where is your honest creationist
argument? Where is your evidence for your belief so that we can
determine who believes in "crap?" Who is dishonestly side stepping
the issues and trying to avoid the obvious?
You could be honest. Just admit that you haven't found an honest
valid creationist argument and that your evidence is so much worse
than the evidence that you think isn't good enough that you are
embarrassed to put it forward. You've already admitted that you have
found a lot of dishonest bull in creationist literature, so present
the honest stuff or admit that you haven't found any that you think
are worth mentioning.
Everyone that knows better can figure out that you may have honestly
been fooled by other creationists, but you know better, now, or you
wouldn't avoid posting the requested material. This isn't funny.
You know for a fact why YEC creationists can't be honest about this
topic. In another thread someone compared you to a used car salesman.
That analogy is more apt than you take it for. A used car salesman
can be a nice and friendly person to his associates, but he has a
problem. He has to sell a lot of known lemons to customers that don't
want to buy a lemon. He has to misrepresent his product or no one
would buy it for the price he is asking. You know for a fact that you
are stuck with a lemon or you would put up your evidence for your
point of view. The only way that you can support selling this lemon
is by misrepresentation. All YEC creationists are stuck with this
problem, and all the ones that try and support their belief in this
arena have to resort to the same dishonest tactics. If you didn't
have a lemon to sell you could be more honest. That is a plain fact.
Wouldn't you rather argue the evidence for your position? Don't you
wish that you had something as good as the molecular data backing up
your position?
Why don't you start off your web page with "Hi I'm your friendly
neighborhood used car salesman, I'm going to try and sell you a lemon
and this is how I'm going to sell it to you...."
You, probably won't see another creationist, writing this kind of
stuff, as honest as that.
Ron Okimoto
Sean Pitman
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03070...@posting.google.com>...
> > > We observe new mutations and new alleles all the time.
> >
> > Yes we do, and they are all extremely simple as far as function is
> > concerned (i.e., antibiotic resistance - which is based on the
> > interference of pre-established molecular interaction and other
> > functions that are based on the potential of a single protein - such a
> > various single protein enzymes). No function that required multiple
> > proteins working together simultaneously has ever been demonstrated to
> > evolve de novo.
>
> I suppose that depends on what you mean by "de novo". If you mean
> that all the components appeared individually from non-coding DNA, I'm
> sure you are correct, but that is a fairly rare occurence even for the
> evolution of single proteins, let alone multi-protein functions.
> Fortunately, no one except you proposes such a thing as a normal
> evolutionary mechanism.
Hmmmm . . . so what "normal evolutionary mechanism would you suggest
to explain the existence of such multi-protein systems of function
where all the protein parts work together at the same time (i.e., have
a specified internal order/relationship with each other)?
> However, functions requiring multiple proteins do seem to have
> evolved. There is, of course, the pentachlorophenol cascade, which
> AIUI evolved by adding a duplicate protein to an existing cascade,
> followed by a mutation to the duplicate, and subsequent mutations
> optimizing the new cascade for the new substrate.
Cascades are different. The individual proteins/enzymes that make up
a cascade do not work together at the same time. Because of this, the
function of the cascade will not be completely destroyed if one of the
start proteins is removed. The rest of the cascade will still
function just fine. An enzymatic cascade is even simpler since a
specified order of the required enzymes is not so important. As long
as all of the required enzymes are there floating around randomly, the
sequential degradation of the substrate will take place just fine.
You see, a specified order of the enzymes is not needed. They can be
in any order here. However, if a function is dependent upon multiple
proteins all working together at the same time, as in the case of
bacterial motility systems like the flagellar apparatus, then the
ballgame is a bit different.
But, even such enzyme cascades are very difficult to evolve from
scratch. If only one or two point mutations are needed to proteins
that are already available to the cell, then such evolution is not a
problem, even if multiple proteins are involved (as was the case with
Hall's E. coli lactase evolution experiments where at least two
independent mutations were required before the lactase function could
be realized). However, if the genes in question are removed
completely, the evolution of even a simple multi-enzyme cascade will
never take place in anyone's lifetime – or even millions of years.
Also, I wouldn't call the genetic engineering in this case natural
evolution by random mutation and natural selection. A fair amount of
intelligent design was involved in this process. As it turns out, the
original wild-type bacteria did in fact have the ability to oxidize
polychlorinated benzenes to at least some degree to begin with. Many
chlorophenol products are known to be degraded by various
microorganisms, and therefore the CYP101 mutants could form the basis
of novel bioremediation systems for polychlorinated benzenes. The
genes encoding the three proteins of the CYP101 system can be
genetically introduced into chlorophenol-degrading micro-organisms to
convert chlorinated benzenes into phenols, which are then degraded by
natural pathways in the host organism. However, you will note that
these three genes are not "evolved" in these organisms, but are placed
there fully formed by intelligent design. A few subsequent mutations
are used later to refine their desired function, but the fact remains
that these required genes did not evolve from scratch at all. I mean,
certainly if Hall's E. coli could not evolve a relatively simple
lactase function from scratch without the ebg or lac genes previously
in place, I don't think that a function that required three complete
genes is going to just spring into existence in a single lifetime or
even in billions or trillions of years. The statistics are just too
much to overcome by purely mindless processes.
> "Molecular analysis of pentachlorophenol degradation", Orser CS, Lamae
> CC, Biodegradation 5:277 Dec 1994
http://intl.ejbiochem.org/cgi/content/full/268/5/1460
In this particular study the authors themselves note that the "De novo
evolution of genes for nitrotoluene degradation during the short
period seems unlikely. Instead, it is more plausible that the pathways
evolve by recruiting genes that encode degradative enzymes for other
compounds to assemble a functional pathway." In other words, the
genes and enzymes themselves did not evolve much at all, but were
already there. Because of this, very few mutations were required to
achieve this relatively simple *cascade-type* enzymatic function. In
fact, three recombinant strains showed activity for all three of the
required enzymes, and the cosmids carried by the strains were
designated pJS314, pJS315, and pJS316.
"Inferences from the comparison of the structural genes of the 2,4-DNT
pathway suggest that the pathway came together from three sources. The
initial dioxygenase appears to have originated from a naphthalene
degradation pathway like that of strain U2. A large portion of the
salicylate hydroxylase oxygenase component is retained but is not
functional. The MNC monooxygenase was probably derived from a pathway
for degradation of chloroaromatic compounds. The presence of the
vestigial (with respect to 2,4-DNT degradation) ortho-ring fission
dioxygenase is consistent with its recruitment from a pathway for
chloroaromatic compounds. The true ring fission enzyme for 2,4-DNT
degradation has a different origin. The sequence of DntD is quite
dissimilar to all other described meta-ring fission enzymes, including
those from naphthalene and chloroarene degradative pathways. The
distinctive sequence of the ring cleavage enzyme reflects the
substrate specificity observed for the THT oxygenase. The distant
relationship between homogentisate dioxygenase and DntD and the
association with homologs from amino acid metabolism (dntE and dntG)
indicate that the lower pathway operon arose from a gene cluster for
amino acid degradation."
Enzymatic activities are relatively simple to achieve. If all the
needed enzymes are already being made to break down a particular
molecular construct in at least some selectably beneficial way
(synthetic or natural), then obviously not much change or evolution is
required to be able to use this 2,3-DNT molecule for energy. Unlike
bacterial motility systems, enzymatic cascades need not self-assemble
themselves in any *particular* way. All that needs to happen is for
all the required enzymes to be present in the intracellular
environment (in any order/arrangement). This is not the case for
other non-cascading functions (i.e., bacterial motility) where all the
protein parts are required to be in a *particular order* all working
together at the same time before the function in question will be
realized. The order of protein parts is not so important in cascading
enzyme functions. Only the presence of the parts is important, but
not so much their order.
However, even though cascading systems of enzymatic function are
relatively simple because of a lack of required specified order of the
individual parts, cascades are still fairly complex. Without the
original enzymes being there preformed, multi-enzyme cascades will
most likely not evolve even in billions of years. As in the case of
2,3-DNT utilization, if all the original enzymes are preformed, some
refining mutations will no doubt contribute to a more effective
interaction with and breakdown of this molecule. However, without the
original genes and enzymes in place to begin with, even this
relatively simple enzymatic function would most likely never have
evolved - even in billions of years. The authors themselves state as
much when they note that the "De novo evolution of genes for
nitrotoluene degradation during the short period of time seems
unlikely."
What I am proposing is that even with billions of years available,
such evolution of even this relatively simple cascading enzymatic type
function would still be unlikely if the required enzymes were not
already there preformed. Another thing is that these scientists did
not demonstrate the evolution of this function in real time.
Certainly I am not saying that this function did not evolve in real
time. It obviously did. However, these scientists were not able to
reproduce the actual evolution of this function in the lab. They came
to their conclusions by studying the pre-existing genes and functions
in those bacteria that had already evolved this function. They made
comparisons between the existing genes and other known genes in other
types of bacteria. Because of this, their hypothesized pathways and
series of mutational events are limited in that several gaps in
knowledge are involved. One of these gaps involves the gene encoding
the methylhydroxyquinone reductase for the 2,4-DNT pathway - which has
not been identified. As such, this experiment is not only limited in
its explanatory value over a real time demonstration, but even what it
proposes to explain doesn't even come close to an explanation of a
multi-protein system where each of the parts work together at the same
time (i.e., where a specific internal order of the individual protein
parts is important).
http://jb.asm.org/cgi/content/full/184/15/4219?view=full&pmid=12107140
Thank-you though for the referral to this most interesting article. I
don't see how it helps your evolutionary position out much, but it was
very interesting none-the-less.
> Von Smith
> Fortuna nimis dat multis, satis nulli.
Sean
Sean Pitman
> It may be hilarious to you, but where is your honest creationist
> argument? Where is your evidence for your belief so that we can
> determine who believes in "crap?" Who is dishonestly side stepping
> the issues and trying to avoid the obvious?
You must be extra dense. I have presented the evidence over and over
again. If you don't see what I have presented as convincing, that is
one thing, but it is certainly evidence that can be clearly
interpreted in favor of ID - at least in my opinion. I haven't side
stepped any issues that I am aware of. I have answered a great many
of the ones that you have raised, as well as many others - at least to
my own satisfaction. It is impossible to convince some people of the
truth or of the correct interpretation of the facts. The best you can
do is to present the evidence and let other's make up their own minds.
I mean, I think that have presented the evidence very clearly and yet
you remain unconvinced by what seems to me to be overwhelming
evidence. Likewise, I'm sure you feel the same think about your
presentation of the evidence as you see it. But, in my opinion I
really do think that you bring very little to the table besides
blanket unsupported statements about my supposed dishonesty, ad hoc
statements that I have no evidence, and obviously bogus claims that I
am avoiding the important issues. You know what, such statements are
not convincing to me nor do I think anyone else who honestly considers
my position will find your personal slanders, generalizations, and
just-so stories all that impressive.
> You could be honest. Just admit that you haven't found an honest
> valid creationist argument and that your evidence is so much worse
> than the evidence that you think isn't good enough that you are
> embarrassed to put it forward.
Come on man! Are you really this slow?! I'm starting to doubt if you
have even made it through grad-school. Why don't I just ask you the
same thing? If you are honest, why don't you just admit that you
haven't found an honest valid evolutionist argument and that your
evidence is too embarrassing to put forward? I mean, from my position
is sure seems like you are holding something back because what you
have put forward as "evidence" so far is quite lame.
In any case, this is simply a ridiculous statement and you know it.
You are suggesting that in order for me to be really honest, I must
admit that I'm wrong and that my position is completely ludicrous.
Don't you see how silly this statement is? It would be Just as silly
for me to demand such a thing of you. You cannot admit to being a
fruitcake if you think that you really do have something valuable to
share - that you are right.
> You've already admitted that you have
> found a lot of dishonest bull in creationist literature, so present
> the honest stuff or admit that you haven't found any that you think
> are worth mentioning.
Please! You are just too funny! You're killin me! You do know of
course that I could use this same lame argument on you. I could say
the very same thing about you and your position. You know full well
that there are a lot of evolutionist kooks out there as well as
creationist kooks. You certainly cannot say that YECs have the edge
on kookiness. There are a great many evolutionists who haven't got
the first clue as to what they are saying - and you know it. Their
arguments are so ridiculous as to be rather humerous. They are
patently false to anyone with a smidgen of common sense and exposure
to the biological sciences. I'm sorry to say this, but sometimes it
seems to me that even you are in this category. In fact, I wouldn't
even give you the time of day if it were not for the fact that on some
rare occasions you happen to come up with something interesting. I do
actually think you are intelligent, but you do often seem to hide it
very well.
By the way, what do you have your Ph.D. in? What topic was your
thesis on again? Do you really have a degree?
> Everyone that knows better can figure out that you may have honestly
> been fooled by other creationists, but you know better, now, or you
> wouldn't avoid posting the requested material. This isn't funny.
What requested material are you talking about? I have answered all
pertinent challenges to my position - to include yours. You
constantly ask me to prove negative positions. You should know better
than this since you know that a negative cannot be absolutely proven.
You seem to take comfort in this fact. It is very nice to believe in
something that cannot be disproved absolutely (i.e., a nonfalsifiable
position).
In any case, I have given what I consider to be very good evidence to
show that neutral gaps do exist and that they do indeed seem to expand
exponentially with increasing complexity. You have been unable to
counter my examples and you have been unable to supply a falsifiable
test for your genetic theories of evolution. At least I have
presented a test that would falsify my position (a real time
demonstration of the evolution of a multi-protein system of function
where each of the proteins works together in a specified way at the
same time - like a bacterial motility function), but none of you have
been able to provide such a falsifying example to support your pet
theory. So far then, my theory has very good predictive value.
> You know for a fact why YEC creationists can't be honest about this
> topic.
Since when is this a fact? This is a ridiculous statement that does
not become true by simply saying it over and over again. I personally
know many YEC creationists who are not only honest, but very well
educated brilliant men and women of science. I myself am a YEC
creationist and I assure you, I can be and I am honest in my beliefs
and approach to this topic.
> In another thread someone compared you to a used car salesman.
Someone who is already an evolutionist and who admittedly doesn't know
much about genetics. Anyone can attack other person's motives if they
disagree with that person. However, it is another thing entirely to
back this up with some sort of rational reason. This wasn't done by
this person. The best this person could say was that they couldn't
put their finger on it, but they just KNEW that I was trying to be
slick and deceptive. There just HAS to be something wrong with what I
am saying even though that can't explain exactly what it is. . .
What a crock. I could also say the same thing about you, but that
wouldn't make it true. I could say, simply because I don't agree with
you, that you make a piece of crap sound soooooo good, just like a
used car salesman. But, that is simply meaningless throwing of mud.
It is a completely unsubstantiated bit of slander that only those who
are gullible will swallow. Unfortunately though, very few people
actually take the time to think for themselves and these types will
believe lies like this without investigating it for themselves. But
hey, that is no skin off my nose. I am talking to those who actually
want to think for themselves. I am also presenting my ideas here for
my own benefit more than for anyone else.
> That analogy is more apt than you take it for. A used car salesman
> can be a nice and friendly person to his associates, but he has a
> problem. He has to sell a lot of known lemons to customers that don't
> want to buy a lemon. He has to misrepresent his product or no one
> would buy it for the price he is asking. You know for a fact that you
> are stuck with a lemon or you would put up your evidence for your
> point of view.
Again, I could say that you know for a fact that you are stuck with a
lemon that you are trying to pawn off with misrepresentation.
However, this is an outlandish statement since obviously you do not
know that you are stuck with the lemon that you really are trying to
sell. You really believe that what you have is the Real Macoy when in
reality it is just about the worst lemon theory in history.
Of course, you believe the same thing about me, but you certainly
cannot say that I "know for a fact that I am stuck with a lemon." In
fact, you know that I think no such thing and that I do in fact
present very good evidence to support my point of view (or else why do
you spend so much of your time, and it must be a lot of time indeed,
challenging me in particular?). I even take my evidence from the work
of mainstream scientists and you know this. I even read the entire
journals before I start blasting someone about an article in question
- unlike those like yourself who think you are above the reading of
anything more than abstracts when you start your attacks on my
interpretation of an experiment. Please . . . start coming up with
some real evidence and stop spending all of your time making nonsense
personal attacks on my character, motives, and false statements that I
do not present my own ideas or any evidence to support myself. This
is simply ridiculous, a waist of your time and mine, and not very
convincing to anyone but the lowest denominator of those who frequent
this forum.
> The only way that you can support selling this lemon
> is by misrepresentation. All YEC creationists are stuck with this
> problem, and all the ones that try and support their belief in this
> arena have to resort to the same dishonest tactics.
Such generalizations and gross over-statements are not only false but
only hurt your own position. Don't you see that such grossly
over-exaggerated claims only hurt your own credibility and give my
position increased credibility as well as a lot of publicity?
> If you didn't
> have a lemon to sell you could be more honest.
So could you . . .
> That is a plain fact.
LOL - Plain to who? You think you just know it all don't you? The
fact of the matter is that you could be just as wrong as anyone. You
have no edge on intelligence, logic, or the use of the scientific
method of determining truth. So, what you think to be "plain fact"
may in fact be "plain wrong". Who are you to judge? Certainly you
must judge for yourself, but to be so adamant that others must see
things your way or be classed as "dishonest" is simply hilariously
blind and closed minded.
> Wouldn't you rather argue the evidence for your position? Don't you
> wish that you had something as good as the molecular data backing up
> your position?
But I do think I have the molecular data backing me up. I think that
the molecular data will actually be the downfall of Darwinism.
Looking at morphologic phenotypes alone it was pretty hard for Darwin
to think other than he did. However, with genetics, the picture is
much more clearly in favor of ID. Of course, I could be wrong, but
for now, I actually think that I'm right. I really do think that your
blindness has caused you and many others to look rather silly indeed.
But hey, it is what you really do believe and that is the wonderful
thing about a free country isn't it? It doesn't matter if others
think you are silly, you can believe whatever you want.
> Why don't you start off your web page with "Hi I'm your friendly
> neighborhood used car salesman, I'm going to try and sell you a lemon
> and this is how I'm going to sell it to you...."
Why don't YOU start off each of YOUR posts with this statement? I
mean, from my perspective, you would only be telling the truth! Of
course, you can't do this now can you because you are honest and you
really do think that you have the real thing - and you will be shocked
someday when you discover that you have really been selling lemons the
entire time. Perhaps you will feel tricked and perhaps regretful once
your inevitable paradigm shift reveals to you the true lemony nature
of the lemons that you have sold here in this forum. But hey, the
same thing could happen to me. But, like you, I doubt it.
> You, probably won't see another creationist, writing this kind of
> stuff, as honest as that.
That's because, like you, there are many creationists who actually
believe that the stuff they write IS honest already.
> Ron Okimoto
Sean
Zachriel
>
> You must be extra dense. I have presented the evidence over and over
> again.
> I myself am a YEC creationist and I assure you, I can be and I am honest
in my beliefs and approach to this topic.
You are a YEC. Let us assume there really is some disagreement on the
subject of "neutral gaps." Nevertheless, the age of the earth is not
dependent on biological proofs. The great age of the earth has been verified
by examination of the geologic column; with measurements by scientists in a
completely unrelated field, nuclear physics; by astronomers with their
detailed surveys of solar system and other stellar systems; and
incidentally, is consistent with the fossil evidence and with evolutionary
biology. So, even if there were some sort of disagreement about neutral
gaps, that just means there is a problem with understanding the process. It
does not mean that life has not evolved over that last billion years or so.
Modern DNA-genetics is a profound and definitive validation of the Theory of
Evolution, which posits that there exists a messenger of heredity, which
varies from individual to individual, is subject to mutation, and is
followed by environmental selection. The messenger, DNA, has those
properties.
At its heart, the Theory of Evolution is a theory of heredity. You may
"debate" your misunderstanding of genetics, but scientists are even now
modifying the heredity of crops, cloning sheep, and manufacturing human
proteins in vats of genetically manipulated bacteria.
Sean Pitman
> "Sean Pitman" <seanpi...@naturalselection.0catch.com> wrote in message
> news:80d0c26f.03071...@posting.google.com...
> >
> > You must be extra dense. I have presented the evidence over and over
> > again.
> .. . .
> > I myself am a YEC creationist and I assure you, I can be and I am honest
> in my beliefs and approach to this topic.
> <snipped>
>
> You are a YEC. Let us assume there really is some disagreement on the
> subject of "neutral gaps." Nevertheless, the age of the earth is not
> dependent on biological proofs. The great age of the earth has been verified
> by examination of the geologic column; with measurements by scientists in a
> completely unrelated field, nuclear physics; by astronomers with their
> detailed surveys of solar system and other stellar systems; and
> incidentally, is consistent with the fossil evidence and with evolutionary
> biology.
When it comes to the age of the universe or the age of the actual
planet called Earth, I don't have a problem with billions of years of
time since their formation. What I have a problem with is the
evidence for the length of time that life has been on this earth being
millions and billions of years old. The Earth it self my be quite old
indeed, but life on this planet as well as the "geologic column" seem
to be quite recent developments - at least as I view the evidence.
However, the best evidence for the problems of evolution can be found
in genetics. Statistically, evolution simply cannot do what it claims
to have done - even given 4 or 5 billion years. There is no adequate
evolutionary mechanism. Random mutation and mindless natural
selection are capable of many simple changes, but they are quite
limited when it comes to the evolution of much of anything beyond the
most simple of genetic functions.
For a more detailed discussion of my views on the geologic column,
fossil record, and genetic evolution see:
www.naturalselection.0catch.com
> So, even if there were some sort of disagreement about neutral
> gaps, that just means there is a problem with understanding the process. It
> does not mean that life has not evolved over that last billion years or so.
If the process is not understood, certainly it does not mean that
evolution did not occur, but it means that no one should claim that
evolution is a clearly understood process or science or that other
potential explanations are all crazy and should not be considered. In
other words, if the process is not understood, even in fuzzy detail,
Darwinism just might be wrong.
> Modern DNA-genetics is a profound and definitive validation of the Theory of
> Evolution, which posits that there exists a messenger of heredity, which
> varies from individual to individual, is subject to mutation, and is
> followed by environmental selection. The messenger, DNA, has those
> properties.
This is an ad hoc statement that is not supported. This is the entire
issue up for debate in this thread. Upon what basis do you make the
claim that modern genetics is the definitive validation of the theory
of evolution when you have just suggested that the very process of
genetic evolution may not be so clearly understood?
Also, I'm not saying that mutations and natural selection are not real
forces for change. They certainly are. And, as such, a certain
degree of evolution does indeed occur. The problem is that these
mindless processes are extremely limited in what they can do. This is
where the whole issue of neutral gaps comes into play. Neutral gaps
limit the ability of natural selection to select, thereby stalling out
the theory of evolution at a very low level of functional complexity.
> At its heart, the Theory of Evolution is a theory of heredity.
So is the theory of intelligent design.
> You may
> "debate" your misunderstanding of genetics, but scientists are even now
> modifying the heredity of crops, cloning sheep, and manufacturing human
> proteins in vats of genetically manipulated bacteria.
LOL - Yes they are.
Do you hear yourself? You said that scientists with intelligent minds
are modifying various life forms. Scientists use *intelligent minds*
in this process. Are you really meaning to suggest that these
creations of intelligent scientists are examples of evolution in
action? You really do need to stick with examples of what the
*mindless* processes of random mutation and mindless nature can and
cannot do.
Sean
Ron Okimoto
> roki...@mail.uark.edu (Ron Okimoto) wrote in message
> > It may be hilarious to you, but where is your honest creationist
> > argument? Where is your evidence for your belief so that we can
> > determine who believes in "crap?" Who is dishonestly side stepping
> > the issues and trying to avoid the obvious?
>
> You must be extra dense. I have presented the evidence over and over
> again.
I'm having line length problems with Netscape again. I hope that I've fixed it.
Usually when I try everything gets messed up.
This is what I posted Sunday to this thread in response to this same type of
waffling:
[> What would you call a person's own work? I present my own ideas in
> this forum at great length all the time. I really do not see how you
> can possibly say that I never present my own ideas or "work"? Are
> you off your rocker?!
When asked to present a single honest creationist argument, you have
never presented your own work and you still avoid stating one of your
arguments that you have found to be honest and valid. I stand by that
statement and this waffling only makes you look bad. If you have an
honest argument present it.] end quote
> If you don't see what I have presented as convincing, that is
> one thing, but it is certainly evidence that can be clearly
> interpreted in favor of ID - at least in my opinion. I haven't side
> stepped any issues that I am aware of. I have answered a great many
> of the ones that you have raised, as well as many others - at least to
> my own satisfaction. It is impossible to convince some people of the
> truth or of the correct interpretation of the facts. The best you can
> do is to present the evidence and let other's make up their own minds.
> I mean, I think that have presented the evidence very clearly and yet
> you remain unconvinced by what seems to me to be overwhelming
> evidence. Likewise, I'm sure you feel the same think about your
> presentation of the evidence as you see it. But, in my opinion I
> really do think that you bring very little to the table besides
> blanket unsupported statements about my supposed dishonesty, ad hoc
> statements that I have no evidence, and obviously bogus claims that I
> am avoiding the important issues. You know what, such statements are
> not convincing to me nor do I think anyone else who honestly considers
> my position will find your personal slanders, generalizations, and
> just-so stories all that impressive.
Just more waffling. No evidence or arguments here. Is it slander? Is
waffling honest. If you present your evidence we can discuss that. We
really got on this honesty issue when you claimed that you didn't have to
weigh evidence. When you claimed that the fact that you refused to put
forward the evidence for your model wasn't an issue. It is an issue in the
honest evaluation of any problem. If you can't support your model what
good is it to tear another model down that is better supported than your
alternative? You don't need an alternative to criticize some theory or
interpretation of the data, but when you do have an alternative it is just
stupid not to weigh it against the one that you don't think is good enough.
Until you do this you are just lying to yourself. No scientific theory is
perfect, you don't even have a scientific theory to compare to the one you
don't like.
>
>
> > You could be honest. Just admit that you haven't found an honest
> > valid creationist argument and that your evidence is so much worse
> > than the evidence that you think isn't good enough that you are
> > embarrassed to put it forward.
>
> Come on man! Are you really this slow?! I'm starting to doubt if you
> have even made it through grad-school. Why don't I just ask you the
> same thing? If you are honest, why don't you just admit that you
> haven't found an honest valid evolutionist argument and that your
> evidence is too embarrassing to put forward? I mean, from my position
> is sure seems like you are holding something back because what you
> have put forward as "evidence" so far is quite lame.
>
> In any case, this is simply a ridiculous statement and you know it.
> You are suggesting that in order for me to be really honest, I must
> admit that I'm wrong and that my position is completely ludicrous.
> Don't you see how silly this statement is? It would be Just as silly
> for me to demand such a thing of you. You cannot admit to being a
> fruitcake if you think that you really do have something valuable to
> share - that you are right.
You keep admitting it by not providing an honest valid argument and
the evidence for your position. This isn't my problem. Isn't this just
more waffling? There doesn't seem to be an honest valid argument in
these two paragraphs, or do you think that this counts?
We observe evolution happening. We can measure the rate of change.
We have the fossil record, the morphological comparisons and the
molecular evidence that tells us a pretty consistent story. Evolution
requires a genetic mechanism for it to work and that is what we find.
Your model doesn't require any of these things, but you just claim
that these clothes can fit your emperor too. This is a much weaker
argument and you know it. Then there is the fact that your model
doesn't really fit the morphological and molecular evidence that tells
us the order of creation of the various lifeforms. Your models has
the order wrong. What does the morphological and molecular
evidence tell us about when the birds were created? When are birds
created in your model?
>
>
> > You've already admitted that you have
> > found a lot of dishonest bull in creationist literature, so present
> > the honest stuff or admit that you haven't found any that you think
> > are worth mentioning.
>
> Please! You are just too funny! You're killin me! You do know of
> course that I could use this same lame argument on you.
In science we find a lot of arguments turn out to be incorrect, but unlike
you, we find that a lot of them are mostly correct. Where are such
creationist arguments? You know the ones that you have verified and
not found to be wanting. We both know that you probably have bogus
arguments on your web page, but you claim that as long as you close
your eyes and pretend that they aren't bogus you can honestly continue
to use them. Just present one argument that you have verified to be valid.
> I could say
> the very same thing about you and your position. You know full well
> that there are a lot of evolutionist kooks out there as well as
> creationist kooks.
There are a lot of kooks in every field, but your problem is that is all you
are stuck with and we have some really good people that aren't kooks.
These people have valid arguments that they can back up. Where are the
creationists like this? Where are their valid arguments?
> You certainly cannot say that YECs have the edge
> on kookiness. There are a great many evolutionists who haven't got
> the first clue as to what they are saying - and you know it. Their
> arguments are so ridiculous as to be rather humerous. They are
> patently false to anyone with a smidgen of common sense and exposure
> to the biological sciences. I'm sorry to say this, but sometimes it
> seems to me that even you are in this category. In fact, I wouldn't
> even give you the time of day if it were not for the fact that on some
> rare occasions you happen to come up with something interesting. I do
> actually think you are intelligent, but you do often seem to hide it
> very well.
We can filter the kooks and still have something left. You can't say
that or you would present a valid argument.
>
> By the way, what do you have your Ph.D. in? What topic was your
> thesis on again? Do you really have a degree?
Getting desperate? Too bad you lose on slimy arguments too. I graduated
an undergraduate genetics major at UC Berkeley. I did my PhD work in
molecular biology and molecular evolution. If you do a PubMed search
you will find 5 or 6 papers on my thesis research on nematodes. You can
read the one on ribosomal RNA in the Journal of Molecular Evolution to get
some feel for the complexities of the research back then (late 1980's and
early 1990's).
>
>
> > Everyone that knows better can figure out that you may have honestly
> > been fooled by other creationists, but you know better, now, or you
> > wouldn't avoid posting the requested material. This isn't funny.
>
> What requested material are you talking about? I have answered all
> pertinent challenges to my position - to include yours. You
> constantly ask me to prove negative positions. You should know better
> than this since you know that a negative cannot be absolutely proven.
> You seem to take comfort in this fact. It is very nice to believe in
> something that cannot be disproved absolutely (i.e., a nonfalsifiable
> position).
Remember that statement that I put up at the beginning. Waffling is not
presenting the requested material.
>
>
> In any case, I have given what I consider to be very good evidence to
> show that neutral gaps do exist and that they do indeed seem to expand
> exponentially with increasing complexity. You have been unable to
> counter my examples and you have been unable to supply a falsifiable
> test for your genetic theories of evolution. At least I have
> presented a test that would falsify my position (a real time
> demonstration of the evolution of a multi-protein system of function
> where each of the proteins works together in a specified way at the
> same time - like a bacterial motility function), but none of you have
> been able to provide such a falsifying example to support your pet
> theory. So far then, my theory has very good predictive value.
I assume that since I have been asking for your best evidence for your
model that this must be it. You have shown that neutral gaps can exist.
You have never shown that they exist in the numbers that you need
between selectable events to make your assertion work. You admit that
you need 20-30 or more neutral changes between selectable events to get
your assertion to work, but you haven't come up with an example of
where even 3 neutral mutations occurred before the changes became
selectable. You know that to really test your assertion you have to know
the starting material for making the complex structures and you have to
have some idea of the order that the structure came together. No one I
know seriously thinks that the flagellum came together in a few months
or years. This is the sort of thing that could have taken hundreds of
millions of years to produce. The guys you got this argument from admit
that unless they can rule out all biologically relevant pathways they don't
have an argument. They can't do this, so they don't have an argument.
It is really that simple. They know this for a fact or they would have tried
to teach it in Ohio. This is simply an argument from ignorance. It carries
very little weight in science.
Compare this to the evidence that we have. We base our assertions on
things that we can demonstrate. We observe genetic change, we observe
new mutations that produce new functions (you have begun to call them
trivial). We can see the relationship of the various proteins of the flagellum
to other proteins in the bacteria. In short we have a mechanism to produce
the variation that we observe in nature. What is your equivalent evidence
for any mechanism that you want to put forward to bridge these neutral gaps
of yours. How is it done? When was it done? When we look at the
various flagellum we get the idea that it could have happened billions of
years ago. Why did your designer make so many different, but obviously
related flagellum? Why are some either missing parts or maybe the others
gained parts, some seem to do a little of both. Who has the weaker
argument in this case?
If this is your best and if you don't know that you have the weaker argument
you better have as much malpractice insurance as you can get. Why didn't
you just present this argument before as your evidence for your belief?
Was it so hard? You have to demonstrate that someone has validated this
argument before you can call it valid. Can you do this? Compared to the
evidence that you don't like how would you rate the validity of your neutral
argument? We can verify our evidence. Even you could reproduce some of
our evidence. How has your neutral assertion been verified?
Is this really evidence for your model? Would it be better evidence that space
aliens mucked with bacteria billions of years ago? What about an unknown
biological mechanism or natural lifeforce acting in these cases? Dosen't the
flagellum sequence data indicate that your young earth scenario is wrong?
Why are all the flagellar genes so different in sequence. They seem to be
related, but how long would it take to develop that much diversity? What
evidence do you have for the existence of some supernatural designer that
would be able to bridge your neutral gaps?
>
>
> > You know for a fact why YEC creationists can't be honest about this
> > topic.
>
> Since when is this a fact? This is a ridiculous statement that does
> not become true by simply saying it over and over again. I personally
> know many YEC creationists who are not only honest, but very well
> educated brilliant men and women of science. I myself am a YEC
> creationist and I assure you, I can be and I am honest in my beliefs
> and approach to this topic.
Where are their arguments supporting their religious beliefs. You can be a
good scientist and be very religious. If any of these honest scientists have a
valid scientific argument for their creationist beliefs why haven't you put it
forward? If you put it forward we can evaluate them. Is it honest to not
weigh the evidence? How old is the earth? Why are you justified in ignoring
all the data that consistently tells us that you are wrong? Is this your idea of
being honest about a topic?
>
>
> > In another thread someone compared you to a used car salesman.
>
> Someone who is already an evolutionist and who admittedly doesn't know
> much about genetics. Anyone can attack other person's motives if they
> disagree with that person. However, it is another thing entirely to
> back this up with some sort of rational reason. This wasn't done by
> this person. The best this person could say was that they couldn't
> put their finger on it, but they just KNEW that I was trying to be
> slick and deceptive. There just HAS to be something wrong with what I
> am saying even though that can't explain exactly what it is. . .
> What a crock. I could also say the same thing about you, but that
> wouldn't make it true. I could say, simply because I don't agree with
> you, that you make a piece of crap sound soooooo good, just like a
> used car salesman. But, that is simply meaningless throwing of mud.
> It is a completely unsubstantiated bit of slander that only those who
> are gullible will swallow. Unfortunately though, very few people
> actually take the time to think for themselves and these types will
> believe lies like this without investigating it for themselves. But
> hey, that is no skin off my nose. I am talking to those who actually
> want to think for themselves. I am also presenting my ideas here for
> my own benefit more than for anyone else.
You are laughably wrong about my genetic knowledge. Just because you
do not understand a topic doesn't mean that other people have the same
problem. I teach a class in genetics, in fact I'm teaching it again next
semester. I've offered to explain nesting to you so that you can't remain
ignorant of the data that tells you that you are wrong, but you refused to
take me up on it. Why do you still think that your molecular arguments
are valid, when you don't understand what it means when we say that
the similarity is nested and not just gross similarity? If you do know the
difference why do you use the data as if it were just gross similarity that
we are talking about.
>
>
> > That analogy is more apt than you take it for. A used car salesman
> > can be a nice and friendly person to his associates, but he has a
> > problem. He has to sell a lot of known lemons to customers that don't
> > want to buy a lemon. He has to misrepresent his product or no one
> > would buy it for the price he is asking. You know for a fact that you
> > are stuck with a lemon or you would put up your evidence for your
> > point of view.
>
> Again, I could say that you know for a fact that you are stuck with a
> lemon that you are trying to pawn off with misrepresentation.
> However, this is an outlandish statement since obviously you do not
> know that you are stuck with the lemon that you really are trying to
> sell. You really believe that what you have is the Real Macoy when in
> reality it is just about the worst lemon theory in history.
You've just admitted from your neutral argument above that you have the
lemon.
>
>
> Of course, you believe the same thing about me, but you certainly
> cannot say that I "know for a fact that I am stuck with a lemon."
Now you do.
> In
> fact, you know that I think no such thing and that I do in fact
> present very good evidence to support my point of view (or else why do
> you spend so much of your time, and it must be a lot of time indeed,
> challenging me in particular?). I even take my evidence from the work
> of mainstream scientists and you know this. I even read the entire
> journals before I start blasting someone about an article in question
> - unlike those like yourself who think you are above the reading of
> anything more than abstracts when you start your attacks on my
> interpretation of an experiment. Please . . . start coming up with
> some real evidence and stop spending all of your time making nonsense
> personal attacks on my character, motives, and false statements that I
> do not present my own ideas or any evidence to support myself. This
> is simply ridiculous, a waist of your time and mine, and not very
> convincing to anyone but the lowest denominator of those who frequent
> this forum.
Your about the only one that presents any data at all. Why should I waste
time on guys that quote scripture as if it means anything? Or guys that just
make vacuous statements about nothing like Pagano, or guys that have
secret agendas that they won't tell anyone about like MG. You have quite
a group of guys that you probably wish were not on your side of the fence,
but that is about all we get around here.
Demonstrate that I needed more than the abstracts to counter your position?
I really have no interest in Halls work. You have to give some reason that I
should. You never do this. I don't need a reference to tell you that you
don't have any evidence that 30 consecutive neutral mutations have to have
occurred in the evolution flagellum because you know that you don't have
any evidence. What would such a reference look like, anyway?
>
>
> > The only way that you can support selling this lemon
> > is by misrepresentation. All YEC creationists are stuck with this
> > problem, and all the ones that try and support their belief in this
> > arena have to resort to the same dishonest tactics.
>
> Such generalizations and gross over-statements are not only false but
> only hurt your own position. Don't you see that such grossly
> over-exaggerated claims only hurt your own credibility and give my
> position increased credibility as well as a lot of publicity?
By presenting your neutral argument you have demonstrated that you do
have the lemon. If this is your best argument you are in even bigger trouble.
Just because you can lie to yourself about it, doesn't change that fact. If it
isn't a fact demonstrate that anyone has demonstrated that the neutral
argument is valid. Since you can't even demonstrate that your argument can
be supported well enough to be considered evidence, where does that leave
you? Compare that to the evidence that you don't think is good enough.
You are stuck with the lemon. That is why you have waffled and you are
reluctant to put forward the evidence for your model. You know that
whatever you have isn't as good as the stuff that you think isn't good
enough. You know this for a fact because the evidence that really makes
you believe your model is scripture and you know that has zero value in
science.
>
>
> > If you didn't
> > have a lemon to sell you could be more honest.
>
> So could you . . .
There are more than two cars on the lot, but I can be honest and claim that
my car is the best one on the lot. You have to misrepresent your car to call
it that. You avoid even referring to your car and support the sale of your
lemon by bad mouthing the other cars on the lot. Don't you wish that your
car was really the most reliable, don't you wish that you could open the hood
and instead of finding nothing to find a real engine in there? We have an
engine in our car, where is your engine and what evidence do you have that
it exists? Don't you wish that you could actually watch your car drive down
the street, like we can observe evolution in action? Even if you never see the
car go from one town to the other you know that we have real evidence that
it could get there, and you can't even get your car to roll off the lot. I don't
have to be dishonest to sell my car. It is the best car on the lot. It isn't a
perfect car, but it still is the best one.
>
>
> > That is a plain fact.
>
> LOL - Plain to who? You think you just know it all don't you? The
> fact of the matter is that you could be just as wrong as anyone. You
> have no edge on intelligence, logic, or the use of the scientific
> method of determining truth. So, what you think to be "plain fact"
> may in fact be "plain wrong". Who are you to judge? Certainly you
> must judge for yourself, but to be so adamant that others must see
> things your way or be classed as "dishonest" is simply hilariously
> blind and closed minded.
Justify that you have the better car. Since you know that you can't do
this in any meaningful way, why should you be laughing? I'd be crying
if I were in your shoes, esspecially if I was basing my religious faith on
something as stupid as this.
>
>
> > Wouldn't you rather argue the evidence for your position? Don't you
> > wish that you had something as good as the molecular data backing up
> > your position?
>
> But I do think I have the molecular data backing me up. I think that
> the molecular data will actually be the downfall of Darwinism.
> Looking at morphologic phenotypes alone it was pretty hard for Darwin
> to think other than he did. However, with genetics, the picture is
> much more clearly in favor of ID. Of course, I could be wrong, but
> for now, I actually think that I'm right. I really do think that your
> blindness has caused you and many others to look rather silly indeed.
> But hey, it is what you really do believe and that is the wonderful
> thing about a free country isn't it? It doesn't matter if others
> think you are silly, you can believe whatever you want.
Fit the data to your model of creation. When are birds created? Why doesn't
this scenario fit the molecular data? If you want to claim that the molecular
data supports your model, you have to demonstrate that this is really the case.
Biological evolution requires a genetic mechanism. Even Darwin knew this.
Your model does not require a genetic mechanism. ID does not require a
genetic mechanism. Creationism does not require a system that allows descent
with modification, but that is the system that we have, and that is what we
observe, descent with modification. Biological evolution requires such a
system. It isn't my blindness at issue. Fit the data to your model. When
were birds created? Can you justify this by the genetic data? You can't just
make baseless assertions, you have to back them up and test them. Test the
data against your model. Your order of creation is incorrect.
>
>
> > Why don't you start off your web page with "Hi I'm your friendly
> > neighborhood used car salesman, I'm going to try and sell you a lemon
> > and this is how I'm going to sell it to you...."
>
> Why don't YOU start off each of YOUR posts with this statement? I
> mean, from my perspective, you would only be telling the truth! Of
> course, you can't do this now can you because you are honest and you
> really do think that you have the real thing - and you will be shocked
> someday when you discover that you have really been selling lemons the
> entire time. Perhaps you will feel tricked and perhaps regretful once
> your inevitable paradigm shift reveals to you the true lemony nature
> of the lemons that you have sold here in this forum. But hey, the
> same thing could happen to me. But, like you, I doubt it.
Because I'm not trying to sell the lemon on the lot. It is as simple as that.
>
>
> > You, probably won't see another creationist, writing this kind of
> > stuff, as honest as that.
>
> That's because, like you, there are many creationists who actually
> believe that the stuff they write IS honest already.
So who has the lemon and if you deny it, can you deny it honestly?
>
>
> > Ron Okimoto
>
> Sean
Ron Okimoto
Lenny Flank
"Sean Pitman" <seanpi...@naturalselection.0catch.com> wrote in message
news:80d0c26f.03071...@posting.google.com...
news:<63afe69c.03071...@posting.google.com>...
>
> > It may be hilarious to you, but where is your honest creationist
> > argument? Where is your evidence for your belief so that we can
> > determine who believes in "crap?" Who is dishonestly side stepping
> > the issues and trying to avoid the obvious?
>
> You must be extra dense. I have presented the evidence over and over
> again. If you don't see what I have presented as convincing, that is
> one thing, but it is certainly evidence that can be clearly
> interpreted in favor of ID - at least in my opinion.
That's nice. Would you mind please telling us all what the scientific
theory of ID is and how we can test it using the scientific method? What,
according to this scientific theory of intelligent design, does the designer
DO, exactly. What mechanisms does it use do do whatever it is that it does.
Where can we see these mechanisms in action.
I look forward to your sidestepping, evading and not answering these simple
questions.