Kenneth Miller's and Barry Hall's challenge of Michael Behe
Sean Pitman M.D.
http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
In chapter four of his controversial book, Darwin's Black Box, Michael
Behe presents the argument that Rube Goldberg machines exist in living
things and that such machines are "irreducibly complex." Behe
presents the argument that the existence of such machines cannot be
explained by naturalistic mechanisms and are thus examples of
deliberate design. After all, anyone who has watched cartoons as a
child knows what a Rube Goldberg machine is and that this machine will
not work if any one part is removed. As an example, consider the
following scenario where Behe describes a popular cartoon about the
loud-mouthed rooster Foghorn Leghorn.
"… Foghorn would be walking along, notice a dollar bill or some other
bait on the ground, and pick it up. The dollar was tied by a string
to a stick that was propped against a ball. When the dollar bill was
moved, the attached string pulled down the stick, and the ball would
start to roll away as Foghorn stared slack-jawed at the developing
action. The ball then would fall of a cliff onto the raised end of a
seesaw, smacking it down and sending a rock with an attached piece of
sandpaper hurtling into the air. On its upward journey the sandpaper
would strike a match sticking out of the cliff, which lit the fuse to
a cannon. The cannon would fire; on its downward track the cannonball
would hit the rim of a funnel (the only allowance for error in the
whole scenario), roll around the edge a few times, and fall through.
As it came out of the funnel, the cannonball would hit against a lever
that started a circular saw. The saw would cut through a rope, which
was holding up a telephone pole. Slowly the telephone pole would
begin to fall, and too late Foghorn Leghorn would realize that the
fascinating show was at his expense. As he turns to run, the very tip
of the telephone pole smacks him on the head and drives him like a peg
into the ground." 1
Behe goes on to say that this Foghorn Leghorn cartoon contraption, as
a Rube Goldberg-like machine, is "irreducibly complex." This of
course means that if any one part is removed, the whole machine fails
and the desired end result or function, does not occur. Behe compares
such thought contraptions to real life systems of functions within
living things, such as the clotting cascade in the blood coagulation
pathway. This clotting cascade works in just about the same way that
Foghorn Leghorn was whacked into the ground by the telephone pole.
Each event in the clotting cascade must happen before the next event
can occur. If any one event is blocked, clotting will not occur at
all. Behe wonders how such a system could have evolved by
naturalistic mechanisms?
Well, we must first ask if Rube Goldberg machines really are
"irreducibly complex"? It is true that if one part is removed the
cascade is interrupted at that point. It is kind of like taking a
domino out of a line of dominos that are balanced on their ends. The
dominos after this point will not be knocked over by the previously
cascading dominos. In this way, the cascade is rendered useless.
However, a common argument is that by the very nature of cascades,
more parts can be added on the originating end of the cascade to make
it longer and longer still... like adding more and more dominos onto
the end of a chain of dominos. At first you start with one domino,
then two, three, four and so on until you have a very long cascade set
up. Consider the Foghorn Leghorn cascade again from this perspective.
What if the entire cascade describing Foghorn Leghorn's demise
started simply? Foghorn picks up the dollar that is attached directly
to the telephone pole by a string. When the string is pulled, the
carefully balanced telephone pole falls over and drives Foghorn into
the ground like a tent peg. Granted, this certainly is not nearly as
interesting or entertaining. But, it would work… right? Now, what if
we add just one little part to the cascade? Lets add the rope that
holds up the telephone pole and a saw that cuts the rope. The string
is attached to the switch on the saw. When pulled, the string turns
the saw on and it cuts the rope and the pole falls. A bit more
interesting and it still works. Now lets add one more little part.
Lets add the cannon. The string pulls a match and ignites the cannon
and the cannon ball hits the saw switch which cuts the rope that holds
the pole… and now we are getting a lot more interesting! We are
evolving a complex cascade one small part at a time… right? It sure
looks that way.
This argument is in fact commonly used as an explanation for the
origins of such apparently complex cascades as occur in blood clotting
systems, visions systems, and energy metabolism systems to name just a
few. After all, according to the theory of evolution, very large and
apparently impossible tasks are broken up into manageable parts. This
is Dawkins's main argument in his book, Climbing Mount Improbable. An
impossible statistical cliff that cannot be scaled in a single bound
by natural selection is scaled in small little evolutionary steps.
Actual laboratory experiments have been put forward to support such a
concept. What is especially interesting is that these laboratory
experiments actually work! It has been demonstrated in real time that
the addition of unique components onto the end of a metabolic cascade
is in fact possible.
The evolutionary biologist Kenneth Miller described one such
experiment in his recent book, Finding Darwin's God. Miller quotes an
experiment done in 1982 by professor Barry Hall. 2 In this experiment
Hall deleted part of a metabolic pathway in a bacterium called E.
coli. Using the proper environmental pressures, the bacterium
"evolved" the missing piece of its cascade back again! 3 This missing
piece was actually the tip of a long cascade that breaks down sugar
molecules and extracts energy from them. Glucose is the main sugar
utilized by this cascading pathway. There are of course other simple
sugars that can also enter this pathway such as galactose and fructose
etc. Each of these also requires a unique enzyme or enzyme pathway to
convert them to something that can enter the cascade. Then, just like
adding more events to Foghorn's cascade, more events can be added to
the sugar cascade. You see, there are different kinds of sugars.
Some of these sugars are more complex than glucose, but can be broken
down into glucose and/or one of the other simple sugars that are
already part of the existing cascade. Once this break down occurs,
this complex sugar molecule becomes just another part of an extended
sugar metabolism cascade. The problem is that unique enzymes are
needed to break down complicated sugar molecules. Some sugars may
even need more than one unique enzyme to break them down to a point
where they can enter the established cascade. However, the benefits
of obtaining these necessary enzymes (proteins) are great. If such
cascades of complex sugar breakdown can be established, any bacterium
with such capabilities would survive better than its peers in such an
environment. The ability to evolve such advantageous enzymes would
certainly enhance the survival of the species. In fact, the "evolved"
bacteria in Hall's experiments quickly outgrew those that had not yet
evolved the needed enzyme. Of course, this is only natural. It is
the law of survival - the survival of the fittest - right? Hall went
on to demonstrate the evolution of two and even three additional steps
added on to the original sugar cascade.
So, it certainly seems that cascades are not as "irreducibly complex"
as Behe claims. Cascades in living systems are certainly as
complicated and even vastly more complicated than the one that whacked
Foghorn Leghorn, but even such complexity does not seem to be
"irreducible." For a machine to be truly irreducible, all of its
functions must collapse if any one part is removed. However, the
removal of one part of a cascade may not destroy its ability to
perform. The removal of an enzyme that allows the utilization of
complex sugars does not eliminate the cascade's ability to continue to
break down glucose or galactose or fructose. Even the removal of the
enzyme needed to break down glucose itself is not vital to the
function of the rest of the cascade. Even though glucose can no
longer be utilized, fructose still can be, along with several other
types of sugars. A cascade is therefore reducible without the loss of
all function. It need not then be "irreducibly complex." The thing
about cascades is that the entire system is no more complex than its
most complicated subsystem. It is like a link in a chain. The chain
is no stronger or weaker than the weakest link in the chain. So, a
cascade is no more complicated than the most complicated link in its
chain. If this most complicated link can be overcome, then the rest
of the chain is easy to make. The question then is, can this
complicated link be overcome?
Professor Hall showed how simple bacteria can evolve links in a
cascade chain. These links seemed like insignificant hurdles, but
couldn't they simply be added up to produce something quite
significant? Or, are there some limits to this evolution? Hall did
delete the gene needed to produce an enzyme (lactase) that broke down
the sugar lactose into two other sugars called glucose and galactose.
Both glucose and galactose are part of the established sugar
metabolism cascade of E. coli. So obviously, without lactase, an E.
coli bacterium can no longer utilize lactose for energy. Hall deleted
that lactase genes to see if the E. coli bacteria would "evolve" back
the ability to utilize lactose when grown on a lactose enriched media.
Hall's experiments were a stunning and dramatic success. His colonies
of E. coli quickly "evolved" the ability to use lactose. There is
just one little catch. Hall did not delete a spare tire gene (ebgA)
that required just one point mutation to produce an enzyme with a
fairly high level of lactase activity. But what if the E. coli had
not been so fortunate as to have this spare tire gene? What would
have happened then? Hall wondered about this himself. He then
deleted the spare tire gene as well as the lacZ genes. Would there be
lactase evolution now? So far, none of these colonies has ever
evolved lactase ability despite being subjected to highly selective
media over many years. Evidently, no other gene could lend its
information by itself or in combination with any other gene to aid in
the bacterial "evolution" of lactase. Hall described these particular
bacterial colonies as having "limited evolutionary potential." 3 But
why did these colonies have limited evolutionary potential?
It turns out that there are statistical gaps that separate unique
protein/enzymatic functions from each other. Not every protein
sequence will be recognized by a given bacterium. In fact, the vast
majority of possible protein sequences will not be recognized as
having function. Because of this problem, if proteins are not already
very very close in sequencing to begin with, the statistical odds that
one will "evolve" into another are remote because they are separated
by a vast number of non-functional amino acid sequences.
Non-recognized or non-functional proteins cannot be guided by natural
selection along any evolutionary path whatsoever. Why? Because
nature only sees function. Nature cannot guide if it is blind. Thus,
nature cannot guide evolution across non-functional gaps. Then,
without this guidance of natural selection, evolution is dead.
So, although cascades are not irreducibly complex in and of
themselves, the evolution of their individual component parts is still
statistically impossible because of the gaps of non-function that
separate each part from its nearest neighbor. Professor Hall never
evolved anything that crossed a gap of non-function that was more than
two mutations wide. The single non-functional gap of two mutations
that he did cross, he could not explain. In fact, by his own
calculations, he figured this feat to be impossible… taking an average
of 100,000 years to cross. The apparent success of the crossing of
even this tiny gap of non-function astounded him. He attempted to
explain the success of this crossing by saying, "under some conditions
spontaneous mutations are not independent events." 3 He went on to
say that this is, "heresy, I am aware." If it is difficult for
professor Hall to imagine the crossing of such a small gap of
non-function, what would it take to cross a three mutation gap… or a
four mutation gap? Consider now that these proteins are hundreds or
even thousands of amino acids in length. The problem seems clear. In
fact, because of this problem all living things may have "limited
evolutionary potential." Bacterial colonies such as Salmonella,
Proteus, and Pseudomonas can be grown on Hall's selective media or any
selective media in any sequence until the cows come home… and none of
them will ever evolve the lactase enzyme (Some of Hall's E. coli
colonies will never evolve it back either). If this relatively simple
function does not evolve in certain creatures with "limited
evolutionary potential" what about functions that require multiple
proteins or systems working together simultaneously? How would such a
function evolve... gradually? For example, bacterial motility can
come in many different forms to include flagella, cilia, undulating
membranes etc. However, all known motility systems require many
"parts" working together. How could the function of any one of these
motility systems evolve gradually? The problem is that the vast
majority of possible combinations of the parts in a given cell will
not result in any function at all, much less a motility function. The
odds are that the motility function is separated from all other
cellular functions by a rather large gap of non-function or neutral
function. Non-functional or neutral mutations cannot be selected by
natural selection since they are not functionally or phenotypically
different from what came before. This means that it is up to random
chance alone to cross the gap toward the motility function. Random
chance, without natural selection, simply takes too long.
So, it turns out that cascades are limited in their evolution, not by
irreducible complexity, but by gaps of non-function or neutral
function that separate the various functions of a given cell from the
genetic material that forms all other aspects of that cell. If
cascades are relatively simple to build, and yet even their component
parts are too complex to yet be explained in a testable way by a
naturalistic process, try demonstrating the evolution of a truly
irreducibly complex system of function outside of deliberate design.
Such systems do actually exist in the natural world. An irreducibly
complex system is one in which all the individual parts work together
at the same time to produce a desired function. For example, an
electric motor is irreducibly complex. It has a minimum number of
parts working together at the same time in order for it to have a
function. It needs a wire coil, a surrounding magnet, electrical
current and bushings to switch the electrical current back and forth
at the proper moment in time. All these parts must of course be set
up in the proper relation to each other. However, if you take away
any one part, none of the other parts will "work" together… period.
There is no "cascade" of function since all the parts work together at
the same time. So, in order to get any function whatsoever from the
electric motor, all the needed parts must come together in a highly
ordered way... suddenly. An electric motor, minus one of its parts,
has no function. It might as well be sitting in a junk pile at the
city dump.
In fact some bacteria, as Behe points out, have little mechanical
motors that are very similar to electric motors. Just like mechanical
motors they require a minimal number of parts, all working together at
the same time, to produce their rotary motion. These little motors
power structures called flagella. 1 Flagella are long whip-like cords
attached to certain bacteria by a little motor of sorts. The motor
actually spins and causes the flagella to spin. The spinning flagella
propels the bacterium through the liquid that it is swimming in. The
problem here is that the motor that spins the flagella is "irreducibly
complex." It has quite a few parts (fifty or so). Many of these
parts are irreducible. If even one of these irreducible parts is
removed. The flagellar motor will not work, not even a little bit.
Each of these parts is, in itself, complex… just as each link in the
cascade system is complex. However, what separates an irreducibly
complex system from a cascading system is that not only are each of
the parts in an irreducible system separated from each other by huge
statistical gaps in recognition, but the system itself is entirely and
completely dependent upon each one of its parts for function. If the
statistical challenge of evolving just one recognized part is huge,
try evolving many parts when none of them will be recognized until all
of them are present in their proper orientation. The system itself is
an entity that must be recognized in order for natural selection to
"select" it for survival. The system cannot be recognized until it is
functional to some degree. An irreducibly complex system is not
functional in any degree until it has all its parts in working
order... simultaneously. Only then can it be recognized and selected
by nature. The irreducibly complex system, unlike a cascading system,
cannot be built gradually. If the evolution of a cascading system of
function is admittedly of "limited evolutionary potential" then try to
imagine the evolution of a truly irreducible system. It is mind
boggling. Not only has it never been observed and documented, but
such a mechanism has not even been theorized as of today.
Some do try and explain flagellar evolution by proposing that many of
the parts in a flagella are used as parts in other cellular systems of
function. For example, the actual flagella is very similar in
structure to long tube-like secretory structures. In fact, it is
thought that some flagella might function as both a motility structure
as well as a secretory structure. Likewise, many of the other parts
in a flagellar motility system do other similar jobs in other systems
within the cell. Therefore, it seems obvious to many that all these
various parts already existed and therefore might easily come together
to form the motility system diagrammed above. The problem is that the
parts do not naturally self-assemble into a flagellar system, or any
other system of function. They must be directed into their proper
places by a coded message in that cell's DNA. It is like the parts of
a car. Many of the same parts could be used to build a boat, or a
house, or any number of other things. However, planning is needed
because the parts themselves do not self assemble to form any one of
these things. Given a bacterium without a motility system, but with
all the needed parts to make one, there is no series of point
mutations that will get it from what it has to the goal of motility
without the crossing of neutral gaps in function (despite the
selection pressure or advantages of motility should this function
happen to evolve). In other words, there is no way to mutate the
genetic code were each and every mutation will be beneficially
advantageous until motility is achieved. At this point, further
evolution is dependent upon neutral evolution (random drift). Such
neutral evolution simply takes too long to evolve new functions and
this time increases dramatically as the complexity of the needed
functions increase.
So, Miller's attempt to explain Behe's challenge of irreducible
complexity only succeeded in attempting to explain the evolution of
cascades. Even this explanation falls very short. Irreducible
complexity remains untouched as a challenge to evolution and as a
strong voice in favor of intelligent design.
1. Behe, Michael J. Darwin's Black Box, The Free Press, 1996.
2. Miller, Kenneth R., Finding Darwin's God, HarperCollins
Publishers, 1999.
3. B.G. Hall, Evolution on a Petri Dish. The Evolved B-Galactosidase
System as a Model for Studying Acquisitive Evolution in the
Laboratory, Evolutionary Biology, 15(1982): 85-150.
C.J.W.
"Sean Pitman M.D." wrote:
> Evolving Rube Goldberg Machines
> http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
"Here is Behe's reply
On the "acid test" Professor Miller claims that the careful work
of University of Rochester biologist Professor Barry Hall is
an experimental demonstration of the ability of Darwinian
evolution to produce an irreducibly complex biochemical system.
(Barry Hall himself never made such a claim.) I disagree.
The fact that the artificial chemical inducer IPTG was
added to the lactose-utilizing system effectively mitigated
its irreducibility, turning the system into one that could
be improved a step at a time. In his recent essay Miller
wrote:
"Does Barry Hall's ebg system fit the definition of irreducible
complexity? Absolutely. The three parts of the evolved
system are: (1) A lactose-sensitive ebg repressor protein
that controls expression of the galactosidase enzyme; (2)
The ebg galactosidase enzyme; (3) The enzyme reaction
that induces the lac permease. Unless all three are in
place, the system does not function, which is, of course,
the key element of an irreducibly complex system."
Miller's claim is incorrect because in the presence of IPTG
the three features he lists are not all needed. In the presence
of IPTG, the "enzyme reaction that induces the lac
permease" is not required because IPTG itself induces
the lac permease. Thus in the presence of IPTG the
system is not irreducibly complex. And, as I wrote in
my original essay, Barry Hall clearly noted that in the
absence of IPTG--when the system actually is irreducibly
complex--no viable mutants have been found in his
25 years of investigation.
The inclusion of IPTG was the result of the decision of
an intelligent agent (Barry Hall) to deliberately alleviate
the irreducibility of the system. In the absence of that intelligent
action, Darwinian processes alone were ineffective. That
is exactly what intelligent design theorists would expect.
Miller also writes, "the ebg gene is actually only 34%
homologous to the gene whose activity it replaces (meaning
that about 2/3 of the protein is quite different from the
galactosidase gene whose function it replaces)". Yet he
knows as well as I do that 34% general sequence homology
makes it virtually certain that the three-dimensional
structures of the two enzymes are essentially identical.
And since the active sites (the business end) of the enzymes
are much more similar (they are identical in 13 of 15
residues), the ebg enzyme is pretty much a spare copy
of the lac enzyme. Thus it seems to me that the taking
over of lac galactosidase function by ebg hardly
even rises to the level of microevolution.
What is actually surprising--even to a design theorist such
as myself--is Barry Hall's finding that no enzyme other
than ebg could fill in for the missing lac galactosidase.
I would have expected otherwise. Perhaps even changes
we would consider to be "microevolution" are often times
beyond the reach of Darwinian processes. Perhaps
even I give natural selection too much credit."
http://www.arn.org/boards/ubb-get_topic-f-1-t-000637-p-1.html
--
--W
æ»´itler stopped and looked me
in the eyes,舛hristianity is, for
the moment, one of the points in the
programme I have laid down. But
we must look ahead. Rosenberg is a
forerunner, a prophet. His theories
are the expression of the German soul.樗
(Strasser, Otto. Hitler and I. Boston,
Houghton Mifflin Company, 1940. :96)
http://religionandpolitics.web1000.com/
John Harshman
Sean Pitman M.D. wrote:
> Evolving Rube Goldberg Machines
> http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
[snip]
Back again? Is this another post-and-run? Do you ever intend to respond
to any of the arguments made against your claims last time?
> It turns out that there are statistical gaps that separate unique
> protein/enzymatic functions from each other. Not every protein
> sequence will be recognized by a given bacterium. In fact, the vast
> majority of possible protein sequences will not be recognized as
> having function. Because of this problem, if proteins are not already
> very very close in sequencing to begin with, the statistical odds that
> one will "evolve" into another are remote because they are separated
> by a vast number of non-functional amino acid sequences.
I'm afraid that your conclusion doesn't follow from your premises, and
your premises are themselves doubtful. What has been demonstrated is
that *some* proteins can't evolve into *some* other proteins by a chain
of point mutations, each one improving fitness for some *particular,
single* function. It has not been shown that the majority of protein
sequences have no possible function, nor that there is not a path
between any two particular proteins that increases fitness at every step
in some environment.
> Non-recognized or non-functional proteins cannot be guided by natural
> selection along any evolutionary path whatsoever. Why? Because
> nature only sees function. Nature cannot guide if it is blind. Thus,
> nature cannot guide evolution across non-functional gaps.
At least not very large ones. But you have not demonstrated that such
non-functional gaps exist, except in a single case, in a single,
unchanging environment, over a short period of time. This sort of thing
is well known, and is referred to by the label "evolutionary
constraints". Some evolutionary paths exist, and others don't. Showing
that some don't exist doesn't show that none exist. If enough paths
exist, evolution by natural selection works fine. Nobody says natural
selection can follow any conceivable path. I would also bet that no
matter how advantageous it would be, horses will never sprout wings from
their shoulders; but a bipedal dinosaur would be able to recruit its
feathered arms for flight. You raise a non-issue as if it's the
universal answer.
> Then,
> without this guidance of natural selection, evolution is dead.
Not true. If all is as you claim, then evolution solely by natural
selection is dead. We must come up with some mechanism -- perhaps even
divine intervention -- to account for the crossing of such gaps. But our
knowledge of evolution in the sense of common descent does not depend on
knowing the mechanism to be natural selection, or upon knowing the
mechanism at all.
[snip the rest]
Chris Merli
"Sean Pitman M.D." <seanpi...@naturalselection.0catch.com> wrote in
message news:80d0c26f.03040...@posting.google.com...
> Evolving Rube Goldberg Machines
> http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
>
> In chapter four of his controversial book, Darwin's Black Box, Michael
> Behe presents the argument that Rube Goldberg machines exist in living
> things and that such machines are "irreducibly complex." Behe
> presents the argument that the existence of such machines cannot be
> explained by naturalistic mechanisms and are thus examples of
> deliberate design. After all, anyone who has watched cartoons as a
> child knows what a Rube Goldberg machine is and that this machine will
> not work if any one part is removed. As an example, consider the
> following scenario where Behe describes a popular cartoon about the
> loud-mouthed rooster Foghorn Leghorn.
>
> we add just one little part to the cascade? Lets add the rope that
> holds up the telephone pole and a saw that cuts the rope. The string
> is attached to the switch on the saw. When pulled, the string turns
> the saw on and it cuts the rope and the pole falls. A bit more
> interesting and it still works. Now lets add one more little part.
> Lets add the cannon. The string pulls a match and ignites the cannon
> and the cannon ball hits the saw switch which cuts the rope that holds
> evolving a complex cascade one small part at a time. right? It sure
Goal post movement detected
I believe this is the very point that biologist have been trying to get
accross. Evolution is so powerful because it can easily adapt proteins used
for one function to other functions. The fact that it was at all possible
to replace this step is stunning evidence of this power. Think about the
requirements. The system you have described has been fine tuned so that
each part works together and over time small imporvements have continued to
modify them for maximum efficency. Now we are going to obliterate thousands
of generations of careful evolution and yet the organism adapts and creates
a new cog for the system. I am curious as to how many genes you would think
we need to knock out to prove the concept. If he had knocked out ebgA and
another protein had mutated to fill the void would that have been enough?
Need I remind you that the proteins that you are comparing are the very tips
of the evolutionary branch. The truth is the precursor to one or perhaps
both of these genes has a very different sequence. The fact that you can
not get directly from "a" to "b" is not evidence that someone at "c" could
not get to one or both.
>
> So, although cascades are not irreducibly complex in and of
> themselves, the evolution of their individual component parts is still
> statistically impossible because of the gaps of non-function that
> separate each part from its nearest neighbor. Professor Hall never
> evolved anything that crossed a gap of non-function that was more than
> two mutations wide. The single non-functional gap of two mutations
> that he did cross, he could not explain. In fact, by his own
> calculations, he figured this feat to be impossible. taking an average
> of 100,000 years to cross. The apparent success of the crossing of
> even this tiny gap of non-function astounded him. He attempted to
> explain the success of this crossing by saying, "under some conditions
> spontaneous mutations are not independent events." 3 He went on to
> say that this is, "heresy, I am aware." If it is difficult for
> professor Hall to imagine the crossing of such a small gap of
> non-function, what would it take to cross a three mutation gap. or a
> four mutation gap? Consider now that these proteins are hundreds or
> even thousands of amino acids in length. The problem seems clear. In
> fact, because of this problem all living things may have "limited
> evolutionary potential." Bacterial colonies such as Salmonella,
> Proteus, and Pseudomonas can be grown on Hall's selective media or any
> selective media in any sequence until the cows come home. and none of
> any one part, none of the other parts will "work" together. period.
> There is no "cascade" of function since all the parts work together at
> the same time. So, in order to get any function whatsoever from the
> electric motor, all the needed parts must come together in a highly
> ordered way... suddenly. An electric motor, minus one of its parts,
> has no function. It might as well be sitting in a junk pile at the
> city dump.
>
> In fact some bacteria, as Behe points out, have little mechanical
> motors that are very similar to electric motors. Just like mechanical
> motors they require a minimal number of parts, all working together at
> the same time, to produce their rotary motion. These little motors
> power structures called flagella. 1 Flagella are long whip-like cords
> attached to certain bacteria by a little motor of sorts. The motor
> actually spins and causes the flagella to spin. The spinning flagella
> propels the bacterium through the liquid that it is swimming in. The
> problem here is that the motor that spins the flagella is "irreducibly
> complex." It has quite a few parts (fifty or so). Many of these
> parts are irreducible. If even one of these irreducible parts is
> removed. The flagellar motor will not work, not even a little bit.
> Each of these parts is, in itself, complex. just as each link in the
> cascade system is complex. However, what separates an irreducibly
> complex system from a cascading system is that not only are each of
> the parts in an irreducible system separated from each other by huge
> statistical gaps in recognition, but the system itself is entirely and
> completely dependent upon each one of its parts for function. If the
> statistical challenge of evolving just one recognized part is huge,
> try evolving many parts when none of them will be recognized until all
> of them are present in their proper orientation. The system itself is
> an entity that must be recognized in order for natural selection to
> "select" it for survival. The system cannot be recognized until it is
> functional to some degree. An irreducibly complex system is not
> functional in any degree until it has all its parts in working
> order... simultaneously. Only then can it be recognized and selected
> by nature. The irreducibly complex system, unlike a cascading system,
> cannot be built gradually. If the evolution of a cascading system of
> function is admittedly of "limited evolutionary potential" then try to
> imagine the evolution of a truly irreducible system. It is mind
> boggling. Not only has it never been observed and documented, but
> such a mechanism has not even been theorized as of today.
..
Chris Merli
"C.J.W." <watt...@bellatlantic.net> wrote in message
news:3E8C8617...@bellatlantic.net...
So it surprises you that a process that requires thousands of generations to
develop would not be replaced in 1 step? So if I remove the starter from
your car and you had to build a new one you could do it in one step?
>
> The inclusion of IPTG was the result of the decision of
> an intelligent agent (Barry Hall) to deliberately alleviate
> the irreducibility of the system. In the absence of that intelligent
> action, Darwinian processes alone were ineffective. That
> is exactly what intelligent design theorists would expect.
>
> Miller also writes, "the ebg gene is actually only 34%
> homologous to the gene whose activity it replaces (meaning
> that about 2/3 of the protein is quite different from the
> galactosidase gene whose function it replaces)". Yet he
> knows as well as I do that 34% general sequence homology
> makes it virtually certain that the three-dimensional
> structures of the two enzymes are essentially identical.
> And since the active sites (the business end) of the enzymes
> are much more similar (they are identical in 13 of 15
> residues), the ebg enzyme is pretty much a spare copy
> of the lac enzyme. Thus it seems to me that the taking
> over of lac galactosidase function by ebg hardly
> even rises to the level of microevolution.
How much different does the new gene have to be to fullfill your
requirement? My guess is you would only accept tha the genes were different
enough if the gene did not provide the replacement function.
>
> What is actually surprising--even to a design theorist such
> as myself--is Barry Hall's finding that no enzyme other
> than ebg could fill in for the missing lac galactosidase.
> I would have expected otherwise. Perhaps even changes
> we would consider to be "microevolution" are often times
> beyond the reach of Darwinian processes. Perhaps
> even I give natural selection too much credit."
> http://www.arn.org/boards/ubb-get_topic-f-1-t-000637-p-1.html
I get the feeling that your leaps of logic are essentially random.
>
> --
> --W
> "Hitler stopped and looked me
> in the eyes,'Christianity is, for
> the moment, one of the points in the
> programme I have laid down. But
> we must look ahead. Rosenberg is a
> forerunner, a prophet. His theories
> are the expression of the German soul.'"
Ron Okimoto
"Sean Pitman M.D." wrote:
> Evolving Rube Goldberg Machines
> http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
>
This could be interesting if you didn't keep coming back with the same
nonsense. I finally just did a PubMed search on "Hall B AND lactose" and
surprise, surprise I found what you claim is impossible. It was number 5
on the list that came up from the search. The reference below seems to
have found an instance of where three mutations were necessary to get the
gain in function, but the two middle ones were apparently silent. This
seems to have happened by chance in the long study that Hall has
conducted, but long only in relative terms. If this could happen between
1974 and 1995 with only a few thousand experiments at most, why can't it
happen in nature?
Krishnan S, Hall BG, Sinnott ML. 1995. Catalytic consequences of
experimental evolution: catalysis by a 'third-generation' evolvant of the
second beta-galactosidase of Escherichia coli, ebgabcde, and by ebgabcd,
a 'second-generation' evolvant containing two supposedly 'kinetically
silent' mutations. Biochem J 1995 Dec 15;312 ( Pt 3):971-7
It also looks like I am correct and that in the original study Hall is
looking for sustainable growth on lactose. Evolution doesn't happen this
way. Evolution does not depend on a do or die situation. In nature the
organism without the mutation lives happily in the environment. This is
not the case for the Hall experiments. The organism dies in the Hall
environment, no second chances. Evolution doesn't work this way if it
did there would have to be some designer tweeking every new life being
born so that it wouldn't die in some new lethal environment that it was
going to be born into. This is so far from reality, why do you expect it
to support what you are saying about it? I'm not saying that Hall can't
make some very firm conclusions from his study, you just can't make the
ones you are trying to make. Look at the above example. Hall was able
to select for a better enzyme that needed two silent substitutions and a
third mutation before he was able to observe it as growing better in his
system. That is how it works in nature. It looks like Hall has met your
challenge with the system you are trying to say supports your contention
that it is impossible. Why don't you research the work more carefully
before making these types of mistakes? Since this is a 1995 paper if you
had done your homework you wouldn't have had to write all that stuff that
is now refuted by the system of your own choosing. Do your own research
and stop relying on creationist sources. You know that they are out to
lunch. You can use them to get a start in thinking about some problem,
but you know that they have to ignore most of the data to believe what
they do, so you have to look for this data yourself.
Oh, ebg is related to beta galactosidase, but the gene duplication
probably happened 2.2 billion years ago according to the molecular
analysis of related proteins done by Hall. As you might expect after
that long they are very different proteins. If you study this system you
can see just how gene duplication is responsible for the permeases, and
inducer genes of the two cistrons. This is like the blood clotting
system that the ID people have to acknowledge that there is a lot of
evidence that it could have evolved. The proteins in the system are
related to eachother and obviously were created by gene duplication.
What design mechanism would do this? We have a mechanism that we observe
to occur in nature that fits the bill very nicely, but where is your
mechanism and how does it work?
It is good to see you back. It has been pretty boring around here with
just the willfully ignorant moron types posting on the creationist side.
Read the recent posts by Glenn, McCoy, nowhereman, and Zoe but be
prepared to cringe a lot. With guys like those on your side you don't
need me to tell you how bad off your side is. What makes it worse is
that they have been about the only ones supporting the creationist
position.
IC the way Behe uses it is bullshit. Demonstrate that it isn't using his
old or new definitions if you can. He admits that IC systems can evolve,
but he defines his IC systems as those IC systems that can't evolve. So
IC by itself is worthless, it has to be coupled with something else. He
hasn't figured out how to determine if they can't evolve, so he is stuck
with a worthless concept that he can't do anything with.
Ron Okimoto
C.J.W.
Chris Merli wrote:
The whole point of proving irreducible complexity or reducible complexity is the
fact that everything is necessary in one step.
<snip>
--
--W
æ»´itler stopped and looked me
in the eyes,舛hristianity is, for
the moment, one of the points in the
programme I have laid down. But
we must look ahead. Rosenberg is a
forerunner, a prophet. His theories
are the expression of the German soul.樗
Chris Merli
No I am afraid you have misundersttod you own side's arguement. You want to
say the IR system could not have developed in a stepwise fashion. I am
pointing out that, however the system came to be, we would not expect that
as soon as the old gene was removed that a new one would instantly appear to
replace it. The original gene and others in the sequence underwent many
mutation events. A good deal of these were probably also interdependent.
You want to see all of these mutations happen in one magical step.
> <snip>
>
> --
> --W
> "Hitler stopped and looked me
> in the eyes,'Christianity is, for
> the moment, one of the points in the
> programme I have laid down. But
> we must look ahead. Rosenberg is a
> forerunner, a prophet. His theories
> are the expression of the German soul.'"
Sean Pitman
> > Evolving Rube Goldberg Machines
> > http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
>
> This could be interesting if you didn't keep coming back with the same
> nonsense.
Well, if what I present is all "nonsense" and so obviously so, why do
you waist so much of your time with it?
> I finally just did a PubMed search on "Hall B AND lactose" and
> surprise, surprise I found what you claim is impossible. It was number 5
> on the list that came up from the search. The reference below seems to
> have found an instance of where three mutations were necessary to get the
> gain in function, but the two middle ones were apparently silent. This
> seems to have happened by chance in the long study that Hall has
> conducted, but long only in relative terms. If this could happen between
> 1974 and 1995 with only a few thousand experiments at most, why can't it
> happen in nature?
>
> Krishnan S, Hall BG, Sinnott ML. 1995. Catalytic consequences of
> experimental evolution: catalysis by a 'third-generation' evolvant of the
> second beta-galactosidase of Escherichia coli, ebgabcde, and by ebgabcd,
> a 'second-generation' evolvant containing two supposedly 'kinetically
> silent' mutations. Biochem J 1995 Dec 15;312 ( Pt 3):971-7
Actually, after reading the abstract, it is not clear to me that the
"c" and "d" changes were actually "nonfunctional" changes. The
abstract says that they were, "hitherto considered to have no kinetic
effect." However, the abstract goes on to say, "that the c and d
changes in fact accelerate the hydrolysis of the glycosyl-enzyme
intermediate by a factor of 2.5, and also decrease the charge on the
aglycone oxygen atom at the first transition state..."
I have yet to obtain and read the entire paper, but it seems to me
that these c and d mutational changes were initially thought to be
neutral but were later found to actually be functional. In any case,
depending on the size of the protein involved and the complexity of
the function involved a gap of three neutral mutations is not an
unreasonable distance for random/neutral evolution to cross in a
reasonable amount of time. If the complexity of the function is
relatively low, there might be many different protein sequences of a
given length or less that could perform that function. The odds that
two or three random mutations would end up at one of these many
different protein sequences is a lot better than the odds two or three
mutations being "right" for a more complex function where there are
only a relatively few protein sequences of a given length able to
produce a that function. The lactase function may have a fair number
of different protein sequences that could hydrolyze lactose. The fact
that Hall has been unable to find any other genetic sequence, aside
from the lacZ and the ebg genes, able to produce a lactase enzyme
despite heavy selection pressures over hundreds of thousands of E.
coli generations, seems to me to indicate a fairly complex function.
For example, the odds of getting one, two, or even three necessary
mutations "right" in a reasonable amount of time, even in a gene some
3,500 base pairs in length, is not unimaginable . . . since this gene
is starting very close to the "goal" to begin with. As a hypothetical
example, consider the following parameters:
· A stable population of one trillion (1012) E. coli bacteria (equal
to the volume of 10mL or an average hospital syringe)
· A bacterial generation time of 20 minutes (E. coli)
· An average bacterial genome of 4.1 million base pairs (E. coli)
· A mutation rate of 1 x 10-4 mutations per base pair per generation.
(Hall proposes that bacteria undergo "hypermutation" in starvation
states. The average rate is much lower at about 1 x 10-9 mutations per
base pair per generation)
Given these parameters, how long would it take to evolve the first
mutation? The odds that the correct position would be mutated in a
clonal E. coli population would be 1 in 4.1 million. The odds that the
correct base would get mutated at this location are 1/4. The odds that
both would happen are 1 in 16.4 million mutations. With a stable
population of one trillion and a mutation rate of about 410 mutation
per genome per generation, the "correct" mutation will occur in about
25,000,000 bacteria in the first generation.
But, what if the starting sequence was two mutations away from the
desired lactase function? Would that make any difference? The odds of
getting either one of the two needed mutations with the first mutation
are 1 in 8.2 million mutations. The odds of getting the second
mutation right are 1 in 16.4 million mutations. So, the odds of
getting both mutations right are 1 in 134,480,000,000,000 (~1.34
trillion) mutations. With these odds, the correct mutation will occur
in about 315 bacteria in the first generation.
If the starting sequence was three mutations away from the desired
function, the odds of getting all three mutations right shoots up to 1
in 735,157,333,333,333,333,333 (~735 million trillion) mutations. With
these odds, the correct mutation will occur in one bacterium in
1,792,682 generations. With a generation time of 20 minutes, that's a
bit over 68 years.
Four mutations would take about 279,740,233 (~280 million) years.
These predictions also bear up in the laboratory. There are many
bacteria that utilize galactose and glucose and yet they cannot
utilize lactose. For example, practically all of the members of the
bacterial type called Shigella cannot utilize lactose but they do
utilize glucose. The same can be said for the many other bacteria such
as Salmonella, Proteus, and Pseudomonas etc. All of these bacteria
could in fact use a lactase gene if it became available to them. They
would in fact be able to utilize the enzymatic activity of the
galactosidase protein if they had access to it or to any other lactase
enzyme. Why then do they not simply "evolve" any one of these possible
lactase genes?
http://naturalselection.0catch.com/Files/Galactosidase%20Evolution.html
> It also looks like I am correct and that in the original study Hall is
> looking for sustainable growth on lactose. Evolution doesn't happen this
> way. Evolution does not depend on a do or die situation. In nature the
> organism without the mutation lives happily in the environment. This is
> not the case for the Hall experiments. The organism dies in the Hall
> environment, no second chances.
Actually, I think that you have misread Hall's work. The E. coli do
not die in the lactose environment set up by Hall. The media is a
"selective media". It does not kill off those bacteria that do not
evolve the lactase enzyme, but only promote growth and improved
survival of those that do evolve the lactase function. Please, go and
read the paper again. The selective media works very much like a
natural environment where the bacteria live just fine, but could live
better if they had certain functions (such as lactase ability) in a
given environment (one with lactose in it).
> Evolution doesn't work this way if it
> did there would have to be some designer tweeking every new life being
> born so that it wouldn't die in some new lethal environment that it was
> going to be born into. This is so far from reality, why do you expect it
> to support what you are saying about it? I'm not saying that Hall can't
> make some very firm conclusions from his study, you just can't make the
> ones you are trying to make. Look at the above example. Hall was able
> to select for a better enzyme that needed two silent substitutions and a
> third mutation before he was able to observe it as growing better in his
> system. That is how it works in nature.
You can't have it both ways. If Hall's experiment was done with the
use of "lethal environments" as you suggest, then he couldn't just
wait around for neutral mutations to add up because the bacteria would
be killed before the third "functional" mutation came along. In other
words, you just admitted that Hall was in fact using a non-lethal
environment with a selective advantage for certain functions. You
even said, "This is how it works in nature." Come on Ron, get it
together and be consistent. Hall's experiments, both in 1974 and 1995
used non-lethal selective growth media. Your argument is therefore
flawed.
> It looks like Hall has met your
> challenge with the system you are trying to say supports your contention
> that it is impossible.
I never said that a neutral gap of 3 mutations was "impossible." I
said that depending on function complexity that certain gaps of such
lengths or larger would be impossible for neutral evolution to cross
in a reasonable amount of time. Where has Hall demonstrated this to
be incorrect? He still hasn't demonstrated the evolution of the
lactase function in E. coli lacking both the lacZ as well as the ebg
genes. Why is this? The only logical reason for such a limitation to
the evolution of the lactase function in such bacterial colonies
(despite the potential benefits if they were able to evolve this
function) is that there is a gap in function between the lactase
function and the collective genomic real estate potential of Hall's E.
coli colonies... even given hundreds of thousands of generations.
> Why don't you research the work more carefully
> before making these types of mistakes?
LOL - Why don't you? You evidently do not understand the experiments
that you are trying to use to support your position.
> Since this is a 1995 paper if you
> had done your homework you wouldn't have had to write all that stuff that
> is now refuted by the system of your own choosing. Do your own research
> and stop relying on creationist sources. You know that they are out to
> lunch. You can use them to get a start in thinking about some problem,
> but you know that they have to ignore most of the data to believe what
> they do, so you have to look for this data yourself.
Oh, I have done a fair amount of reading/research for myself. You
perhaps should do a bit of your own thinking as well and not rely so
much on the conclusions of mainline popular scientists. Granted, many
if not most YECs don't know the heck what they are talking about.
But, the same can be said for evolutionists. There are a few bright
lights in both camps. So, we must all try and think for ourselves.
You and the evolutionist camp may turn out to be correct. However,
until I understand evolution and how it works for myself, I'm
certainly not going to take anyone's word for it at face value.
That's just not me.
> Oh, ebg is related to beta galactosidase, but the gene duplication
> probably happened 2.2 billion years ago according to the molecular
> analysis of related proteins done by Hall.
Actually, the ebg gene is very different from the lacZ gene (hexomere
vs. tetramer for example). There really is not good reason to believe
that ebg was produced via a dupliction mutation, especially if it
happened 2.2 billion years ago. In far less than 2 billion years,
random mutations would have obliterated the ebg gene out of existence
since it was basically "neutral" when the lacZ gene was operational.
In any case, you seem to be really reaching for something, anything,
to explain this problem. I'm sure you can do better than this... but
maybe not?
> As you might expect after
> that long they are very different proteins. If you study this system you
> can see just how gene duplication is responsible for the permeases, and
> inducer genes of the two cistrons. This is like the blood clotting
> system that the ID people have to acknowledge that there is a lot of
> evidence that it could have evolved. The proteins in the system are
> related to eachother and obviously were created by gene duplication.
If given the "a priori" assumption that evolution is true, then yes,
this is the only logical explanation. However, just because various
genes look quite similar or even identical does not mean that they
necessarily arose via gene duplication. Very similar genes may be
used in very different ways in different systems of function. The
evolution of different systems of function using the same genes is
still quite problematic since the assembly of any new system of
multiple genes would require the crossing of neutral gaps in function.
No such functional system of multiple genes, to my knowledge, has
been demonstrated to have evolved in real time. For example, it is
thought that the motility function of bacterial flagella arose via the
use of existing genes in new combinations so as to produce a new
function of motility. Well, if it is so easy, and there are few or no
neutral gaps to cross, the evolution of such a motility system should
be easy to demonstrate in short order. After all, the necessarily
genes to produce all the necessary parts are all there in the
non-motile cell. What is the problem with using these existing parts
to make a new function? It should be so easy, but it really runs into
the same problem as using the same 20 amino acids to produce new
functions. All the amino acids are there, but making a new function
using the 20 amino acids quickly runs into roadblocks of gaps of
neutral/non-function. The same thing happens when you try to use
existing proteins to make new functions. The gaps are still there and
are even wider than trying to cross gaps in single protein function.
> What design mechanism would do this? We have a mechanism that we observe
> to occur in nature that fits the bill very nicely, but where is your
> mechanism and how does it work?
But you do not have a mechanism that you can detail as to how such
gaps are crossed. It is back to the "God of the Gaps" argument. If
you can explain how to cross the gaps using naturalistic mechanisms,
then I will believe you. Otherwise, you have nothing but wishful
thinking. For example, it is easy to explain how a window could be
broken using a naturalistic mechanism, but it is another thing
entirely to explain how a broken window can be fixed using a
naturalistic mechanism.
> It is good to see you back. It has been pretty boring around here with
> just the willfully ignorant moron types posting on the creationist side.
> Read the recent posts by Glenn, McCoy, nowhereman, and Zoe but be
> prepared to cringe a lot. With guys like those on your side you don't
> need me to tell you how bad off your side is. What makes it worse is
> that they have been about the only ones supporting the creationist
> position.
I have been very busy lately, but thanks for the compliment here.
Really though, telling me that I only have idiots who support me
really doesn't help your position. All it says is that my position is
unpopular and that you are strongly supported by the popular vote.
This means nothing since it explains nothing in a way that I can
understand. It is just an argument of authority, but says nothing of
explanatory substance.
> IC the way Behe uses it is bullshit. Demonstrate that it isn't using his
> old or new definitions if you can. He admits that IC systems can evolve,
> but he defines his IC systems as those IC systems that can't evolve. So
> IC by itself is worthless, it has to be coupled with something else. He
> hasn't figured out how to determine if they can't evolve, so he is stuck
> with a worthless concept that he can't do anything with.
I don't agree with everything Behe says. I think that he is somewhat
confused in certain areas. I do agree with his basic definition of
IC, but I think that he limits himself in what he defines as IC. For
me, I consider all functions to be irreducibly complex. I don't limit
the definition at all. This can be easily demonstrated and supported.
Any particular function that is dependent upon various "parts" for
its operation is IC. Remove certain parts and that function will
cease. This means that a function can be destroyed if the parts are
changed or "reduced". The lactase function is IC. Remove a certain
number of amino acids and that function will end. Obviously then, IC
functions can evolve. However, the problem comes with the type of
function in question. Some functions are very simple functions.
Others functions are much more complex. Simple functions may require
fewer parts and there may be many more arrangements of specified parts
that could still do a simple function. However, more complex
functions might require more parts and there are probably far fewer
relative arrangements of such parts that could produce this given
function. This means that random/neutral mutations would be far less
likely to come across a collection of parts with a more complex
function than a more simple function (such as the motility function
vs. nylonase function).
Behe makes the mistake of trying to limit the definition of IC systems
to those systems of function that he considers to be highly complex.
I feel that this is a significant mistake on his part. However, his
basic concept is a good one and remains as a roadblock to natural
selection as a reasonable mechanism for naturalistic evolution.
> Ron Okimoto
Sean
John Harshman
Sean Pitman wrote:
> Ron Okimoto <roki...@uark.edu> wrote in message news:<3E8CAB80...@mail.uark.edu>...
>
>
>>>Evolving Rube Goldberg Machines
>>>http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
>>>
>>This could be interesting if you didn't keep coming back with the same
>>nonsense.
>>
>
> Well, if what I present is all "nonsense" and so obviously so, why do
> you waist so much of your time with it?
There are several reasons. One is that lurkers may not have seen the
first refutations of your nonsense. Another is the hope that you will
say something new if encouraged, or will begin to understand the
objections to your argument, and may even reply to them.
> For example, the odds of getting one, two, or even three necessary
> mutations "right" in a reasonable amount of time, even in a gene some
> 3,500 base pairs in length, is not unimaginable . . . since this gene
> is starting very close to the "goal" to begin with. As a hypothetical
> example, consider the following parameters:
>
> · A stable population of one trillion (1012) E. coli bacteria (equal
> to the volume of 10mL or an average hospital syringe)
> · A bacterial generation time of 20 minutes (E. coli)
> · An average bacterial genome of 4.1 million base pairs (E. coli)
> · A mutation rate of 1 x 10-4 mutations per base pair per generation.
> (Hall proposes that bacteria undergo "hypermutation" in starvation
> states. The average rate is much lower at about 1 x 10-9 mutations per
> base pair per generation)
I'm not sure these parameters make sense. The hypermutation is in
bacteria that aren't dividing, so combining it with a "generation time"
wouldn't work. But never mind, they are good enough to demonstrate your
point, which is that any particular string of neutral mutations is
vanishingly unlikely, just as any particular ordering of 52 cards in a
deck is vanishingly unlikely (and just as irrelevant to the playing of a
hand of bridge as your claim is to the process of evolution).
> Given these parameters, how long would it take to evolve the first
> mutation? The odds that the correct position would be mutated in a
> clonal E. coli population would be 1 in 4.1 million. The odds that the
> correct base would get mutated at this location are 1/4.
Quibble: 1/3. If you assume a mutation, you have to assume that it's to
a different base than the one that was already there.
[snip demonstration that neutral evolution is not a good way to produce
any specific set of changes]
Pokemoto
>Path:
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>From: seanpi...@naturalselection.0catch.com (Sean Pitman)
>Newsgroups: talk.origins
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One of these changes without the last one has a negative affect on activity,
but what is the affect of the three together? It is neutral in the system
because all they are looking for is if the bacteria can grow on lactose.
>
>I have yet to obtain and read the entire paper, but it seems to me
>that these c and d mutational changes were initially thought to be
>neutral but were later found to actually be functional. In any case,
>depending on the size of the protein involved and the complexity of
>the function involved a gap of three neutral mutations is not an
>unreasonable distance for random/neutral evolution to cross in a
>reasonable amount of time.
Alert, Alert, goal post shift. The challenge was three changes. So what would
you consider to be impossible, now? 5, 6, 10? It looks like 6 is a real
possibility, so you better go with 10, but that would probably be worthless
because you can't come up with an example where that would have to happen.
Things aren't as impossible as you thought, are they?
I'm leaving town, in just a few minutes, but I'll try and get back to the rest
of this post if it is worth it. As you say above it may not be.
Snip:
Ron Okimoto
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
On Thu, 3 Apr 2003 17:59:50 +0000 (UTC),
seanpi...@naturalselection.0catch.com (Sean Pitman M.D.) wrote:
>Evolving Rube Goldberg Machines
>http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
[enormous snip]
>But what if the E. coli had
>not been so fortunate as to have this spare tire gene? What would
>have happened then? Hall wondered about this himself. He then
>deleted the spare tire gene as well as the lacZ genes. Would there be
>lactase evolution now?
See 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)
where they have evolved a beta glactosidase from an enzyme other than
the "spare tyre". I believe I have directed you to this paper before.
>It turns out that there are statistical gaps that separate unique
>protein/enzymatic functions from each other. Not every protein
>sequence will be recognized by a given bacterium.
Again, you are still hung up on the idea that you _must_ have certain
neutral mutations before proceeding to subsequent benefical mutations.
This is not so. let's consider the evolution of Extended
Spectrum Beta Lactamases. Extended beta lactams are synthetic drugs
that were not previously in the natural environment. An example is
cefotaxime, these drugs have bulky side chains added so that the
lactamases cannot hydrolyse them (although they can still bind to the
Dd-petidases), and were introduced (in part) to attack
penicillin-resistant bacteria
Prior to 1981 there were no ESBL expressing bacteria, in 1981
cefotaxime entered clinical use, by 1985 the double mutant TEM3
(E104K/G238S) was isolated clinically. In 1994 (see refs in Orencia)
the triple mutant E104K/M182T/G238S was predicted based on mutagenesis
studies and in 1998 TEM52 (E104K/M182T/G238S) was isolated.
The evolution of TEM's from the first reported isolates has been
rapid. In 1994 around 19 TEM's were known (in contrast to the sole
TEM1 which appeared in the '60's), by 2001 there were 90. Experimental
evolution studies have succeeded in reproducing and _predicting_ the
evolution of mutants of TEM1.
Lets look at some of these 90 evolved variants. For example TEM18
E104K/G238S vs TEM88 E104K/G238S/M128T/G196A. The latter two mutations
appear to be neutral, and have been fixed in the population by drift.
TEM42 differs from TEM1 in 13 positions, of which only 5 are
functional, the rest neutral. Thus, in TEM42, the majority
of mutations are neutral, but they did not _require_ to be in place
before functional mutations could take place.
Again, you are hung up on the idea that there exist systems that
require 3 or more mutations before a new function is found (and that
these systems are common). As I've pointed out before, in most cases
simple mutations are enough to generate weak, but useful new functions
(without the loss of the original function) and the path from Function
A to Function B has intermediates are all functional.
One hypothetical pathway might look like this (where -> indicates a
mutation)
Function A -> Function A very weak function B -> weak Function A weak
Function B -> very weak Function A better Function B -> Function B
The evolution of ESBL's from TEM's looks like this
TEM1 (BL, no effective ESBL) -(E104K)-> TEM1*(BL, very weak ESBL)
-(G238S)-> TEM3 (less BL, robust ESBL) -(M187T)-> TEM52 (modest BL,
excellent ESBL)
As well as improving ESBL M187T also stabilizes the enzyme, making it
more effective.
At each stage you have a working enzyme doing something vital for the
cell. Another example system I used was a DD-peptidase -> Penicillin
binding protein with weak dd-peptidase activity -> penicillin binding
protein with weak Lactamase activity -> Lactamase. At each stage a
usefully activity is occurring, and the beta-lactamase activity can
develop in steps with no "non-functional" intermediates,even though
Dd-peptidase activity is lost. It is interesting that methicillin
resistance is due to the production of an extremely high affinity
penicillin binding protein, which protects the other Dd-peptidases
from attack.
GNIADKOWSKI, M. (2001). Evolution and epidemiology of
extended-spectrum beta-lactamases (ESBLs) and ESBL-producing
microorganisms. Clin Microbiol Infect, 7, 597-608.
ORENCIA, M.C., YOON, J.S., NESS, J.E., STEMMER, W.P. & STEVENS, R.C.
(2001). Predicting the emergence of antibiotic resistance by directed
evolution and structural analysis. Nat Struct Biol, 8, 238-42.
PETROSINO, J., CANTU, C., 3RD & PALZKILL, T. (1998). beta-Lactamases:
protein evolution in real time. Trends Microbiol, 6, 323-7.
RICE, L. (2001). Evolution and clinical importance of
extended-spectrum beta-lactamases. Chest, 119, 391S-396S.
[snip]
>Some do try and explain flagellar evolution by proposing that many of
>the parts in a flagella are used as parts in other cellular systems of
>function. For example, the actual flagella is very similar in
>structure to long tube-like secretory structures. In fact, it is
>thought that some flagella might function as both a motility structure
>as well as a secretory structure.
See
http://www.health.adelaide.edu.au/Pharm/Musgrave/essays/flagella.htm
for one example of step by step assembly of functional motile flagella
from functional non-motile precurrsors.
Cheers! Ian
=====================================================
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
Frank J
(snip)
IIRC you were a young-earther, at least as of a few months back. Now
you're defending Behe, an old-earther who accepts common descent, and
is even more "evolutionist" than "saltationist." Are you coming around
to Behe's model, or will you be trying to refute him too?
Sean Pitman
Just because I agree with one aspect of another person's thinking does
not mean that I agree with everything that person thinks. I agree
with the basic concept/argument of irreducible complexity (IC) as Behe
presents it. However, there are certain important ideas that Behe
claims for IC that I do not agree with. Behe tries to limit IC
systems to those systems which he considers to be of high complexity.
I disagree with this limitation.
I think that all functions are irreducibly complex. Some functions
are more simple than others and therefore have a relatively greater
number systems or arrangement of a given number of parts that can
perform them. They are also more likely to be made up of a relatively
fewer number of parts and are therefore more likely to be closer to
something contained in a given collection of part arrangements (ie:
gene pool). Other functions are much more complex and therefore have
a relatively fewer number of arrangements of a given number of parts
that can perform them. Obviously then, neutral evolution would have
an easier time crossing the smaller neutral gaps between the more
simple functions as compared to the wider neutral gaps that separate
the more complex functions from the current genomic real estate of a
given creature or gene pool.
So yes, I do agree with Behe in some areas, but certainly not in every
area of his thinking.
Sean
Ian
news:80d0c26f.0304...@posting.google.com...
> fn...@comcast.net (Frank J) wrote in message
news:<38c5d0dd.03040...@posting.google.com>...
> > seanpi...@naturalselection.0catch.com (Sean Pitman M.D.) wrote in
message news:<80d0c26f.03040...@posting.google.com>...
> > > Evolving Rube Goldberg Machines
> > > http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
> >
> > (snip)
> >
> > IIRC you were a young-earther, at least as of a few months back. Now
> > you're defending Behe, an old-earther who accepts common descent, and
> > is even more "evolutionist" than "saltationist." Are you coming around
> > to Behe's model, or will you be trying to refute him too?
>
> Just because I agree with one aspect of another person's thinking does
> not mean that I agree with everything that person thinks. I agree
> with the basic concept/argument of irreducible complexity (IC) as Behe
> presents it. However, there are certain important ideas that Behe
> claims for IC that I do not agree with. Behe tries to limit IC
> systems to those systems which he considers to be of high complexity.
> I disagree with this limitation.
>
<chez watt>
> I think that all functions are irreducibly complex.
</chez watt>
Sean Pitman
> Back again? Is this another post-and-run? Do you ever intend to respond
> to any of the arguments made against your claims last time?
Now, I may be wrong, but I "responded" quite a bit to various
arguments against my position(s) "last time." Perhaps I have not
responded to your arguments in particular but I have certainly
responded at great length to many of those responding to my ideas.
You should know this. You were there. In any case, I cannot respond
to everyone since there are a lot more of you guys than there are of
me. I have a job and other interests which limit my time to respond
to everyone who wishes me to discuss their ideas with them. So, I
pick and choose those whose arguments that are of particular interest
to me as I have the time and inclination. Really, I'm sorry. I just
cannot reply to everyone even though many expect me to and even though
I would like to.
> I'm afraid that your conclusion doesn't follow from your premises, and
> your premises are themselves doubtful. What has been demonstrated is
> that *some* proteins can't evolve into *some* other proteins by a chain
> of point mutations, each one improving fitness for some *particular,
> single* function. It has not been shown that the majority of protein
> sequences have no possible function, nor that there is not a path
> between any two particular proteins that increases fitness at every step
> in some environment.
Oh really? It seems quite obvious to me that given a particular
creature, such as a bacterium, that the vast majority of possible
amino acid sequences/proteins of a given length will have no
beneficial function for that creature in its current environment. To
say otherwise is extremely naive in my estimation. Only a very tiny
fraction of the potential amino acid sequences will be recognized by
any given bacterium or living cell in any given creature. Take humans
for example. The vast majority of human DNA does not code for any
functional protein much less a beneficially functional protein. The
proteins that are coded for are somewhat plastic, true, but they are
also very specific. If changed or "denatured" to any significant
degree, they loose all function. This means that the vast majority of
potential protein sequences and three-dimensional shapes are worthless
to a given human cell.
As far as demonstrating a negative (ie: A lack of a functional path
between two different proteins), it is impossible this side of
eternity. A negative finding never means that a positive finding is
impossible. However, the likelihood that a negative finding will
occur can be calculated. The odds can be estimated to give a
predictive power to the hypothesis that a negative finding will arise
for a given situation in a given span of time. Hall's experiment was
interesting in that it seemed to show such a negative finding. Those
bacteria that did not have the lacZ nor the ebg genes never evolved
the lactase function. Given their entire collective genomic real
estate, they had nothing close enough to evolve a gene to produce this
function despite being observed over many thousands of generations.
This seems to indicate the presence of some sort of statistical block
to the evolution of this function starting from hundreds of
"particular" genes. This seems to indicate that there, "is not a path
between any two particular proteins [in this particular gene pool]
that increases fitness at every step in [the given] environment." If
there was such a path, the traversing of this path should happen very
rapidly. The fact that it takes so long to cross this path means that
there simply is not a step-by-step improvement as the path is
traversed. Natural selection has been blinded along the way by two or
more "neutral" steps. With each neutral step that must be traversed,
the time required increases dramatically.
> > Non-recognized or non-functional proteins cannot be guided by natural
> > selection along any evolutionary path whatsoever. Why? Because
> > nature only sees function. Nature cannot guide if it is blind. Thus,
> > nature cannot guide evolution across non-functional gaps.
>
> At least not very large ones. But you have not demonstrated that such
> non-functional gaps exist, except in a single case, in a single,
> unchanging environment, over a short period of time. This sort of thing
> is well known, and is referred to by the label "evolutionary
> constraints". Some evolutionary paths exist, and others don't. Showing
> that some don't exist doesn't show that none exist. If enough paths
> exist, evolution by natural selection works fine. Nobody says natural
> selection can follow any conceivable path. I would also bet that no
> matter how advantageous it would be, horses will never sprout wings from
> their shoulders; but a bipedal dinosaur would be able to recruit its
> feathered arms for flight. You raise a non-issue as if it's the
> universal answer.
This is complete wishful thinking. No one has ever demonstrated the
"lack of gaps" between such complex functions as the modification of
scales into feathers or the evolution of a motility system in a
non-motile bacterial colony. The only evolution that has ever been
demonstrated in real time is the evolution of relatively simple
functions, such as the simple enzymatic functions of single proteins
(ie: lactase, nylonase, antibiotic resistance etc.). Such functions
are so simple that the gaps between what is already there and such
comparatively simple functions are relatively small, requiring only a
very few mutations to achieve. When you start talking about the
evolution of feathers, flight, eyesight, motility, and other such
highly complex functions, you are talking about functions that require
multiple genes and proteins all working together at once. The neutral
gaps between what is there and the development of such highly complex
functions are enormous. If you think that a neutral gap in function
that requires just one protein sequence is hard to cross, try crossing
a gap that requires the evolution of multiple proteins to cross where
hundreds or even many thousands of neutral mutations are needed.
If there were such a path from scales to feathers, then we should be
able to quickly demonstrate such evolution in real time. If each and
every step were beneficially functional in some unique way from what
came before, then such evolution would proceed very much as Dawkins's
experiment with his computer phrase evolution. Dawkins started with a
nonfunctional phrase and then, using a selection mechanism that
compared mutating sequences with the ideal sequences, his computer
evolved the phrase, "Methinks it is like a weasel" in less than 50
phrase "generations". The problem with this experiment, of course, is
that it does not reflect the abilities of natural selection. Natural
selection does not have the ability to recognize nucleic acid or amino
acid sequences directly, but only as they have some sort of function.
However, if each and every change did have a function, then natural
selection would in fact work very much like Dawkins's computer
program. The evolution across such a functional path would occur at
an extremely rapid rate. There would be no need for millions and
billions of years to achieve the diversity that we see in the natural
world for such changes could be and would be realized in short order.
The idea that eons of time are needed for evolution to be successful
means that there is not a path of function where each and every step
is beneficially unique. There are gaps between various functions that
require a lot of time to cross. In fact, many of these gaps seem so
wide that billions or even many trillions upon trillions of years are
simply not enough. This is where the idea of design comes into play.
Intelligence can cross such gaps in short order. Humans can type into
the computer, "Methinks it is like a weasel" far far faster than a
computer can come up with that phrase/function using neutral
evolution. Why? Because humans have access to an intelligent mind
that can be creative were as computers are not intelligent or
creative. Likewise, genes and natural selection are not intelligent
or creative. The gaps and functions are there. The only logical
explanation to explain their existence is intelligent design.
Intelligent design is the only force that exists in the universe, that
we are aware of, that creates functions of the complexity and variety
that we see in living things.
> > Then,
> > without this guidance of natural selection, evolution is dead.
>
> Not true. If all is as you claim, then evolution solely by natural
> selection is dead. We must come up with some mechanism -- perhaps even
> divine intervention -- to account for the crossing of such gaps. But our
> knowledge of evolution in the sense of common descent does not depend on
> knowing the mechanism to be natural selection, or upon knowing the
> mechanism at all.
Oh really? This is an amazing statement! You know that naturalism is
the answer... without knowing how it works? You don't need to know
the mechanism to know that it works? Natural selection really does
not have to be part of the mechanism in order for naturalism to be
creative? Incredible! Well then, what other force do you know of,
besides natural selection, which can help random mutations create such
complex and integrated functions as we see in living things?
You obviously have a very great faith in the power of naturalism to
answer all questions pertaining to the physical universe. For you,
the very notion that there just might be evidence of design in the
natural world/universe is simply out of the question. You approach
all ideas with this "a priori" assumption that naturalism must answer
all that we see in the natural world. However, this is not a
scientific view. The scientific method does not require any a priori
assumptions to be brought to the table. To say that science cannot
detect intelligent design is not scientific nor is it supported by the
evidence that we have available to us. Design is detected and
proposed as a source for many observations that we see on a daily
basis. Why? Because many things that we see around us, such as a
fixed window or a Picaso painting, have no naturalistic explanation.
To say then that living things had to have arisen "naturally", when
one has no clue as to the naturalistic mechanism, seems to me like
deliberate insanity.
> John Harshman <harshman....@pacbell.net> wrote in message news:<3E8DAE72...@pacbell.net>...
>
> > For example, the odds of getting one, two, or even three necessary
> > mutations "right" in a reasonable amount of time, even in a gene some
> > 3,500 base pairs in length, is not unimaginable . . . since this gene
> > is starting very close to the "goal" to begin with. As a hypothetical
> > example, consider the following parameters:
> >
> > · A stable population of one trillion (1012) E. coli bacteria (equal
> > to the volume of 10mL or an average hospital syringe)
> > · A bacterial generation time of 20 minutes (E. coli)
> > · An average bacterial genome of 4.1 million base pairs (E. coli)
> > · A mutation rate of 1 x 10-4 mutations per base pair per generation.
> > (Hall proposes that bacteria undergo "hypermutation" in starvation
> > states. The average rate is much lower at about 1 x 10-9 mutations per
> > base pair per generation)
>
> I'm not sure these parameters make sense. The hypermutation is in
> bacteria that aren't dividing, so combining it with a "generation time"
> wouldn't work.
Yes, mutations (hypermutation or not) happen in a given bacterium
before it divides. However, once the mutations occur, these mutations
are passed on to the bacterium's clonal offspring via the
division/replication/mitotic process. Then, these offspring also
mutate and these new mutations are added the previous mutations and
are all passed on to the next generation... and so on. So you see,
the mutation rate per generation can be calculated. In fact, Hall
does so in his own paper. He makes his own estimations of the
mutation rates for his bacterial colonies, "per generation." Please,
go back and read his paper and reevaluate what you just said.
> But never mind, they are good enough to demonstrate your
> point, which is that any particular string of neutral mutations is
> vanishingly unlikely, just as any particular ordering of 52 cards in a
> deck is vanishingly unlikely (and just as irrelevant to the playing of a
> hand of bridge as your claim is to the process of evolution).
You evidently do not understand the difference between a hand of
bridge and the evolution of novel functions. Every hand in a hand of
bridge, no matter how rare, has a unique function in the game of
bridge. However, not every "hand" or series of nucleotides in a
genome of a given creature has a unique function. In fact, the vast
majority of potential DNA sequences are non-functional or neutral. To
get to a new function requires random neutral drift around a huge sea
of neutral/non-functional sequences. This random wandering takes
time. For the evolution of more and more complex functions, this time
of drift becomes so huge that even trillions of years are nothing
compared to the time needed.
> > Given these parameters, how long would it take to evolve the first
> > mutation? The odds that the correct position would be mutated in a
> > clonal E. coli population would be 1 in 4.1 million. The odds that the
> > correct base would get mutated at this location are 1/4.
>
> Quibble: 1/3. If you assume a mutation, you have to assume that it's to
> a different base than the one that was already there.
In the replacement of a particular base in a sequence of DNA, the
replacement could replace the base at the position in question with
the same base 1/4th of the time. Therefore, the odds that a given
"change" will result in a specific base are 1 in 4.
> [snip demonstration that neutral evolution is not a good way to produce
> any specific set of changes]
Exactly. Neutral evolution does not explain how increasingly complex
novel functions can evolve in the time limit of 4 or 5 billion years
that life has supposedly been here on this planet. Neutral evolution
only explains genotypic changes and how these changes can become
"fixed" in a given gene pool. However, it says very little about how
even fairly small neutral gaps between novel functions can be crossed
in a reasonable amount of time.
Sean
Noelie S. Alito
news:W8Gja.148$_d2.24...@newssvr13.news.prodigy.com...
> "Sean Pitman" <seanpi...@naturalselection.0catch.com> wrote in message
> news:80d0c26f.0304...@posting.google.com...
> > fn...@comcast.net (Frank J) wrote in message
> news:<38c5d0dd.03040...@posting.google.com>...
> > > seanpi...@naturalselection.0catch.com (Sean Pitman M.D.) wrote in
> message news:<80d0c26f.03040...@posting.google.com>...
> > > > Evolving Rube Goldberg Machines
> > > > http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
> > >
> > > (snip)
> > >
> > > IIRC you were a young-earther, at least as of a few months back. Now
> > > you're defending Behe, an old-earther who accepts common descent, and
> > > is even more "evolutionist" than "saltationist." Are you coming around
> > > to Behe's model, or will you be trying to refute him too?
> >
> > Just because I agree with one aspect of another person's thinking does
> > not mean that I agree with everything that person thinks. I agree
> > with the basic concept/argument of irreducible complexity (IC) as Behe
> > presents it. However, there are certain important ideas that Behe
> > claims for IC that I do not agree with. Behe tries to limit IC
> > systems to those systems which he considers to be of high complexity.
> > I disagree with this limitation.
> >
>
> <chez watt>
> > I think that all functions are irreducibly complex.
> </chez watt>
Seconded.
<snip>
Noelie
--
The two happiest days in a man's life are the day he buys his boat,
and the day he sells it. --Former boat-owner
John Wilkins
Hey, I agree with him. It's a purely definitional statement. Of course,
that is no reason to think that each component in an IC function is
equally IC (fallacy of composition), or that such IC things cannot
evolve. We already knew they could...
--
John Wilkins
"Listen to your heart, not the voices in your head" - Marge Simpson
Frank J
In terms of the general origins model, however, it seems that your
differences with his are essentially the same as your differences with
that of mainstream evolution. How about in terms of approach to
science?
http://bostonreview.mit.edu/br22.1/coyne.html
>
> Sean
John Harshman
Sean Pitman wrote:
> John Harshman <harshman....@pacbell.net> wrote in message news:<3E8C588D...@pacbell.net>...
>
>
>
>>Back again? Is this another post-and-run? Do you ever intend to respond
>>to any of the arguments made against your claims last time?
>>
>
> Now, I may be wrong, but I "responded" quite a bit to various
> arguments against my position(s) "last time." Perhaps I have not
> responded to your arguments in particular but I have certainly
> responded at great length to many of those responding to my ideas.
> You should know this.
Perhaps you shouldn't post things you aren't very interested in, then. I
for one would most like to discuss the evidence for and (if any) against
common descent. How about you?
>>I'm afraid that your conclusion doesn't follow from your premises, and
>>your premises are themselves doubtful. What has been demonstrated is
>>that *some* proteins can't evolve into *some* other proteins by a chain
>>of point mutations, each one improving fitness for some *particular,
>>single* function. It has not been shown that the majority of protein
>>sequences have no possible function, nor that there is not a path
>>between any two particular proteins that increases fitness at every step
>>in some environment.
>>
>
> Oh really? It seems quite obvious to me that given a particular
> creature, such as a bacterium, that the vast majority of possible
> amino acid sequences/proteins of a given length will have no
> beneficial function for that creature in its current environment.
Agreed. This is obvious.
> To
> say otherwise is extremely naive in my estimation. Only a very tiny
> fraction of the potential amino acid sequences will be recognized by
> any given bacterium or living cell in any given creature.
Recognized? What meaning are you using for "recognized"?
> Take humans
> for example. The vast majority of human DNA does not code for any
> functional protein much less a beneficially functional protein. The
> proteins that are coded for are somewhat plastic, true, but they are
> also very specific. If changed or "denatured" to any significant
> degree, they loose all function.
You are confusing two forms of change. We were talking about mutation.
Denaturing is a loss of tertiary or quaternary structure, most often as
a result of heating. Nothing to do with what we are referring to. (Also,
I don't understand your distinction between "functional" and
"beneficially functional", or what you mean by "somewhat plastic".)
> This means that the vast majority of
> potential protein sequences and three-dimensional shapes are worthless
> to a given human cell.
This is not quite clear, at least the "vast majority" part. There are
lots of protein sequences that don't do exactly what we would like, but
it does appear that we can find function from random sequences. See
this: Hayashi, Y., H. Sakata, Y. Makino, I. Urabe, and T. Yomo. 2003.
Can an artibrary sequence evolve towards acquiring a biological
function? J. Mol. Evol. 56:162-168.
And the introduction of 3-D shapes only confuses the question.
> As far as demonstrating a negative (ie: A lack of a functional path
> between two different proteins), it is impossible this side of
> eternity. A negative finding never means that a positive finding is
> impossible. However, the likelihood that a negative finding will
> occur can be calculated.
If it can, then you haven't done it yet. This remains to be seen.
Nilsson & Pelger 1994. Or so you claim, without evidence. How do you
know there are such gaps? For eyesight, it has certainly been shown that
there is a continuous series of slight morphological variants, each
advantageous, from a patch of light-sensitive cells to a camera eye. I'm
sure you are familiar with How would one go about demonstrating that
there are or are not such gaps with respect to feathers? We do know that
feathers arose in a bipedal, non-flying dinosaur. That seems clear
enough. Whether they arose by natural selection, or by any naturalistic
pathway, is difficult to determine. I suppose you could, if you liked,
support some kind of theistic evolution in which God gives the
occasional nudge to get a genome across some functional gap. I'm not
sure where you would find evidence for it, as there is for selection,
and I'm pretty sure you would reject such a theory anyway. Right?
> If you think that a neutral gap in function
> that requires just one protein sequence is hard to cross, try crossing
> a gap that requires the evolution of multiple proteins to cross where
> hundreds or even many thousands of neutral mutations are needed.
I agree that this scenario sounds unlikely. I just don't agree that it
is necessary.
> If there were such a path from scales to feathers, then we should be
> able to quickly demonstrate such evolution in real time.
I deny that there is any such expectation. Why should there be? Are you
saying that we should be able to demonstrate every possible occurrence
in the lab? Why? If we are talking about something that took millions of
years, why should we be able to do it in one or two? And this assumes
that we know what steps are necessary, which we don't, at least not yet.
If each and
> every step were beneficially functional in some unique way from what
> came before, then such evolution would proceed very much as Dawkins's
> experiment with his computer phrase evolution. Dawkins started with a
> nonfunctional phrase and then, using a selection mechanism that
> compared mutating sequences with the ideal sequences, his computer
> evolved the phrase, "Methinks it is like a weasel" in less than 50
> phrase "generations". The problem with this experiment, of course, is
> that it does not reflect the abilities of natural selection. Natural
> selection does not have the ability to recognize nucleic acid or amino
> acid sequences directly, but only as they have some sort of function.
> However, if each and every change did have a function, then natural
> selection would in fact work very much like Dawkins's computer
> program. The evolution across such a functional path would occur at
> an extremely rapid rate. There would be no need for millions and
> billions of years to achieve the diversity that we see in the natural
> world for such changes could be and would be realized in short order.
>
> The idea that eons of time are needed for evolution to be successful
> means that there is not a path of function where each and every step
> is beneficially unique.
You have the kernel of an interesting point there, and it's been a
conundrum of evolution for some time. Why is evolution so slow over the
long term, when natural selection is so fast? I think there are several
reasons: waiting for mutations, waiting for the environment (internal
and external) to change so that new selective pressures are seen, and
following a twisty path around constraints rather than the straight path
you seem to think is the only possible one. It's an interesting problem,
but not as you seem to think a disproof of the efficacy of selection.
> There are gaps between various functions that
> require a lot of time to cross. In fact, many of these gaps seem so
> wide that billions or even many trillions upon trillions of years are
> simply not enough.
If there are, name one and show the evidence that it is such a gap.
> This is where the idea of design comes into play.
> Intelligence can cross such gaps in short order. Humans can type into
> the computer, "Methinks it is like a weasel" far far faster than a
> computer can come up with that phrase/function using neutral
> evolution. Why? Because humans have access to an intelligent mind
> that can be creative were as computers are not intelligent or
> creative. Likewise, genes and natural selection are not intelligent
> or creative. The gaps and functions are there. The only logical
> explanation to explain their existence is intelligent design.
> Intelligent design is the only force that exists in the universe, that
> we are aware of, that creates functions of the complexity and variety
> that we see in living things.
That would be true if you were able to show that natural selection can't
do it.
>>> Then,
>>>without this guidance of natural selection, evolution is dead.
>>>
>>Not true. If all is as you claim, then evolution solely by natural
>>selection is dead. We must come up with some mechanism -- perhaps even
>>divine intervention -- to account for the crossing of such gaps. But our
>>knowledge of evolution in the sense of common descent does not depend on
>>knowing the mechanism to be natural selection, or upon knowing the
>>mechanism at all.
>>
>
> Oh really? This is an amazing statement! You know that naturalism is
> the answer... without knowing how it works?
Did I mention naturalism? No. In fact I mentioned divine intervention as
one potential mechanism. So your comments are irrelevant. I'm talking
about common descent. Would you care to argue about the evidence for
common descent?
> You don't need to know
> the mechanism to know that it works? Natural selection really does
> not have to be part of the mechanism in order for naturalism to be
> creative? Incredible! Well then, what other force do you know of,
> besides natural selection, which can help random mutations create such
> complex and integrated functions as we see in living things?
I didn't mention anything about random mutations. I'm talking about
common descent. Common descent is separable from the mechanism that
causes adaptation. You, as a creationist, deny common descent. I'm
saying that if, somehow, you were to show that natural selection is
insufficient as a driving mechanism, then the evidence for common
descent would remain untouched and conclusive.
> You obviously have a very great faith in the power of naturalism to
> answer all questions pertaining to the physical universe. For you,
> the very notion that there just might be evidence of design in the
> natural world/universe is simply out of the question.
I said nothing whatsoever either for or against design. I'm not talking
about design. I'm talking about common descent. Is that clear?
> You approach
> all ideas with this "a priori" assumption that naturalism must answer
> all that we see in the natural world. However, this is not a
> scientific view. The scientific method does not require any a priori
> assumptions to be brought to the table. To say that science cannot
> detect intelligent design is not scientific nor is it supported by the
> evidence that we have available to us. Design is detected and
> proposed as a source for many observations that we see on a daily
> basis. Why? Because many things that we see around us, such as a
> fixed window or a Picaso painting, have no naturalistic explanation.
> To say then that living things had to have arisen "naturally", when
> one has no clue as to the naturalistic mechanism, seems to me like
> deliberate insanity.
Nor did I do any such thing. I happen to believe, based on the evidence,
that natural selection is a pretty good mechanism and that evolution has
indeed proceeded "naturally" (and there is considerable evidence that
evolution has no particular goal), but that's not at all what I'm
talking about here. Your inability to separate "darwinism" into
independent components is causing a communication failure.
>>John Harshman <harshman....@pacbell.net> wrote in message news:<3E8DAE72...@pacbell.net>...
>>
>>
>>>For example, the odds of getting one, two, or even three necessary
>>>mutations "right" in a reasonable amount of time, even in a gene some
>>>3,500 base pairs in length, is not unimaginable . . . since this gene
>>>is starting very close to the "goal" to begin with. As a hypothetical
>>>example, consider the following parameters:
>>>
>>>· A stable population of one trillion (1012) E. coli bacteria (equal
>>>to the volume of 10mL or an average hospital syringe)
>>>· A bacterial generation time of 20 minutes (E. coli)
>>>· An average bacterial genome of 4.1 million base pairs (E. coli)
>>>· A mutation rate of 1 x 10-4 mutations per base pair per generation.
>>>(Hall proposes that bacteria undergo "hypermutation" in starvation
>>>states. The average rate is much lower at about 1 x 10-9 mutations per
>>>base pair per generation)
>>>
>>I'm not sure these parameters make sense. The hypermutation is in
>>bacteria that aren't dividing, so combining it with a "generation time"
>>wouldn't work.
>>
>
> Yes, mutations (hypermutation or not) happen in a given bacterium
> before it divides.
Actually, under normal conditions most mutations occur during DNA
replication, which I believe does occur simultaneously with cell
division in most prokaryotes.
> However, once the mutations occur, these mutations
> are passed on to the bacterium's clonal offspring via the
> division/replication/mitotic process.
Mitosis is something that happens in eukaryotes, not prokaryotes.
> Then, these offspring also
> mutate and these new mutations are added the previous mutations and
> are all passed on to the next generation... and so on. So you see,
> the mutation rate per generation can be calculated.
Once again: hypermutations are observed to occur in bacteria that are
not actively dividing. Generally they happen under starvation conditions
in which the bacteria cannot reproduce. If one bacterium experiences a
mutation that lets it reproduce, then the subsequent colony descends
from that one. Actively dividing bacteria do not experience these
hypermutational rates.
> In fact, Hall
> does so in his own paper. He makes his own estimations of the
> mutation rates for his bacterial colonies, "per generation." Please,
> go back and read his paper and reevaluate what you just said.
Are these hypermutational rates, i.e. a response to stress? I'm afraid I
don't have the paper available in front of me.
>>But never mind, they are good enough to demonstrate your
>>point, which is that any particular string of neutral mutations is
>>vanishingly unlikely, just as any particular ordering of 52 cards in a
>>deck is vanishingly unlikely (and just as irrelevant to the playing of a
>>hand of bridge as your claim is to the process of evolution).
>>
>
> You evidently do not understand the difference between a hand of
> bridge and the evolution of novel functions. Every hand in a hand of
> bridge, no matter how rare, has a unique function in the game of
> bridge. However, not every "hand" or series of nucleotides in a
> genome of a given creature has a unique function. In fact, the vast
> majority of potential DNA sequences are non-functional or neutral.
Every analogy is imperfect, but I think we can get a little more out of
this one. Let's define a "non-functional" bridge hand as one with less
than 13 points, and a "functional" one as having 13 points or more. If
this is so, then even though there are many more nonfunctional than
functional hands, and even though any given functional hand is
vanishingly rare, still there are enough functional hands dealt to keep
a game going. So with life. We are not picking a fixed target and
attempting to approach it with mutations. There are many possible goals
and many paths to each one. Even if most changes lead nowhere, it's
enough that some changes lead somewhere.
> To
> get to a new function requires random neutral drift around a huge sea
> of neutral/non-functional sequences.
You assume this but there is no reason to suppose it, and no reason to
suppose a single target as all your calculations assume.
> This random wandering takes
> time. For the evolution of more and more complex functions, this time
> of drift becomes so huge that even trillions of years are nothing
> compared to the time needed.
>
>
>>>Given these parameters, how long would it take to evolve the first
>>>mutation? The odds that the correct position would be mutated in a
>>>clonal E. coli population would be 1 in 4.1 million. The odds that the
>>>correct base would get mutated at this location are 1/4.
>>>
>>Quibble: 1/3. If you assume a mutation, you have to assume that it's to
>>a different base than the one that was already there.
>>
>
> In the replacement of a particular base in a sequence of DNA, the
> replacement could replace the base at the position in question with
> the same base 1/4th of the time. Therefore, the odds that a given
> "change" will result in a specific base are 1 in 4.
If a base is replaced with the same base we don't call it a mutation. We
don't call it anything, except maybe "replication". A mutation rate that
includes "no change" would be a rate of 1 per site per generation, since
every site will either change or not change. You really need to fix this.
>>[snip demonstration that neutral evolution is not a good way to produce
>>any specific set of changes]
>>
>
> Exactly. Neutral evolution does not explain how increasingly complex
> novel functions can evolve in the time limit of 4 or 5 billion years
> that life has supposedly been here on this planet.
Nor does anybody proposes that it does. So what's the problem? Neutral
evolution may provide some of the variation that natural selection
eventually picks up and works with. But nobody supposes that neutral
changes build eyes.
> Neutral evolution
> only explains genotypic changes and how these changes can become
> "fixed" in a given gene pool.
It explains some genotypic changes, i.e. the neutral ones.
> However, it says very little about how
> even fairly small neutral gaps between novel functions can be crossed
> in a reasonable amount of time.
Well, it does say how neutral gaps can be crossed. With low probability,
getting lower as the size of the gap increases. If there is a large
neutral gap between two functional proteins it is unlikely to be
crossed. But who says that such gaps are prevalent?
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
On Sat, 5 Apr 2003 20:05:02 +0000 (UTC),
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
[big snip]
>You evidently do not understand the difference between a hand of
>bridge and the evolution of novel functions.
You evidently don't understand what a neutral mutation is.
>Every hand in a hand of
>bridge, no matter how rare, has a unique function in the game of
>bridge. However, not every "hand" or series of nucleotides in a
>genome of a given creature has a unique function.
No, some of them have multiple functions, or duplicate the function of
other genes (the upregulation of protein kinase C alpha to cope with
deletion of protein kinase C beta is an example of such a duplicate
function).
>In fact, the vast
>majority of potential DNA sequences are non-functional or neutral.
You really don't understand what neutral means do you?
>To
>get to a new function requires random neutral drift around a huge sea
>of neutral/non-functional sequences.
No it doesn't. This is a very peculiar notion you have, that sequences
MUST traverse neutral sequences before reaching a functional sequence.
They don't, as I have explained using the TEM beta lactamases.
The ancestral TEM1 first originated in 1965, by 1998 TEM42 had
evolved. TEM42 differs from TEM1 in 13 positions, of which only 5 are
functional, the rest neutral. Thus, in TEM42, the majority
of mutations are neutral, yet TEM42 evolved in a mere 33 years across
what you would call an unbrigeable 8 neutral mutation gap. But the
thing is that these mutations did not _require_ to be in place before
functional mutations could take place. Neutral mutations occur in the
background, in all genes, ticking away like a clock, without regard to
the production or otherwise of benefical mutations. A sequence left
alone will aquire much the same number of neutral mutations as a
sequence undergoing selection for a change in function.
>This random wandering takes
>time. For the evolution of more and more complex functions, this time
>of drift becomes so huge that even trillions of years are nothing
>compared to the time needed.
But as they DON'T have to wander through neutral sequences, this is
irrelevant.
[snip]
>Exactly. Neutral evolution does not explain how increasingly complex
>novel functions can evolve in the time limit of 4 or 5 billion years
>that life has supposedly been here on this planet.
No, ordinary evolution does that.
>Neutral evolution
>only explains genotypic changes and how these changes can become
>"fixed" in a given gene pool.
Only certain kinds of genotypic changes. Functional changes are fixed
by selection.
>However, it says very little about how
>even fairly small neutral gaps between novel functions can be crossed
>in a reasonable amount of time.
There are no neutral "gaps".
Hayashi, Y., H. Sakata, Y. Makino, I. Urabe, and T. Yomo. 2003.
Can an artibrary sequence evolve towards acquiring a biological
function? J. Mol. Evol. 56:162-168.
Which other people have pointed you to, is an example of evolving a
functional protein from a random sequence in a relatively short time
using muation and selection, without encountering any "neutral gaps".
However, alos of interest, the paper references other experiments,
some of which show that a vast percentage of random protein sequences
are esterases.
Ron Okimoto
> Ron Okimoto <roki...@uark.edu> wrote in message news:<3E8CAB80...@mail.uark.edu>...
>
> > > Evolving Rube Goldberg Machines
> > > http://naturalselection.0catch.com/Files/Rube%20Goldberg.html
> >
>
> I have yet to obtain and read the entire paper, but it seems to me
> that these c and d mutational changes were initially thought to be
> neutral but were later found to actually be functional. In any case,
> depending on the size of the protein involved and the complexity of
> the function involved a gap of three neutral mutations is not an
> unreasonable distance for random/neutral evolution to cross in a
> reasonable amount of time. If the complexity of the function is
> relatively low, there might be many different protein sequences of a
> given length or less that could perform that function. The odds that
> two or three random mutations would end up at one of these many
> different protein sequences is a lot better than the odds two or three
> mutations being "right" for a more complex function where there are
> only a relatively few protein sequences of a given length able to
> produce a that function. The lactase function may have a fair number
> of different protein sequences that could hydrolyze lactose. The fact
> that Hall has been unable to find any other genetic sequence, aside
> from the lacZ and the ebg genes, able to produce a lactase enzyme
> despite heavy selection pressures over hundreds of thousands of E.
> coli generations, seems to me to indicate a fairly complex function.
>
> For example, the odds of getting one, two, or even three necessary
> mutations "right" in a reasonable amount of time, even in a gene some
> 3,500 base pairs in length, is not unimaginable . . . since this gene
> is starting very close to the "goal" to begin with. As a hypothetical
> example, consider the following parameters:
Why is it starting very close to the goal? You acknowledge that it is
a very different protein. Why should this matter? Was it present by
design or just chance?
>
> · A stable population of one trillion (1012) E. coli bacteria (equal
> to the volume of 10mL or an average hospital syringe)
> · A bacterial generation time of 20 minutes (E. coli)
> · An average bacterial genome of 4.1 million base pairs (E. coli)
> · A mutation rate of 1 x 10-4 mutations per base pair per generation.
> (Hall proposes that bacteria undergo "hypermutation" in starvation
> states. The average rate is much lower at about 1 x 10-9 mutations per
> base pair per generation)
>
> Given these parameters, how long would it take to evolve the first
> mutation? The odds that the correct position would be mutated in a
> clonal E. coli population would be 1 in 4.1 million. The odds that the
> correct base would get mutated at this location are 1/4. The odds that
> both would happen are 1 in 16.4 million mutations. With a stable
> population of one trillion and a mutation rate of about 410 mutation
> per genome per generation, the "correct" mutation will occur in about
> 25,000,000 bacteria in the first generation.
I don't know if I agree with your numbers, but all they indicate is
that we are more on the right track than you are. You have to keep
these mutations from happening. We observe them to happen. What is
your problem?
>
> But, what if the starting sequence was two mutations away from the
> desired lactase function? Would that make any difference? The odds of
> getting either one of the two needed mutations with the first mutation
> are 1 in 8.2 million mutations. The odds of getting the second
> mutation right are 1 in 16.4 million mutations. So, the odds of
> getting both mutations right are 1 in 134,480,000,000,000 (~1.34
> trillion) mutations. With these odds, the correct mutation will occur
> in about 315 bacteria in the first generation.
How does this help you out? These calculation just make our model
look better.
>
> If the starting sequence was three mutations away from the desired
> function, the odds of getting all three mutations right shoots up to 1
> in 735,157,333,333,333,333,333 (~735 million trillion) mutations. With
> these odds, the correct mutation will occur in one bacterium in
> 1,792,682 generations. With a generation time of 20 minutes, that's a
> bit over 68 years.
You can't calculate the probabilities like that because they aren't
independent. You have to calculate the probabilities based on the
actual situation. Once you have one mutation, you don't have to get
it again. You can as often as you like, but the second mutation would
occur in a bacterium that already had the mutation. Like you
indicated by your own calculations 315 bacteria would have any one of
the three. Close to 1000 in just the first generation would have one
of the three. How many in the second generation? The 100th? The
chance of two is the mutation rate in those bacteria that already have
one. Your numbers collapse dramatically, and even more dramatically
if the mutations were not neutral, but had some selective advantage
that allowed them to increase in frequency in the population.
>
> Four mutations would take about 279,740,233 (~280 million) years.
> These predictions also bear up in the laboratory. There are many
> bacteria that utilize galactose and glucose and yet they cannot
> utilize lactose. For example, practically all of the members of the
> bacterial type called Shigella cannot utilize lactose but they do
> utilize glucose. The same can be said for the many other bacteria such
> as Salmonella, Proteus, and Pseudomonas etc. All of these bacteria
> could in fact use a lactase gene if it became available to them. They
> would in fact be able to utilize the enzymatic activity of the
> galactosidase protein if they had access to it or to any other lactase
> enzyme. Why then do they not simply "evolve" any one of these possible
> lactase genes?
The probabilities are not independent. How did Hall get these three
in the few experiments that he did? How many mammal guts did it take
to evolve the first lac operon?
>
> http://naturalselection.0catch.com/Files/Galactosidase%20Evolution.html
>
>
> > It also looks like I am correct and that in the original study Hall is
> > looking for sustainable growth on lactose. Evolution doesn't happen this
> > way. Evolution does not depend on a do or die situation. In nature the
> > organism without the mutation lives happily in the environment. This is
> > not the case for the Hall experiments. The organism dies in the Hall
> > environment, no second chances.
>
> Actually, I think that you have misread Hall's work. The E. coli do
> not die in the lactose environment set up by Hall. The media is a
> "selective media". It does not kill off those bacteria that do not
> evolve the lactase enzyme, but only promote growth and improved
> survival of those that do evolve the lactase function. Please, go and
> read the paper again. The selective media works very much like a
> natural environment where the bacteria live just fine, but could live
> better if they had certain functions (such as lactase ability) in a
> given environment (one with lactose in it).
You have never given the procedure that they used. I just give what I
saw in what came up in the search. I didn't look at all of the
references only the first 5 or so before I stopped, but explain where
I am going wrong, and how I am misinterpreting this quote from one of
the abstracts "Wild-type ebg beta-galactosidase, encoded by ebgA, is a
catalytically feeble enzyme that does not hydrolyze lactose or other
beta-galactosidase efficiently enough to permit growth on those
substrates." Hall BG 1999. FEMS Microbiol Lett. 174: 1-8. The way
that these selection experiments work (by researchers like Cairns and
Campbell) is to plate the bacterium out on a plate where they have
minimal metabolic capability. They have to work their DNA repair
mechanism and be able to transcribe the new mutations in the DNA to
mRNA or they will not express the new mutations, but they do not grow
well or divide very well. After a period of time in this semi stasis
most of them die on the plate. You can't revive them even if you add
medium that they can grow on. I don't know when you call a bacteria
dead, but if it never divides again that gets my vote.
What did Hall do and would it be considered to be the way things
usually work in nature?
>
> > Evolution doesn't work this way if it
> > did there would have to be some designer tweeking every new life being
> > born so that it wouldn't die in some new lethal environment that it was
> > going to be born into. This is so far from reality, why do you expect it
> > to support what you are saying about it? I'm not saying that Hall can't
> > make some very firm conclusions from his study, you just can't make the
> > ones you are trying to make. Look at the above example. Hall was able
> > to select for a better enzyme that needed two silent substitutions and a
> > third mutation before he was able to observe it as growing better in his
> > system. That is how it works in nature.
>
> You can't have it both ways. If Hall's experiment was done with the
> use of "lethal environments" as you suggest, then he couldn't just
> wait around for neutral mutations to add up because the bacteria would
> be killed before the third "functional" mutation came along. In other
> words, you just admitted that Hall was in fact using a non-lethal
> environment with a selective advantage for certain functions. You
> even said, "This is how it works in nature." Come on Ron, get it
> together and be consistent. Hall's experiments, both in 1974 and 1995
> used non-lethal selective growth media. Your argument is therefore
> flawed.
They were two different experiments. He had a bacteria that could
grow on lactose. He was looking for ones that grew faster. These
bacteria already had two mutations (ebgab) that enabled them to grow
and divide on lactose medium. Before they had at least one of these
mutations they couldn't. When he looked for better growth he got the
ones with 5 total mutations (ebgabcde). This is more like what you
see in nature. The bacteria can divide and multiply in the
environment and you are only selecting for the colonies that grow
faster than most of the others.
>
> > It looks like Hall has met your
> > challenge with the system you are trying to say supports your contention
> > that it is impossible.
>
> I never said that a neutral gap of 3 mutations was "impossible." I
> said that depending on function complexity that certain gaps of such
> lengths or larger would be impossible for neutral evolution to cross
> in a reasonable amount of time. Where has Hall demonstrated this to
> be incorrect?
Yes, by any standard. How many man hours do you think the experiment
took. Probably less than 6 months worth of experiments, and more
likely just a couple of weeks. He may have been working on this
problem since the 1970s but his bacteria were probably in the freezer
most of that time.
He still hasn't demonstrated the evolution of the
> lactase function in E. coli lacking both the lacZ as well as the ebg
> genes. Why is this?
He doesn't do the experiments like they would happen in nature? He
never lets the bacterium have a chance to evolve the number of
mutations that are needed to get activity using some other protein?
The only logical reason for such a limitation to
> the evolution of the lactase function in such bacterial colonies
> (despite the potential benefits if they were able to evolve this
> function) is that there is a gap in function between the lactase
> function and the collective genomic real estate potential of Hall's E.
> coli colonies... even given hundreds of thousands of generations.
This is pretty bogus because you have to admit that it happened once
in only 2000 proteins found in E. coli. From the couple of other
bacteria that he has been able to do this with it has happened in them
too, and different proteins were involved in those activities. So
what is your problem. It seems like it isn't so special. Demonstrate
that it is. If it is so hard, why was he able to do it again in other
species?
>
> > Why don't you research the work more carefully
> > before making these types of mistakes?
>
> LOL - Why don't you? You evidently do not understand the experiments
> that you are trying to use to support your position.
Demonstrate that you understand the experiments, and that they tell
you what you think that they are telling you.
>
> > Since this is a 1995 paper if you
> > had done your homework you wouldn't have had to write all that stuff that
> > is now refuted by the system of your own choosing. Do your own research
> > and stop relying on creationist sources. You know that they are out to
> > lunch. You can use them to get a start in thinking about some problem,
> > but you know that they have to ignore most of the data to believe what
> > they do, so you have to look for this data yourself.
>
> Oh, I have done a fair amount of reading/research for myself. You
> perhaps should do a bit of your own thinking as well and not rely so
> much on the conclusions of mainline popular scientists. Granted, many
> if not most YECs don't know the heck what they are talking about.
> But, the same can be said for evolutionists. There are a few bright
> lights in both camps. So, we must all try and think for ourselves.
> You and the evolutionist camp may turn out to be correct. However,
> until I understand evolution and how it works for myself, I'm
> certainly not going to take anyone's word for it at face value.
> That's just not me.
So how did you miss the 1995 paper? As long as you use creationist
literature, expect to be wrong about 100% of the time. That is just a
fact that you know and have run into so many times that it must hurt.
The "evolutionist" that matter are the professional biologist. Joe
Blow down the street doesn't carry much weight in science, but for
some reason he carries the weight of creationism on his shoulders.
That is the difference between science and creationism. You know
this, I shouldn't have to tell you that. Why try and make it look
like the guys that don't matter, matter? If you don't know what you
are talking about, you don't get much attention in science. Look at
all the ID supporters, until they come up with something to evaluate,
science wouldn't give them the time of day. They only get attention
because of the dishonest things that they are doing in politics.
>
> > Oh, ebg is related to beta galactosidase, but the gene duplication
> > probably happened 2.2 billion years ago according to the molecular
> > analysis of related proteins done by Hall.
>
> Actually, the ebg gene is very different from the lacZ gene (hexomere
> vs. tetramer for example). There really is not good reason to believe
> that ebg was produced via a dupliction mutation, especially if it
> happened 2.2 billion years ago. In far less than 2 billion years,
> random mutations would have obliterated the ebg gene out of existence
> since it was basically "neutral" when the lacZ gene was operational.
> In any case, you seem to be really reaching for something, anything,
> to explain this problem. I'm sure you can do better than this... but
> maybe not?
You don't know how they evaluate these proteins do you. There are
sequence motifs that are very unlikely to have evolved their
similarity by chance. They are very different in sequence, but the
family as a whole has specific simiarites that allow us to determine
that they are related. That they now form hexamers instead of
tetramers only makes your position look less likely. We place certain
restriction on the evolution of proteins using our understanding of
chemistry and the molecular biology of the genes, but whether a
protein can switch from being a active tetramer to an active hexamer
is not one of those limitations. The 2/2 billion year estimate just
indicates that beta gal separated and was doing something else long
before mammals evolved around 200 million years ago. The progenitor
would have been in the same boat as ebg. It would have been evolving
for 2 billion years, probably with no lactase activity, but it was
able to evolve that ability when mammals started to provide milk for
their young and it became available as a food source for the bacterial
flora in the mammal guts. Just like ebg did when beta gal was taken
away.
>
> > As you might expect after
> > that long they are very different proteins. If you study this system you
> > can see just how gene duplication is responsible for the permeases, and
> > inducer genes of the two cistrons. This is like the blood clotting
> > system that the ID people have to acknowledge that there is a lot of
> > evidence that it could have evolved. The proteins in the system are
> > related to eachother and obviously were created by gene duplication.
>
> If given the "a priori" assumption that evolution is true, then yes,
> this is the only logical explanation. However, just because various
> genes look quite similar or even identical does not mean that they
> necessarily arose via gene duplication.
Give your alternative mechanism and the evidence for it.
Very similar genes may be
> used in very different ways in different systems of function. The
> evolution of different systems of function using the same genes is
> still quite problematic since the assembly of any new system of
> multiple genes would require the crossing of neutral gaps in function.
> No such functional system of multiple genes, to my knowledge, has
> been demonstrated to have evolved in real time.
You have a problem in that you haven't been able to find a system
where you can claim that this has ocurred. Shouldn't you demonstrate
that there is a problem before you claim it is a problem. Give
specific examples and how you determined that the changes had to be
neutral.
For example, it is
> thought that the motility function of bacterial flagella arose via the
> use of existing genes in new combinations so as to produce a new
> function of motility. Well, if it is so easy, and there are few or no
> neutral gaps to cross, the evolution of such a motility system should
> be easy to demonstrate in short order. After all, the necessarily
> genes to produce all the necessary parts are all there in the
> non-motile cell. What is the problem with using these existing parts
> to make a new function? It should be so easy, but it really runs into
> the same problem as using the same 20 amino acids to produce new
> functions. All the amino acids are there, but making a new function
> using the 20 amino acids quickly runs into roadblocks of gaps of
> neutral/non-function. The same thing happens when you try to use
> existing proteins to make new functions. The gaps are still there and
> are even wider than trying to cross gaps in single protein function.
Demonstrate that the changes had to be neutral and what order that you
think that they occurred in.
It could be easy to evolve a flagellum, but we have a problem. We
don't know what the first one looked like. It has changed in the
billions of years since it first evolved. Looking at the different
flagellum we can see that they probably did evolve from some original
one, but some have different parts. Some parts seem to have been
lost, some may have been gained, some lost and regained. It has been
a very long time. What did the original flagellum look like? What
proteins and their sequences were available as basic material that it
evolved from? Without this basic knowledge how do you expect us to
reproduce the evolution of flagellum? Look at ebg, a billion years
ago it's sequence may not have been able to evolve Beta gal activity
in a single mutation, but hundreds of amino acid changes since then
now provide a substrate for beta gal evolution. You need to know the
sequences of the proteins like the ATPases at the time that flagella
were evolving in order to try and figure out how hard it would be to
get one to form the hexamer needed by the flagellum. Maybe the
original flagellum only had a tetramer arrangement, maybe only a
dimer. Do you know this kind of stuff? Can you recreate the
conditions under which flagellum were evolving? You know that these
details are very important. Different starting sequences will give
you different results.
>
> > What design mechanism would do this? We have a mechanism that we observe
> > to occur in nature that fits the bill very nicely, but where is your
> > mechanism and how does it work?
>
> But you do not have a mechanism that you can detail as to how such
> gaps are crossed.
What was the mechanism used for ebg evolution. Random mutation,
genetic drift and natural selection. If you have some other mechanism
just lay it out and compare it to the mechanism that we have actual
evidence is working in nature.
It is back to the "God of the Gaps" argument. If
> you can explain how to cross the gaps using naturalistic mechanisms,
> then I will believe you.
I just did, and I used a real verfied example.
Otherwise, you have nothing but wishful
> thinking. For example, it is easy to explain how a window could be
> broken using a naturalistic mechanism, but it is another thing
> entirely to explain how a broken window can be fixed using a
> naturalistic mechanism.
Evolution isn't fixing broken windows. The window was never really
intact it just adds pieces. Halls example is fixing a broken window,
but real life evolution doesn't have to do that except in dire cases
that probably usually result in extinction. All evolution has to do
is make the window more solid than it was. If you have a better
mechanism state it and the evidence for it.
>
> > It is good to see you back. It has been pretty boring around here with
> > just the willfully ignorant moron types posting on the creationist side.
> > Read the recent posts by Glenn, McCoy, nowhereman, and Zoe but be
> > prepared to cringe a lot. With guys like those on your side you don't
> > need me to tell you how bad off your side is. What makes it worse is
> > that they have been about the only ones supporting the creationist
> > position.
>
> I have been very busy lately, but thanks for the compliment here.
> Really though, telling me that I only have idiots who support me
> really doesn't help your position. All it says is that my position is
> unpopular and that you are strongly supported by the popular vote.
> This means nothing since it explains nothing in a way that I can
> understand. It is just an argument of authority, but says nothing of
> explanatory substance.
It says more than that your position is unpopular. Most or a large
chunk of the people in the US probably side with you. The problem is
that they do it because they are ignorant, and certain people play off
this ignorance to get them to do stupid things.
>
> > IC the way Behe uses it is bullshit. Demonstrate that it isn't using his
> > old or new definitions if you can. He admits that IC systems can evolve,
> > but he defines his IC systems as those IC systems that can't evolve. So
> > IC by itself is worthless, it has to be coupled with something else. He
> > hasn't figured out how to determine if they can't evolve, so he is stuck
> > with a worthless concept that he can't do anything with.
>
> I don't agree with everything Behe says. I think that he is somewhat
> confused in certain areas. I do agree with his basic definition of
> IC, but I think that he limits himself in what he defines as IC. For
> me, I consider all functions to be irreducibly complex. I don't limit
> the definition at all.
How can you say this when you can evolve function using antibodies
that had no enzymatic function before or evolve function from random
sequences, or evolve new fuctions for existing proteins like ebg?
Your definition makes less sense than Behe's. Behe's first definition
was found to be worthless because his IC defined systems could evolve
and he acknowledged that. His new definition is just plain worthless
because he can't demonstrate that it applies to anything.
This can be easily demonstrated and supported.
> Any particular function that is dependent upon various "parts" for
> its operation is IC. Remove certain parts and that function will
> cease. This means that a function can be destroyed if the parts are
> changed or "reduced". The lactase function is IC. Remove a certain
> number of amino acids and that function will end. Obviously then, IC
> functions can evolve. However, the problem comes with the type of
> function in question. Some functions are very simple functions.
> Others functions are much more complex. Simple functions may require
> fewer parts and there may be many more arrangements of specified parts
> that could still do a simple function. However, more complex
> functions might require more parts and there are probably far fewer
> relative arrangements of such parts that could produce this given
> function. This means that random/neutral mutations would be far less
> likely to come across a collection of parts with a more complex
> function than a more simple function (such as the motility function
> vs. nylonase function).
This is just the same old bull of the creationist probability argument
when you can't even begin to calculate the probabilities. Quantify
the difference between nylonase and motility complexes. Some motility
complexes are simpler than others. Try and calculate the
probabilities when you don't even know what the first flagellum looked
like.
>
> Behe makes the mistake of trying to limit the definition of IC systems
> to those systems of function that he considers to be highly complex.
> I feel that this is a significant mistake on his part. However, his
> basic concept is a good one and remains as a roadblock to natural
> selection as a reasonable mechanism for naturalistic evolution.
The definition that if you take away a part then the system doesn't
work isn't any good in determining if the system could have evolved or
not. You basically admit that these systems have been observed to
evolve. You have to have something more. Just saying it is
improbable is pretty silly since you can't even begin to calculate the
probabilities because even if you did have all the information I'd
like to see you deal with all the non independent variables.
How improbable would it be to co-opt an ATPase for flagellar work if
you only needed a single aminoacid substitution to do it? What was
the sequence of that ATPase and how many mutations were needed to get
it to do its new function? Maybe no mutations had to happen in the
ATPase. Some mutation in another protein that made it interact with
the ATPase and form a structure needed for flagellar development may
have happened. Make up your own story, but you have to rule them all
out before you can claim that they are impossible.
Ron Okimoto
>
> > Ron Okimoto
>
>
> Sean
howard hershey
Sean Pitman wrote:
> John Harshman <harshman....@pacbell.net> wrote in message news:<3E8C588D...@pacbell.net>...
>
>
[snip]
>
>
>>I'm afraid that your conclusion doesn't follow from your premises, and
>>your premises are themselves doubtful. What has been demonstrated is
>>that *some* proteins can't evolve into *some* other proteins by a chain
>>of point mutations, each one improving fitness for some *particular,
>>single* function. It has not been shown that the majority of protein
>>sequences have no possible function, nor that there is not a path
>>between any two particular proteins that increases fitness at every step
>>in some environment.
>
>
> Oh really? It seems quite obvious to me that given a particular
> creature, such as a bacterium, that the vast majority of possible
> amino acid sequences/proteins of a given length will have no
> beneficial function for that creature in its current environment.
*If* a gene (not the allele of a gene, but the gene in all its permuted
and mutated forms) produced a protein of no beneficial or harmful
function for that creature in that current environment, the gene in
question would be both superfluous (redundant) and selectively neutral.
Mutation in such a gene would neither be selected for nor against and
drift would ensure that eventually such a gene would no longer produce
any protein.
*If* a mutation in an *allele* of a gene produces a deleterious
phenotype in any pairwise combination (e.g., recessive deleterious
mutations only produce deleterious phenotypes in the homozygous state),
then it will be selected against when in that state.
*If* a mutation in an *allele* of a gene produces a selectively neutral
variant (that is, one that is functionally identical to other alleles),
the frequency of that allele in the population will drift randomly.
> To
> say otherwise is extremely naive in my estimation. Only a very tiny
> fraction of the potential amino acid sequences will be recognized by
> any given bacterium or living cell in any given creature. Take humans
> for example. The vast majority of human DNA does not code for any
> functional protein much less a beneficially functional protein.
The vast majority of human DNA does not encode *any* protein, period.
> The
> proteins that are coded for are somewhat plastic, true, but they are
> also very specific.
Proteins of quite different amino acid sequences can serve the same
'function'. Only a small part of most enzymes are crucial to function.
Much of the sequence of proteins involves merely a mechanism for
ensuring that the active sites are properly aligned to each other.
> If changed or "denatured" to any significant
> degree, they loose all function.
As I just said, proteins with quite different amino acid sequences (as
little as 10% identity in some cases) can serve the same function, so
*amount* of "change", per se, is not what determines function.
"Denaturation", of course, *means* that the normal 3-dimensional
structure of a protein has been destroyed, usually by heat or acid or
strong denaturing agents and has nothing to do with sequence change at all.
> This means that the vast majority of
> potential protein sequences and three-dimensional shapes are worthless
> to a given human cell.
>
> As far as demonstrating a negative (ie: A lack of a functional path
> between two different proteins), it is impossible this side of
> eternity. A negative finding never means that a positive finding is
> impossible. However, the likelihood that a negative finding will
> occur can be calculated.
But only under the assumptions that you arbitrarily assign. You
*assume* that no *selective* pathway exists between protein sequences
that perform different functions. You *assume* that all the
intermediate steps are selectively neutral. And you *assume* that most
evolutionary change involves intermediate states of no utility at all!
> The odds can be estimated to give a
> predictive power to the hypothesis that a negative finding will arise
> for a given situation in a given span of time. Hall's experiment was
> interesting in that it seemed to show such a negative finding. Those
> bacteria that did not have the lacZ nor the ebg genes never evolved
> the lactase function.
Whatever gave you the idea that evolution is unconstrained and can
always come up with a new enzymatic activity in the time frame you judge
sufficient? Evolution doesn't work that way.
> Given their entire collective genomic real
> estate, they had nothing close enough to evolve a gene to produce this
> function despite being observed over many thousands of generations.
> This seems to indicate the presence of some sort of statistical block
> to the evolution of this function starting from hundreds of
> "particular" genes. This seems to indicate that there, "is not a path
> between any two particular proteins [in this particular gene pool]
> that increases fitness at every step in [the given] environment."
Whatever makes you think that evolution works by converting *any* old
random protein from one state to the new one it needs? If there is no
protein which can provide a sensible pathway to beta-galactosidase
activity within a human lifetime in E. coli, there may be one in B.
subtilis, in which case it may well be B. subtilis that evolves the
activity and not E. coli (although E. coli may acquire it later by
horizontal transfer). Or there may need to be a duplication in order to
generate a mutation in a gene that otherwise is necessary for life.
> If
> there was such a path, the traversing of this path should happen very
> rapidly. The fact that it takes so long to cross this path means that
> there simply is not a step-by-step improvement as the path is
> traversed.
So *if* you remove all the genes that *do* provide a sensible pathway
between that protein and the needed activity, you are shocked, shocked
to discover that it is much more difficult to find yet a different
pathway to the activity you want. And if a different pathway does
arise, then if you remove that one, too, will you be shocked, shocked to
discover that it is even more difficult?
> Natural selection has been blinded along the way by two or
> more "neutral" steps. With each neutral step that must be traversed,
> the time required increases dramatically.
Under your false assumption that multiple (more than two or three)
selectively neutral steps are usually involved.
>>>Non-recognized or non-functional proteins cannot be guided by natural
>>>selection along any evolutionary path whatsoever.
It has been stated before, but "non-recognized" and "non-functional" are
NOT the same as "selectively neutral". "Non-recognized" and
"non-functional" proteins are almost always selectively deleterious, not
selectively neutral. "Selectively neutral" means that the protein is
*just* as useful for all functions it performs as the alternative
protein is. Until you understand this and reflect that understanding in
your argument, you entire argument is nonsense.
>>>Why? Because
>>>nature only sees function. Nature cannot guide if it is blind. Thus,
>>>nature cannot guide evolution across non-functional gaps.
>>
>>At least not very large ones. But you have not demonstrated that such
>>non-functional gaps exist, except in a single case, in a single,
>>unchanging environment, over a short period of time. This sort of thing
>>is well known, and is referred to by the label "evolutionary
>>constraints". Some evolutionary paths exist, and others don't. Showing
>>that some don't exist doesn't show that none exist. If enough paths
>>exist, evolution by natural selection works fine. Nobody says natural
>>selection can follow any conceivable path. I would also bet that no
>>matter how advantageous it would be, horses will never sprout wings from
>>their shoulders; but a bipedal dinosaur would be able to recruit its
>>feathered arms for flight. You raise a non-issue as if it's the
>>universal answer.
>
>
> This is complete wishful thinking. No one has ever demonstrated the
> "lack of gaps" between such complex functions as the modification of
> scales into feathers
Have you read the recent Scientific American article on this very point?
Feathers may not have evolved directly from scales (but clearly used
many of the genetic mechanisms used in scale production). But all the
"complex functions" needed to produce feathers clearly pre-existed in
dinosaurs before feathers did. Dinosaurs did produce keratins well
before feather keratins were needed. The mechanism for producing the
pattern of where and how to position feathers was already there. Like
most evolutionary change, feathers (or the hair of mammals, which also
arose similarly) are modifications of pre-existing structures and functions.
> or the evolution of a motility system in a
> non-motile bacterial colony.
There may well be mechanisms of bacterial motility that are secondary to
other functions, such as gliding motility.
> The only evolution that has ever been
> demonstrated in real time is the evolution of relatively simple
> functions, such as the simple enzymatic functions of single proteins
> (ie: lactase, nylonase, antibiotic resistance etc.). Such functions
> are so simple that the gaps between what is already there and such
> comparatively simple functions are relatively small, requiring only a
> very few mutations to achieve.
Repeated steps can take you from New York to California, but not in one
day. It is quite often the case that evolution is sporadic in nature,
with a subsequent period of further mutation that adapts the organism to
a bigger change.
> When you start talking about the
> evolution of feathers, flight, eyesight, motility, and other such
> highly complex functions, you are talking about functions that require
> multiple genes and proteins all working together at once.
And, in essentially every one of those cases, it appears that the
multiple genes and proteins already existed and (in many cases) served
other functions. Evolution is not in the business of inventing
novelties out of thin air like creationism does. Nor does evolution
plan to generate necessary novelties. Evolution is non-teleological.
Evolution modifies whatever exists, sometimes creating things that an
outside observer might call "novelty" unless he or she was aware of the
intermediate steps and evidence of those steps.
> The neutral
> gaps between what is there and the development of such highly complex
> functions are enormous.
So you assert without any evidence. What selectively neutral gap do you
posit between the eyespot and the focusing eye? Nilsson and Pegler
see a selective advantage to the intermediate steps between these two
end points, where each intermediate stage has increased visual acuity.
Eye crystallins are, interestingly enough, not generated from scratch.
The biochemistries of vision (vertebrate and invertebrates have
different chemistries beyond the first few steps) basically involve
linking those first two steps to neural biochemistry pathways that
already existed.
> If you think that a neutral gap in function
> that requires just one protein sequence is hard to cross, try crossing
> a gap that requires the evolution of multiple proteins to cross where
> hundreds or even many thousands of neutral mutations are needed.
>
> If there were such a path from scales to feathers, then we should be
> able to quickly demonstrate such evolution in real time.
Why do you think this? No evolutionary biologist thinks the path to
flight feathers had no intermediates. See the recent Scientific American
article. At each intermediate step, the product had improved
functionality for *some* function (not necessarily flight).
> If each and
> every step were beneficially functional in some unique way from what
> came before, then such evolution would proceed very much as Dawkins's
> experiment with his computer phrase evolution.
What evidence do you have *specifically* of features with many
intermediate stages of no possible utility? Not selective neutrality,
but no possible utility.
> Dawkins started with a
> nonfunctional phrase and then, using a selection mechanism that
> compared mutating sequences with the ideal sequences, his computer
> evolved the phrase, "Methinks it is like a weasel" in less than 50
> phrase "generations". The problem with this experiment, of course, is
> that it does not reflect the abilities of natural selection. Natural
> selection does not have the ability to recognize nucleic acid or amino
> acid sequences directly, but only as they have some sort of function.
Yes? Which means that a number of evolutionary changes in sequence are
not due to selection but are due to neutral drift. But that is not the
real problem with thinking that Dawkin's model is exactly like
evolution. Rather, it is the teleological nature of Dawkin's model that
is more problematic. That and the brittle nature of English sentences
that makes selection in English hard if the intermediates are to have
functional utility (i.e., be meaningful English). And, of course, the
fact is that evolution is more like going from "Methinks she is like a
weasel" to "Methinks it is like a weasel" (whereby only part of the
sentence is changed). But then Dawkin's model was never intended to be
a perfect analogy to evolution, but only to demonstrate the rapidity of
a process involving a filtering mechanism over one involving chance alone.
> However, if each and every change did have a function, then natural
> selection would in fact work very much like Dawkins's computer
> program. The evolution across such a functional path would occur at
> an extremely rapid rate.
That might be the case if evolution were teleological in nature. It
isn't. Organisms do not decide that they would be better off with wings
and proceed to invent feathers directly and expeditiously. Feathers,
almost assuredly, did not arise for the purpose of allowing flight.
There were many intermediate states where feathers served different
functions entirely (such as insulation and display).
> There would be no need for millions and
> billions of years to achieve the diversity that we see in the natural
> world for such changes could be and would be realized in short order.
Only in a teleological world unlike the real world.
>
> The idea that eons of time are needed for evolution to be successful
> means that there is not a path of function where each and every step
> is beneficially unique.
It means no such thing. It only means that each step in a multistep
process must have independent utility *at that time*. There is no
teleological goal which must reached for "evolution to be successful".
Each step represent success.
> There are gaps between various functions that
> require a lot of time to cross. In fact, many of these gaps seem so
> wide that billions or even many trillions upon trillions of years are
> simply not enough.
You have not presented any evidence of such gaps. *You* must
demonstrate that all the proposed and or necessary intermediate steps
have absolutely no independent utility to the organism that has them.
All you have done is wave your hands and look at a beginning state which
has no wings used for flying and look at what you consider to be the
necessary goal and assert that no possible intermediate could have any
independent utility to any organism until the "goal" is reached. If
necessary or observed interemediate states have utility to the organism
that has those states, your whole argument falls apart. That there
exist many intermediate states of eye complexity in living organisms
demonstrates that such intermediate states can have utility to the
organisms that have them, and, in some cases may be of greater utility
in particular environments than the features you regard as the "goal" of
evolution.
> This is where the idea of design comes into play.
> Intelligence can cross such gaps in short order. Humans can type into
> the computer, "Methinks it is like a weasel" far far faster than a
> computer can come up with that phrase/function using neutral
> evolution.
Dawkins does not generate the phrase by using neutral evolution. It is
selection that generates the phrase.
> Why? Because humans have access to an intelligent mind
> that can be creative were as computers are not intelligent or
> creative. Likewise, genes and natural selection are not intelligent
> or creative. The gaps and functions are there. The only logical
> explanation to explain their existence is intelligent design.
> Intelligent design is the only force that exists in the universe, that
> we are aware of, that creates functions of the complexity and variety
> that we see in living things.
>
>
>>> Then,
>>>without this guidance of natural selection, evolution is dead.
>>
>>Not true. If all is as you claim, then evolution solely by natural
>>selection is dead. We must come up with some mechanism -- perhaps even
>>divine intervention -- to account for the crossing of such gaps. But our
>>knowledge of evolution in the sense of common descent does not depend on
>>knowing the mechanism to be natural selection, or upon knowing the
>>mechanism at all.
>
>
> Oh really? This is an amazing statement! You know that naturalism is
> the answer... without knowing how it works? You don't need to know
> the mechanism to know that it works? Natural selection really does
> not have to be part of the mechanism in order for naturalism to be
> creative? Incredible!
Your reading comprehension leaves much to be desired. He said that even
*if* natural selection were not the mechanism, the evidence would still
support common descent. Indeed, he specifically included "divine
intervention" as a possible alternative explanation *if* such gaps exist
and need to be crossed. The last time I looked, "divine intervention"
was not a naturalistic explanation.
> Well then, what other force do you know of,
> besides natural selection, which can help random mutations create such
> complex and integrated functions as we see in living things?
Natural selection works to retain complex and integrated functions once
they exist. Random mutation will still produce novelty and complexity
and novel integration (aka variation). Natural selection will still
exist in your world, I presume? What evidence do you have that some
other force is needed?
> You obviously have a very great faith in the power of naturalism to
> answer all questions pertaining to the physical universe. For you,
> the very notion that there just might be evidence of design in the
> natural world/universe is simply out of the question. You approach
> all ideas with this "a priori" assumption that naturalism must answer
> all that we see in the natural world. However, this is not a
> scientific view. The scientific method does not require any a priori
> assumptions to be brought to the table.
It brings the assumption that it can only deal with the material or
natural world. By definition, supernatural events are unknowable and so
irregular that we can learn nothing about the material world from them.
> To say that science cannot
> detect intelligent design is not scientific nor is it supported by the
> evidence that we have available to us.
Anthropologists and sociologists do it all the time. However, their
"intelligent designer" is supported by evidence and the capacities,
materials, methods, and intentions of that designer are always considered.
> Design is detected and
> proposed as a source for many observations that we see on a daily
> basis. Why? Because many things that we see around us, such as a
> fixed window or a Picaso painting, have no naturalistic explanation.
Sure they do. They were made by a biological organism. Last I looked,
biological organisms were not supernatural.
> To say then that living things had to have arisen "naturally", when
> one has no clue as to the naturalistic mechanism, seems to me like
> deliberate insanity.
>
Evolution is concerned with the descent with modification of organisms,
not the singular abiogenesis event that produced the first one.
All hands of bridge are equally rare.
> However, not every "hand" or series of nucleotides in a
> genome of a given creature has a unique function. In fact, the vast
> majority of potential DNA sequences are non-functional or neutral. To
> get to a new function requires random neutral drift around a huge sea
> of neutral/non-functional sequences.
Are you saying that single mutational events cannot have beneficial
selective consequences in particular environments? That it *always* or
almost *always* requires three or four independent mutational events
before there can be a beneficial selective consequence? What is your
evidence for this. Does the same reasoning hold for mutations with
deleterious selective consequences? You are aware that the terms
"beneficial", "deleterious", and "neutral" are conditional (dependent
upon environment) and not inate terms for describing mutations, aren't you?
Sean Pitman
> Perhaps you shouldn't post things you aren't very interested in, then. I
> for one would most like to discuss the evidence for and (if any) against
> common descent. How about you?
I don't post things that I'm not interested in. Why would you get
that idea?
As far as the evidence for and against common descent, I think that a
discussion of evolutionary mechanisms (or the lack thereof) is quite
relevant to this topic.
> > It seems quite obvious to me that given a particular
> > creature, such as a bacterium, that the vast majority of possible
> > amino acid sequences/proteins of a given length will have no
> > beneficial function for that creature in its current environment.
>
>
> Agreed. This is obvious.
>
> > Only a very tiny
> > fraction of the potential amino acid sequences will be recognized by
> > any given bacterium or living cell in any given creature.
>
> Recognized? What meaning are you using for "recognized"?
Take for example the insulin protein. Not every cell in the body
"recognizes" the insulin amino acid sequence. Other cells, having the
proper surface receptors, do recognize the insulin protein and perform
various functions when insulin comes around. So, for some cells the
insulin protein really has no function or meaning while for other
cells it does. It is like different words for different languages. A
given word might have some meaning in Spanish, but none in English.
The same is true for protein "words" in living cells. A given
protein/amino acid sequence might have function or "recognition" for
one cell, but have no function/meaning/recognition for another cell.
If a given part performs some sort of function in a given system of
functional parts, then that part is "recognized" by that particular
system. The system "knows" what to do with that part. It "knows"
what function that part has. For example, the term "recognition" is
often used when describing the interactions of antibodies with
antigens. When the antibody comes in contact with a particular
antigen that it fits with, the antibody is said to "recognize" the
antigen. Does this make sense now?
> > Take humans
> > for example. The vast majority of human DNA does not code for any
> > functional protein much less a beneficially functional protein. The
> > proteins that are coded for are somewhat plastic, true, but they are
> > also very specific. If changed or "denatured" to any significant
> > degree, they loose all function.
>
> You are confusing two forms of change. We were talking about mutation.
> Denaturing is a loss of tertiary or quaternary structure, most often as
> a result of heating. Nothing to do with what we are referring to. (Also,
> I don't understand your distinction between "functional" and
> "beneficially functional", or what you mean by "somewhat
plastic".)
I mention protein "denaturing" to emphasize the idea that changes in
protein sequence *and* structure affect protein function. We are
talking about protein function in general here. Whatever changes a
protein (mutation, heat, chemicals etc) can affect its function in a
given system of function since protein function is dependent upon its
3D shape/structure.
Also, a protein can be functional without being "beneficially"
functional. For example, a protein can have a "detrimental" function.
> > This means that the vast majority of
> > potential protein sequences and three-dimensional shapes are worthless
> > to a given human cell.
>
> This is not quite clear, at least the "vast majority" part. There are
> lots of protein sequences that don't do exactly what we would like, but
> it does appear that we can find function from random sequences. See
> this: Hayashi, Y., H. Sakata, Y. Makino, I. Urabe, and T. Yomo. 2003.
> Can an artibrary sequence evolve towards acquiring a biological
> function? J. Mol. Evol. 56:162-168.
Of course one would expect that various random sequences could be
found that do actually have some sort of function in a given cellular
system of function. Some of these might even have a "beneficial"
function in a given cell and environment. However, the vast majority
of potential sequences of a given length and 3D structure will not
have a function at all. You admitted as much above. When I said, "It
seems quite obvious to me that given a particular creature, such as a
bacterium, that the vast majority of possible amino acid
sequences/proteins of a given length will have no beneficial function
for that creature in its current environment", you said, "Agreed. This
is obvious." Well then, what are you trying to do here? You seem to
be contradicting yourself in the same breath.
I see it much like a language system of function. Pick a given
sequence length of words. Lets pick a sequence length of 3-letter
words. How many 3-letter words are defined by the English language
system? Quite a few, but probably not 17,576 which is the total
number of possible 3-letter words. Surely there is a sizable
percentage of defined 3-letter words as compared to the total possible
number of 3-letter words... true. Therefore, it is relatively easy to
change a letter in a 3-letter word and get to a new functional word
such as the evolution of "cat to hat to bat to bad to bid to did to
dig to dog." However, will this work so easily when we are talking
about say, 6-letter words? There are 308,915,776 different 6-letter
sequences or potential 6-letter words out there. Relative to this
number, the number of defined or "functional" 6-letter words in the
English language system of function, are few. It is much more
difficult to "randomly" pick out of this pile of 6-letter words a word
that will have some sort of function or "recognition" when spoken in
an English speaking crowd.
So yes, one would expect that there would be "lots of protein
sequences" that could be picked at random out of a mix of protein
"words" that would have some function for a given cell in a given
environment. However, I am willing to bet that these functions are
usually quite simple, having to do with enzymatic activities that
require relatively short amino acid sequences to perform them (like
3-letter words). Such functional sequences would be found to be
relatively common in a random mix of proteins. However, when one
starts increasing the complexity, the difficulty for picking a protein
with a function of higher complexity becomes more and more difficult
(As with the challenge of picking, at random, a functional 6-letter
word from a mix of 6-letter sequences). It might not be "impossible"
to randomly pick such a sequence, but it would take a lot longer time
to be successful on average.
The average time involved becomes the problem because, with increasing
complexity, the total number of sequences with potential function
decreases dramatically leaving larger and still larger gaps in
function between those sequences that would actually have function for
a given cell in a given environment. The random drift or "selection"
involved in getting from one sequence with function to any other
sequence with a different function of comparable complexity requires
greater and still greater amounts of time.
> And the introduction of 3-D shapes only confuses the question.
Actually, the 2-D sequence of proteins really is not what does the
job. The 3D structure is what really matters when it comes to protein
function. The same sequence can be folded in different ways. And,
depending upon which way the protein is folded; function may be gained
or lost. Proteins do not always spontaneously fold in the proper way
to realize their function. There are other proteins that fold new
proteins as they are made. If the 3D structure of a particular
protein is "unfolded" and then allowed to "refold" by itself, it most
likely will not fold properly and its function will be lost. So,
really, we talk about the 2D sequence because it is easier to talk
about, but in reality, the 3D structure is very important to function
and only compounds the problem of complexity since even more
differences can be realized for a given amino acid sequence than a
simple 2D sequence analysis would suggest. For a 2D sequence of 10
amino acids, the total number of potential proteins is:
10,240,000,000,000 (~10 trillion). However, the total number of
different proteins would actually be much higher than this because of
all the added differences in 3D structures that are not being included
in the total number. This makes for even less of a chance of picking
those sequences/3D structures of amino acids that actually have some
sort of function, much less beneficial function, for a given cell in a
given environment.
> > As far as demonstrating a negative (ie: A lack of a functional path
> > between two different proteins), it is impossible this side of
> > eternity. A negative finding never means that a positive finding is
> > impossible. However, the likelihood that a negative finding will
> > occur can be calculated.
>
> If it can, then you haven't done it yet. This remains to be seen.
Well, of course I disagree. Can you prove that these gaps do not
exist or explain how they might not exist? For example, can you show
how a relatively complex function, such a bacterial motility (Any
type, not necessarily flagellar motility), could evolve where no
genetic gaps in function would need to be crossed? There are those
who suggest that there is no goal in evolution. Therefore, the
testing of a specific "goal" such as the evolution of a specific
function, such as motility, is not a valid challenge of evolution
since a given type of bacteria may evolve other equally complex
functions before motility is ever evolved.
This is a great argument. For one thing, without a goal to defend,
there is no need to move goal posts as YECs are so often accused of
doing. Just because a particular function does not evolve, such as
the lactase function in certain of Hall's bacteria, does not mean that
evolution is having problems. It only means that evolution does not
need to travel down any particular path, regardless of the benefits
that would be realized if that path was traversed. Well, Ok... lets
go there. Naturalistic evolution obviously does not "know" which path
to choose. It can go down any path in any direction and eventually
get somewhere with some beneficial function. Sure it can. However,
what if each starting point is completely surrounded by a huge ocean
of neutral function or nonfunction? Consider that if there were 1
million defined 6-letter words that each word would, on average, be
surrounded by 300 non-defined words. No matter which way evolution
went, odds are that it would quickly run into a gap of nonfunction
that separates current function from new function. Try it. Starting
with a 6-letter word, how far can you go before you are blocked by a
gap of nonfunction? Now, if that seems hard, try to evolve a larger
sequence of letters, such as a sentence of words, one letter at a time
and see how far you can go before you are blocked by sequences of
nonfunction.
> How do you
> know there are such gaps? For eyesight, it has certainly been shown that
> there is a continuous series of slight morphological variants, each
> advantageous, from a patch of light-sensitive cells to a camera eye.
A series of morphologic variants that appear to follow a smooth
evolution of very small steps is deceptive in that is covers up the
complexity of the genetics involved. If in fact every "slight"
morphologic variant was the result of an equivalently "slight" change
in the genetic code then you would be correct in your statement that
such a series of morphologic variants give convincing evidence of
common descent. However, there are several problems with such an
automatic assumption. One problem is that apparently small
morphologic changes often require relatively large changes in the
underlying genetic code. The same is true for computer functions.
Apparently "simple" or "small" changes in a program's function often
require comparably large changes in the underlying code. For example,
going from a "simple" eye spot or collection of light sensitive cells
to a slightly concave eye cavity spot, seems morphologically simple,
but the genetics involved are quite complex. All the cells involved in
the formation of this cavity must be programmed to relate with the
other cells in this area in a very specific way to form this
concavity. This orchestration requires many very specific genetic
changes. Gaps in beneficial function are certainly involved. Another
problem is that function is arbitrarily attached to code. Very
different codes can and do code for the same or similar functions and
very similar codes can and do code for very different functions.
Because of this arbitrary nature of code, a change in the code will
probably not result in an equivalent change in code function or
"morphology". Very small changes in code can result in huge changes
in morphology. Also, very large changes in code might not change
morphology/function very much at all.
An argument based on morphology alone might seem compelling if that is
all that one had, but we know more now than Darwin knew. We know that
there is an underlying code or genotype that gives rise to morphology
or phenotype. If you can explain, genetically, how the gaps between
these various "small" differences in morphology can be explained, then
you would certainly win the Nobel Prize. As of yet, I have found no
detailed genetic explanation or real-time experiment that explains or
demonstrates how the evolution of morphologic variants, such as the
morphologic eye variants or various bacterial motility systems,
evolved or even could have evolved.
> I'm
> sure you are familiar with How would one go about demonstrating that
> there are or are not such gaps with respect to feathers?
Yes, try to evolve a feather or a feather-like structure or to
estimate how long it would take based on genetic sequence analysis,
mutations rates, functional genetic intermediates, and the length of
the average genetic pathway to such a function in a given creature.
Detail the genetic codes involved in coding for feathers and then
compare these codes to the codes that are available in other
non-feathered creatures and see if a genetic path could be detailed
and how long it would take to cross this path.
> We do know that
> feathers arose in a bipedal, non-flying dinosaur. That seems clear
> enough.
Oh really? How so? Is there a gradual step-by-step demonstration of
this evolution in the fossil record? Not any more than could be
detailed various creatures all living at the same time today. It is
the same argument as the evolution of simple to complex eyes. Get a
bunch of different kinds of eyes and line them up in a morphologic
sequence from more "simple" to more "complex". Obviously, once this
lineup is complete, the conclusion must follow that the simple eyes
gave rise to the more complex eyes. This might seem reasonable at
first glance, but this is not necessarily a correct conclusion.
Practically any collection of objects can be categorized in such a
manner, but this does not mean that these various object arose via
common descent... especially if the mechanism to adequately explain
such variations is weak. For example, the various books on my
bookshelf can be categorized in this manner, and just as convincingly,
from more "simple" to more "complex." But, this does not mean that
the more complex books arose via common descent from the less complex
books even if the changes between them seem to be relatively small.
You see, without an ability to detail a mechanism of change, the
differences and similarities, by themselves, do not necessarily
support the position of common descent.
> Whether they arose by natural selection, or by any naturalistic
> pathway, is difficult to determine. I suppose you could, if you liked,
> support some kind of theistic evolution in which God gives the
> occasional nudge to get a genome across some functional gap. I'm not
> sure where you would find evidence for it, as there is for selection,
> and I'm pretty sure you would reject such a theory anyway. Right?
The evidence that you have is one of morphology alone, not of
genetics. The morphologic evidence is not compelling enough to
adequately support the theory of common descent. You need genetic
evidence or some way to explain how the genetic gaps can be crossed.
Also, I find the standard interpretation of fossils and the geologic
column unconvincing and quite biased or colored by the a priori
assumptions of evolution and naturalism. I see no clear evidence that
feathers must have evolved from featherless creatures. The fossil
record is a static record and is thus quite limited in what it can
tell us about the lives and changes of creatures over time. You need
real-time examples detailing the actual genetic changes in life forms.
Relying on morphology is easy to do, but it is rather weak when it
comes to explaining how the genetic codes themselves evolved via some
naturalistic process.
> > If you think that a neutral gap in function
> > that requires just one protein sequence is hard to cross, try
crossing
> > a gap that requires the evolution of multiple proteins to cross where
> > hundreds or even many thousands of neutral mutations are needed.
>
>
> I agree that this scenario sounds unlikely. I just don't agree that it
> is necessary.
Why not? What *genetic* explanation do you have to account for the
differences then?
> > If there were such a path from scales to feathers, then we should be
> > able to quickly demonstrate such evolution in real time.
>
> I deny that there is any such expectation. Why should there be? Are you
> saying that we should be able to demonstrate every possible occurrence
> in the lab? Why? If we are talking about something that took millions of
> years, why should we be able to do it in one or two? And this assumes
> that we know what steps are necessary, which we don't, at least not yet.
If it took millions of years... why did it take so long if there was a
beneficially functional path each step (mutation) of the way?
> You have the kernel of an interesting point there, and it's been a
> conundrum of evolution for some time. Why is evolution so slow over the
> long term, when natural selection is so fast? I think there are several
> reasons: waiting for mutations, waiting for the environment (internal
> and external) to change so that new selective pressures are seen, and
> following a twisty path around constraints rather than the straight path
> you seem to think is the only possible one. It's an interesting problem,
> but not as you seem to think a disproof of the efficacy of selection.
Mutations occur quite rapidly. For humans, the average mutation rate
is around 250 mutations per individual per generation. In a large
population, such mutations, if a fair proportion were directed in some
way, would result in rapid evolution along a great variety of
evolutionary paths. Feathers, wings, eyes, legs, arms, and a host of
potentially beneficial functions would evolve in short order. The
problem is that the path is quite "twisty" indeed. The path is not
straight. That is the problem. The path is very curvy because of the
random drift problem. If each and every step is not selectively
advantageous, then evolution starts to wander around a neutral sea of
function. The wandering is very curvy or nonlinear. In fact, it is
such a curvy path that millions, billions, and trillions upon
trillions of years are simply not enough to traverse this path. The
"efficacy of selection" is dependent upon nature's ability to select
between different genetic changes. If the changes are "neutral" in
function then natural cannot select between different genetic
sequences that have the same function (or nonfunction). At this point
the "efficacy" of natural selection is severely limited.
> > There are gaps between various functions that
> > require a lot of time to cross. In fact, many of these gaps seem so
> > wide that billions or even many trillions upon trillions of years are
> > simply not enough.
>
> If there are, name one and show the evidence that it is such a gap.
I already have. Depending on the complexity of the function in
question, the evidence for non-evolution can be found in comparing
what is available with what is needed. The lactase function in E.
coli is a good example of this non-evolution. When lacZ and ebg genes
are deleted from E. coli, they simply do not use any other genetic
sequence to evolve the lactase function despite being observed for
many thousands of generations while growing on selective media that
would benefit them if they were ever to evolve the lactase function
again. B. G. Hall himself described such E. coli colonies as having,
"limited evolutionary potential." Obviously these limits are there
and they are found in the form of neutral/nonfunctional genetic gaps
in function. All codes/language systems have these gaps. Human
languages, computer languages, and even genetic languages/codes have
these gaps. Natural selection cannot cross gaps in function in any
directed way. Without direction, mutations are purely random and
random changes wander around a very curvy path that simply takes to
long to come across new beneficial functions.
> > You know that naturalism is
> > the answer... without knowing how it works?
>
> Did I mention naturalism? No. In fact I mentioned divine intervention as
> one potential mechanism. So your comments are irrelevant. I'm talking
> about common descent. Would you care to argue about the evidence for
> common descent?
The theory of common descent is a naturalistic theory. It is an
argument from the position that nature and naturalistic processes can
explain the variety in living forms. You are therefore "mentioning
naturalism." You mentioned "divine intervention as one potential
mechanism" but you do not believe that this is the mechanism over the
idea that a naturalistic process is a more likely or reasonable
explanation. For myself, I'm not so much arguing for the identity of
the designer as I am for the fact that there is evidence of design,
from some intelligent source somewhere, in living things. Humans are
also capable of such designs in code and systems of function. Are we
therefore "divine"? No, but we certainly are capable of
"supernatural" activities in the sense that non-intelligent natural
processes, such as random mutation and natural selection, are
incapable of performing. A tree limb, as it is blown by the wind, may
break a window without relying on deliberate design or creative
intelligence. However, there is no naturalistic process for fixing
the window and putting it back in its place outside of deliberate
design/creative intelligence... regardless of where this intelligence
came from... be it divine or human or an intelligent alien from the
planet Zorg. Whatever the source of intelligence, the fact that
"supernatural" intelligence (ie: above the naturalistic
non-intelligent processes of a mindless nature) was required can be
detected.
> I didn't mention anything about random mutations. I'm talking about
> common descent. Common descent is separable from the mechanism that
> causes adaptation. You, as a creationist, deny common descent. I'm
> saying that if, somehow, you were to show that natural selection is
> insufficient as a driving mechanism, then the evidence for common
> descent would remain untouched and conclusive.
Not so. Without a knowledge of the mechanism of common descent, the
evidence for common descent is far from "conclusive." Common descent
is not a forgone conclusion, especially if the mechanistic explanation
fails.
> > You obviously have a very great faith in the power of naturalism to
> > answer all questions pertaining to the physical universe. For you,
> > the very notion that there just might be evidence of design in the
> > natural world/universe is simply out of the question.
>
> I said nothing whatsoever either for or against design. I'm not talking
> about design. I'm talking about common descent. Is that clear?
When you are arguing in favor of common descent, you are arguing
against design. The theory of common descent is a theory that tries
to propose a naturalistic cause, outside of design, to the existence
of various life forms. So, really, you are talking about design.
Whether or not you admit it or realize it is another issue.
>I happen to believe, based on the evidence,
> that natural selection is a pretty good mechanism and that evolution has
> indeed proceeded "naturally" (and there is considerable evidence
that
> evolution has no particular goal), but that's not at all what I'm
> talking about here. Your inability to separate "darwinism" into
> independent components is causing a communication failure.
You would like to think that one component has no bearing on the other
components of the theory, but the fact of the matter is that all the
components of Darwinism are intimately intertwined. If one basic
component fails, the whole thing fails. I suppose you could say that
the theory of evolution is... "irreducibly complex." ; )
> Actually, under normal conditions most mutations occur during DNA
> replication, which I believe does occur simultaneously with cell
> division in most prokaryotes.
Yes, this is true. However, these mutations, once they occur, are
passed on from one generation to the next.
> > However, once the mutations occur, these mutations
> > are passed on to the bacterium's clonal offspring via the
> > division/replication/mitotic process.
>
> Mitosis is something that happens in eukaryotes, not prokaryotes.
True again, but prokaryotic replication/division is similar to
eukaryotic mitosis. The offspring are "clonal" in both cases.
> Once again: hypermutations are observed to occur in bacteria that are
> not actively dividing. Generally they happen under starvation conditions
> in which the bacteria cannot reproduce. If one bacterium experiences a
> mutation that lets it reproduce, then the subsequent colony descends
> from that one. Actively dividing bacteria do not experience these
> hypermutational rates.
True again. However, in my calculations I wanted to raise the
mutation rate as much as possible in favor of the evolution of new
traits in a reasonable amount of time. Hall also used other mutagens
to increase the mutation rate in his colonies. In any case, the point
of the high mutation rate is to show the difficulty in crossing
apparently small gaps in function.
> > In fact, Hall
> > does so in his own paper. He makes his own estimations of the
> > mutation rates for his bacterial colonies, "per generation."
> Are these hypermutational rates, i.e. a response to stress? I'm afraid I
> don't have the paper available in front of me.
The mutation rates that I used in my calculations are higher than
those used by Hall in his calculations. The mutation rates that he
uses are increased over normal because he used various mutagens to
increase the mutational diversity in his experiments.
> Every analogy is imperfect, but I think we can get a little more out of
> this one. Let's define a "non-functional" bridge hand as one with less
> than 13 points, and a "functional" one as having 13 points or more. If
> this is so, then even though there are many more nonfunctional than
> functional hands, and even though any given functional hand is
> vanishingly rare, still there are enough functional hands dealt to keep
> a game going. So with life. We are not picking a fixed target and
> attempting to approach it with mutations. There are many possible goals
> and many paths to each one. Even if most changes lead nowhere, it's
> enough that some changes lead somewhere.
Given 52 different cards in a deck and 5 cards in a hand, there would
be 380,204,032 different possible hands. If only 1 million hands had
a "function" what would the odds be that a "functional" hand would be
drawn any given round? 1 in 380 tries... right? If each try takes 10
minutes, the average time needed to draw a functional hand would be
~2.5 days. You see, each functional hand, on average, would be
separated from every other functional hand by a relatively small sea
of nonfunctional hands. Still though, no matter which direction you
would happen to go, the odds are that you would end up with many
nonfunctional hands before you would come across *any* other
functional hand.
As you said, "So it is with life. We are not picking a fixed target
and attempting to approach it with mutations. There are many possible
goals and many paths to each one." The problem is that every path is
long no matter which path is taken. In fact, when it comes to certain
complex functions in living things, the average distance of a path to
any one of a number of possible goals is so large that even with a
huge population taking many different paths, the time required to
reach any of the potentially beneficial targets is still huge. For
example, take those functions that require at least 100 amino acids to
perform them. How many of these functions would be beneficial to a
given organism in a particular environment? Maybe a billion? or a
trillion? Maybe a trillion trillion? Maybe, but most likely not
anywhere near the 1 x 10e130 different potential 2D sequences that
could be had. By far the vast majority of these 1 x 10e130 proteins
would be of no beneficial use to any particular organism. If even a
trillion trillion functions could be of some beneficial use, this is
still a tiny fraction of the total leaving only slightly less than 1 x
10e130 different proteins that would not be beneficially functional.
This means that each one of the trillion trillion functions would be
surrounded by 1 x 10e106 proteins that would not be beneficially
functional. In moving from one function to any one of the other
trillion trillion functional sequences out there, one would have to
cross a vast sea of nonfunction... no matter which direction one
started out in. These functions are like tiny islands in a vast sea.
No matter how many beneficial functional islands there might be out
there somewhere in this ocean, the waters of nonfunction that separate
them are vast indeed. The boat of neutral evolution just drifts
around on this sea randomly until it comes across some new function
that can be recognized as beneficial by natural selection. However,
until this new function is realized, natural selection is blind to all
neutral/nonfunctional genetic changes that occur in the meantime.
This leaves random chance as the loan power for change. And, random
chance alone simply takes too long to cross this sea to any one of the
billions, trillions or even zillions of possible functions that may be
out there.
It is like a lottery where there are a million winning numbers. It
seems like a cinch to win by picking at least one of so many winning
numbers until one realizes that for every winning number there are a
zillion loosing numbers. How long, on average, will it take to come
across any one of the one million winning numbers if there are
trillions upon trillions of loosing numbers for each winning number?
You see, the deck is heavily stacked in favor of loosing when it comes
to the realization of any sort of complex function that requires the
crossing of even a relatively short gap of neutral change.
> > To
> > get to a new function requires random neutral drift around a huge sea
> > of neutral/non-functional sequences.
> You assume this but there is no reason to suppose it, and no reason to
> suppose a single target as all your calculations assume.
There is plenty of reason to "suppose" this. You yourself admitted
that there are most likely far more nonfunctional sequences than
functional sequences. My calculations use a single function as an
example, but I need not assume a single target at all. Even given
millions of potential targets, the problem remains that each one of
these targets is still surrounded by a huge sea of nonfunction. The
Bridge Game analogy is very good in this regard, but it is limited in
that the odds in favor of getting a functional hand, within your
definition of function, are still pretty good because of the limited
nature of each hand of bridge. However, when you expand the hands to
compare with the size and complexity certain genetic functions, the
odds get much much worse. Instead of having a hand of only a few
cards, try using a hand of 1,000+ cards while only having a few
million winning hands out there.
> > In the replacement of a particular base in a sequence of DNA, the
> > replacement could replace the base at the position in question with
> > the same base 1/4th of the time. Therefore, the odds that a given
> > "change" will result in a specific base are 1 in 4.
>
> If a base is replaced with the same base we don't call it a mutation. We
> don't call it anything, except maybe "replication". A mutation rate that
> includes "no change" would be a rate of 1 per site per generation, since
> every site will either change or not change. You really need to fix this.
Ok... I've thought about this point further and you've got me here. I
will fix this. Thanks for pointing out this error, but it really has
no significant bearing on the point at hand. Be the odds 1 in 4 or 1
in 3 makes no real difference as far as the problem is concerned.
> Well, it [neutral evolution] does say how neutral gaps can be crossed. With low probability,
> getting lower as the size of the gap increases. If there is a large
> neutral gap between two functional proteins it is unlikely to be
> crossed. But who says that such gaps are prevalent?
You are one of the more reasonable evolutionists that I have come
across. At least you recognize the problem and seek a reasonable
solution, such as the idea that such gaps do not exist. If such gaps
really did not exist, then yes, evolution would not present a problem
at all. However, it seems like you understand that if such gaps do
exist that they would actually present a significant problem for your
theory. You see that a gap crossing of low probability requires more
time to be overcome and that this time increases with the size of the
neutral gap. But, you believe in evolution so much, based on other
evidences, that such gaps really must not actually be there. They
might be there for certain targeted functions in certain narrow
situations, but certainly not for all functions. You propose that
there are so many potentially beneficial functions out there that all
the various paths that might be taken are bound to come across at
least a few of them in a reasonable amount of time, even if they be
quite complex... such as bacterial motility or camera-like eyesight.
Well, let me turn the tables here and ask you to defend this
hypothesis of yours. Upon what basis do you propose that these gaps
do not exist? You obviously "agree" that the vast majority of
possible amino acid sequences of a given length would have no
beneficial function for a particular organism in a particular
environment. Given this agreement, how do you propose that no gaps
exist between functional sequences? Are they all clustered together
like a bunch of islands in an archipelago? Even the "functional
hands" in your hypothetical game of bridge are each separated from
each other by many nonfunctional hands. These are "gaps" in function
between functional hands of bridge. Since these gaps exist in your
hypothetical example, how then can you propose that they do not exist
in the genetic cards/deck of a given gene pool? Please, upon what
evidence do you propose the absence of significant gaps between
various genetic functions as these functions move up the continuum
from more simple to more complex?
Sean
Ron Okimoto
> John Harshman
>
All this whining about neutral mutations is pretty bogus until you can
put forward a system that you can use to demonstrate that this is a
problem. Just because we don't know something doesn't mean very much.
You have to use what we know to support your position. Since you
can't what good is your argument. It is simply worthless because you
can't test it.
Take the flagellum, point out the changes that had to be neutral to
evolve the flagellum and demonstrate that they had to be neutral.
This will be a neat trick because you don't know what the starting
material was or what the original flagellum looked like. If you can't
do this how do you know that they were neutral changes? It is just
that simple. You have to come up with some way to test your ideas.
It isn't up to the real science to do it for you. When we don't know
something what is the problem. We don't know a lot, but we do know
somethings, so what is your beef with what we know? Making
unreasonable demands when you can't even tell us that any of the
changes had to be neutral is pretty bogus.
There is so much genetic evidence for common descent that even guys
like Behe and Dembski have to admit that it is pretty much of a fact
and you can't say that these guys have a naturalistic bias. So common
descent must not exclude the possibility of design or designers, so
again you are wrong. There is so much evidence for common descent
that the ID advocates have to give it lip service or they look like
lunatics. One of the best evidences for common descent is the "sea of
neutral mutations" in the genome. The vast majority of mutations have
no affect on the orgainism. We share a lot of these neutral mutations
with our close relatives the apes. We share them in a specific
pattern that makes it very apparent that if the designer exists that
he created using common descent. The designer would have had to take
an existing genetic template and change it a bit. Neutral mutations
would happen for a few million years and he would take this template
and again change it. You skipped out on learning what nesting was so
you don't understand how we know these things, but guys like Behe will
tell you that it is a fact of nature. Just because you refuse to
learn what the data is and what it tells you doesn't mean a whole lot
to science.
Humans and chimps are over 98% identical in their genetic template.
It looks like the designer used an ape template to make us. He seems
to have used a different ape template to make chimps and humans than
he used to make orangs and it looks like he used a monkey template to
make all ape templates. How did the designer do this and place the
sea of neutral mutations in the genomes to make it look like he used
common descent? That should be your challenge. We have a very simple
and direct answer, what is yours?
Ron Okimoto
Snip:
Sean Pitman
> > For example, the odds of getting one, two, or even three necessary
> > mutations "right" in a reasonable amount of time, even in a gene some
> > 3,500 base pairs in length, is not unimaginable . . . since this gene
> > is starting very close to the "goal" to begin with.
>
> Why is it starting very close to the goal? You acknowledge that it is
> a very different protein. Why should this matter? Was it present by
> design or just chance?
Even though the ebg gene produces a very different protein from the
one produced by the lacZ gene, this protein was only one point
mutation away from the lactase function. A single point mutation was
all that was required to realize a beneficial lactase function. At
this point, purely random chance is all that is needed to gain the
beneficial function in short order.
> I don't know if I agree with your numbers, but all they indicate is
> that we are more on the right track than you are. You have to keep
> these mutations from happening. We observe them to happen. What is
> your problem?
You just don't seem to get it do you? I'm not trying to "keep these
mutations from happening." I am well aware that they do happen. The
problem is that as the neutral gaps in function get wider, the time
required to cross these gaps gets exponentially longer and longer
until zillions of years are needed.
> > But, what if the starting sequence was two mutations away from the
> > desired lactase function? Would that make any difference? The odds of
> > getting either one of the two needed mutations with the first mutation
> > are 1 in 8.2 million mutations. The odds of getting the second
> > mutation right are 1 in 16.4 million mutations. So, the odds of
> > getting both mutations right are 1 in 134,480,000,000,000 (~1.34
> > trillion) mutations. With these odds, the correct mutation will occur
> > in about 315 bacteria in the first generation.
>
> How does this help you out? These calculations just make our model
> look better.
Not really… Although I have since revised the numbers significantly in
keeping with my new understanding of the probabilities involved (with
the help of the binomial equation), the statistics certainly don't
help you out of the gap-crossing problem.
> > If the starting sequence was three mutations away from the desired
> > function, the odds of getting all three mutations right shoots up to 1
> > in 735,157,333,333,333,333,333 (~735 million trillion) mutations. With
> > these odds, the correct mutation will occur in one bacterium in
> > 1,792,682 generations. With a generation time of 20 minutes, that's a
> > bit over 68 years.
>
> You can't calculate the probabilities like that because they aren't
> independent. You have to calculate the probabilities based on the
> actual situation. Once you have one mutation, you don't have to get
> it again. You can as often as you like, but the second mutation would
> occur in a bacterium that already had the mutation. Like you
> indicated by your own calculations 315 bacteria would have any one of
> the three. Close to 1000 in just the first generation would have one
> of the three. How many in the second generation? The 100th? The
> chance of two is the mutation rate in those bacteria that already have
> one. Your numbers collapse dramatically, and even more dramatically
> if the mutations were not neutral, but had some selective advantage
> that allowed them to increase in frequency in the population.
First off, by definition a "neutral" mutation has no selective
advantage. This is the point. Because of this, nature does not
preferentially select to increase their frequency in a population.
This is the basis of my whole point… you understand.
However, your main point is quite interesting. I have had to revise
my probability calculations significantly because of it. I wrote a
computer program based on your argument to see just how fast the
"numbers would collapse." I started with a colony of a given number
of individuals, non of whom had any of the "correct" mutations. I
hypothesized a neutral gap between current function and a new
beneficial function of three point mutations in a genome of 4 million
base pairs. After one generation I calculated the average number of
individuals that would have at one, two, and three "correct"
mutations. Then the program calculated the number of individuals with
one correct mutation that would gain a second "correct" mutation as
well as the number that would loose the correct mutation that they
already had and move to the group with no correct mutations. I did
the same for those in the 2 and 3 "correct mutation groups." After
running this program over and over again, I noticed something very
interesting. In about 60,000 generations, regardless of the
population size or the size of the gap, the population reached
equilibrium where each group maintained a constant population size.
For E. coli with a generation time of around 20 minutes, this
equilibrium is reached in just over 2 years.
So, what does this mean? As it turns out, a population of a trillion
bacteria can cross a neutral gap of 3 or 4 point mutations in a few
weeks, not hundreds or thousands of years as I had previously
calculated. In fact, a population of a trillion E. coli bacteria
could cross a neutral gap of 20 mutations in around 2 years.
The problem can be visualized by considering the total number of
options there are for a given neutral gap. For example, consider a
gap of 2 point mutations. How many different possibilities are there
for a gap of just 2 point mutations? Well, there are 4 options for
each position so the total number of potential combinations of the
options in two positions is 4 to the power of 2, or 16. There are
only 16 possible combinations total. At equilibrium, all of these
possible combinations would have the same chance of being "occupied".
Starting with a trillion cloned individuals at one of the 16 possible
positions, all of these 16 positions would be rapidly filled with the
given mutation rate of 400 per individual per generation. But, what
happens when the gap is doubled to 4 point mutations? Does the total
number of options also double? No, it increases by a power of 2.
Squaring 16 gives us 256 total options for a gap of 4. Still, a
population of a trillion individuals will quickly fill all of these
options with many individuals. At equilibrium, each option, to
include the "correct" option, will have 3,906,250,000 representatives.
Doubling the gap to 8 again causes the total number of potential
options to increase by a power of 2 to yield 65,536 possible
combinations. Again, a trillion individuals would quickly fill all of
these possibilities with 15,258,789 at each position at equilibrium.
Obviously then, such a large population can cross such gaps in short
order. However, when the gap gets to be around 20, there aren't
enough individuals to fill every potential option at equilibrium. A
gap of 20 has 1,099,511,627,776 different possibilities. Each
possibility would only have 0.909 individuals occupying that position
at any given point in time. This would call for a bit of "random
walk" on the part of these individuals. A given position or option
might be empty during a given generation. There would be an average
time where this option had no representation in the population of a
trillion.
Now, consider a gap of 30. A gap of 30 has 1,152,921,504,606,846,976
(~ 1 million trillion) options. This means that at equilibrium there
will be 1 million non-occupied positions for every position that is
occupied. If each individual bacterium in a steady state population
of 1 trillion changes this sequence of 30 to a new sequence every
generation, it would still take an average of 1 million generations to
come up with at least one individual with the "correct" sequence.
This works out to be around 38 years. However, a gap of 40 has
1,208,925,819,614,629,174,706,176 (~ 1 trillion trillion) options. A
population of a trillion would come up with the "correct" option in
around 38,051,750 years.
So you see, the problem continues to stand. A gap of 30 or 40 is
nothing compared to the complexity of the functions that exist in
living things. A sequence of 30 base pairs would only code for an
amino acid sequence of 10. Consider that the lacZ and ebg genes are
over 1,500 base pairs in length… and this is what is needed to code
for the relatively simple enzymatic lactase function of a single
protein. It turns out that populations of bacteria forming a ball the
size of the galaxy or even the known universe would not be enough to
keep up with the time required to cross neutral gaps of even 100 or
200 base pairs.
http://faculty.vassar.edu/lowry/binom_stats.html
Interestingly enough, Hall himself discusses this problem:
"Given a gene of 1000 base pairs there are over 10e34 sequences that
differ from the wild-type sequences by 10 or fewer mutations. Not
only can we not explore all of those possible variants, life itself
has barely had sufficient time to explore all of those possibilities.
The mass of the earth's oceans is about 1.4 x 10e24g. Even if living
cells constituted a 10e-4 of the mass of the oceans, given about 10e12
bacterial cells per gram, a reproduction rate of about 1 cell
generation per day and a mutation rate of about 10e-9 per cell
generation and 4 billion years of life there has been sufficient time
to explore only 1.6 x 10e34 variants of a single 1000-bp sequence.
However, evolution does not proceed by exploring all possible variants
but by incorporating single mutations, selecting the fittest of those
variants, expanding the population of the fittest variants, and
incorporating additional single changes."
Hall goes on to explain, "If the evolved sequence differs from the
wild-type at n sites there are n possible first-step amino acid
replacement mutants. Each of those single mutants can be created by
site directed mutagenesis and the effect on fitness determined by
competition experiments. The best (fittest) of those amino acid
replacements can be chosen and the n31 possible second-step mutants
created, the fittest double mutant chosen, the n32 possible third-step
mutations introduced, etc. The effect of this exercise is to mimic an
evolutionary pathway in which the fittest single mutant is fixed into
the population, that population expands, the fittest double mutant
arises and is fixed into the population, etc. Orr has recently shown
on theoretical grounds that adaptive evolution is expected to proceed
in exactly this fashion in which the first mutations to be fixed are
those that have the greatest positive effect."
Of course, all of Hall's single steps here are functionally
beneficial. What happens if there are true gaps in function? What
happens to evolution?
Hall continues: "If that sequence involves six amino acid
replacements, we might find that after introducing three replacements,
each of which further improves fitness, none of the three remaining
replacements improves fitness. Assuming that the final six-mutant
sequence is significantly fitter than the triple mutant, that result
means that two, or perhaps even three, of the remaining substitutions
must be introduced simultaneously to further improve fitness. This
simultaneous occurrence of two or more specific mutations is obviously
highly unlikely, but what about the possibility that one of the two
mutations will arise, by selectively neutral, but be fixed into the
population by drift? Were that to occur the second mutation would
quickly be incorporated by selection. The probability that a newly
arisen neutral mutation will be fixed into the population is the
reciprocal of the population size. When populations are large enough
that the probability of the occurrence of the mutation is very high,
e.g., the population size approaches the reciprocal of the spontaneous
mutation rate, then the probability of the fixation is very low.
Although neutral variants arise constantly, it is very unlikely that
the particular neutral variant we require will be fixed into the
population. Thus, unless each of the mutations confers a selective
advantage relative to its parent, it is unlikely that the final
six-mutant sequence would evolve naturally. In the example above we
would conclude that the evolutionary potential may well be limited to
the triple mutant."
http://www.eeb.uconn.edu/Courses/EEB449/Hall%20FEMS.pdf
So you see, even Hall admits that even relatively small neutral gaps
of three mutations might be enough to "limit" further evolution.
Thus, such functions that are isolated from other functions by neutral
gaps might be quite difficult for a theory of purely naturalistic
evolution to explain.
> > > It also looks like I am correct and that in the original study Hall is
> > > looking for sustainable growth on lactose. Evolution doesn't happen this
> > > way. Evolution does not depend on a do or die situation. In nature the
> > > organism without the mutation lives happily in the environment. This is
> > > not the case for the Hall experiments. The organism dies in the Hall
> > > environment, no second chances.
> >
> > Actually, I think that you have misread Hall's work. The E. coli do
> > not die in the lactose environment set up by Hall. The media is a
> > "selective media". It does not kill off those bacteria that do not
> > evolve the lactase enzyme, but only promote growth and improved
> > survival of those that do evolve the lactase function. Please, go and
> > read the paper again. The selective media works very much like a
> > natural environment where the bacteria live just fine, but could live
> > better if they had certain functions (such as lactase ability) in a
> > given environment (one with lactose in it).
>
> You have never given the procedure that they used. I just give what I
> saw in what came up in the search. I didn't look at all of the
> references only the first 5 or so before I stopped, but explain where
> I am going wrong, and how I am misinterpreting this quote from one of
> the abstracts "Wild-type ebg beta-galactosidase, encoded by ebgA, is a
> catalytically feeble enzyme that does not hydrolyze lactose or other
> beta-galactosidase efficiently enough to permit growth on those
> substrates." Hall BG 1999. FEMS Microbiol Lett. 174: 1-8.
Yes, that is true. However, Hall used a lac-TET plate (Tetrazolium
lactose agar) as a selective media. Tetrazolium lactose agar (TZ
lactose) is a rich medium containing amino acids, nucleosides,
vitamins, lactose and the indicator substance
2,3,5-triphenyltertrazolium chloride. The indicator substance is
initially colorless, but is reduced to a deep red color by the growth
of colonies unless the colonies metabolize the lactose. (The acid
produced as a by-product of lactose metabolism inhibits the reduction
reaction.) (Note: LacZ- mutants sometimes give a weaker response on
TZ-lactose than do LacY- mutants.)
In other words, this agar does in fact allow grow of E. coli that lack
lactase ability, but indicates when such an ability is achieved. This
is a selective media that does not "kill" those that are not selected.
> The way
> that these selection experiments work (by researchers like Cairns and
> Campbell) is to plate the bacterium out on a plate where they have
> minimal metabolic capability. They have to work their DNA repair
> mechanism and be able to transcribe the new mutations in the DNA to
> mRNA or they will not express the new mutations, but they do not grow
> well or divide very well. After a period of time in this semi stasis
> most of them die on the plate. You can't revive them even if you add
> medium that they can grow on. I don't know when you call a bacteria
> dead, but if it never divides again that gets my vote.
>
> What did Hall do and would it be considered to be the way things
> usually work in nature?
Other researchers may have done things differently, but Hall used a
non-lethal selective media in his experiments, closely simulating real
life non-lethal situations where the gain of a particular function
would enhance survival and reproduction.
Exactly… but the environments in both cases were non-lethal. In other
words, they allowed for the build up of additional mutations.
> > > It looks like Hall has met your
> > > challenge with the system you are trying to say supports your contention
> > > that it is impossible.
> >
> > I never said that a neutral gap of 3 mutations was "impossible." I
> > said that depending on function complexity that certain gaps of such
> > lengths or larger would be impossible for neutral evolution to cross
> > in a reasonable amount of time. Where has Hall demonstrated this to
> > be incorrect?
>
> Yes, by any standard. How many man hours do you think the experiment
> took. Probably less than 6 months worth of experiments, and more
> likely just a couple of weeks. He may have been working on this
> problem since the 1970s but his bacteria were probably in the freezer
> most of that time.
Still, 10s or even hundreds of thousands of generations were in fact
observed… still with no evolution of certain specific functions.
Also, there are many other types of bacteria out there that have not
been in any freezers since the 1970s (ie: Salmonella, Proteus, etc)
that still do not have lactase ability, despite its relative
simplicity of function, and despite having experience over a million
generations with huge populations sizes under selection pressures that
would benefit such bacteria if they ever did evolve the lactase
function.
> > He still hasn't demonstrated the evolution of the
> > lactase function in E. coli lacking both the lacZ as well as the ebg
> > genes. Why is this?
>
> He doesn't do the experiments like they would happen in nature? He
> never lets the bacterium have a chance to evolve the number of
> mutations that are needed to get activity using some other protein?
Yes, Hall does in fact do the experiments as they would be expected to
happen in nature. This is a non-argument. The reason why the
bacteria aren't given a chance to evolve the number of mutations that
are needed is because the time required to evolve such specified
mutations is more time that Hall has left in his life… even if he were
to live thousands or millions of years.
> > The only logical reason for such a limitation to
> > the evolution of the lactase function in such bacterial colonies
> > (despite the potential benefits if they were able to evolve this
> > function) is that there is a gap in function between the lactase
> > function and the collective genomic real estate potential of Hall's E.
> > coli colonies... even given hundreds of thousands of generations.
>
> This is pretty bogus because you have to admit that it happened once
> in only 2000 proteins found in E. coli. From the couple of other
> bacteria that he has been able to do this with it has happened in them
> too, and different proteins were involved in those activities. So
> what is your problem. It seems like it isn't so special. Demonstrate
> that it is. If it is so hard, why was he able to do it again in other
> species?
The reason why it is a problem is that when you remove the egb gene,
it never happens again… nor does it happen in many other bacterial
species despite 50+ years of observation and selective pressures.
Granted, the lactase function does appear to be a rather simple
enzymatic function that can be performed by a single protein sequence
working alone. The fact that such a relatively simple function is
difficult to evolve in various types of bacteria is quite interesting.
If a simple enzymatic function is so difficult to evolve, what about
more complex functions that require multiple proteins all working
together simultaneously? The gaps rapidly get quite enormous as the
complexity of function increases. If you think it is fortunate for 1
out of 2000 proteins to be able to evolve a relatively simple function
like the lactase function, try figuring out the odds of getting a more
complex multi-protein function to evolve… such as bacterial motility.
> > > Why don't you research the work more carefully
> > > before making these types of mistakes?
> >
> > LOL - Why don't you? You evidently do not understand the experiments
> > that you are trying to use to support your position.
>
> Demonstrate that you understand the experiments, and that they tell
> you what you think that they are telling you.
See above…
> > > Since this is a 1995 paper if you
> > > had done your homework you wouldn't have had to write all that stuff that
> > > is now refuted by the system of your own choosing. Do your own research
> > > and stop relying on creationist sources. You know that they are out to
> > > lunch. You can use them to get a start in thinking about some problem,
> > > but you know that they have to ignore most of the data to believe what
> > > they do, so you have to look for this data yourself.
> >
> > Oh, I have done a fair amount of reading/research for myself. You
> > perhaps should do a bit of your own thinking as well and not rely so
> > much on the conclusions of mainline popular scientists. Granted, many
> > if not most YECs don't know the heck what they are talking about.
> > But, the same can be said for evolutionists. There are a few bright
> > lights in both camps. So, we must all try and think for ourselves.
> > You and the evolutionist camp may turn out to be correct. However,
> > until I understand evolution and how it works for myself, I'm
> > certainly not going to take anyone's word for it at face value.
> > That's just not me.
>
> So how did you miss the 1995 paper?
I didn't miss the 1995 paper. There was nothing in it that
contradicted the previous papers or anything that I had said. Hall
himself is the one that made the statement that a neutral gap of 3
mutations would be, for all practical purposes, impossible to cross.
I am in fact more in favor with your argument here than Hall himself
is. I think that Hall is limiting the abilities of neutral evolution
too much here. The limiting gap seems to be a bit wider than Hall's
calculations allow. So, who is misreading who here? You evidently
haven't read anything more than abstracts. Try reading the entire
paper for a change.
> As long as you use creationist
> literature, expect to be wrong about 100% of the time.
That's bogus. There are in fact many creationists that are well
educated, honest, and insightful in their thinking and writings.
Outlandish statements such as this only speak against your
credibility. I don't say such things about evolutionists. I think
that there are many brilliant evolutionists who are very well
educated, brilliant, honest, as well as insightful. I have found the
same to be true of many, though certainly not all or even most,
creationists.
> That is just a
> fact that you know and have run into so many times that it must hurt.
> The "evolutionist" that matter are the professional biologist. Joe
> Blow down the street doesn't carry much weight in science, but for
> some reason he carries the weight of creationism on his shoulders.
You evidently do not understand that there are many well educated
professional biologists and other scientists who are in fact
creationists or design theorists. To make such generalizations that
all creationists are poorly educated idiots is simply ridiculous.
> That is the difference between science and creationism. You know
> this, I shouldn't have to tell you that. Why try and make it look
> like the guys that don't matter, matter? If you don't know what you
> are talking about, you don't get much attention in science. Look at
> all the ID supporters, until they come up with something to evaluate,
> science wouldn't give them the time of day. They only get attention
> because of the dishonest things that they are doing in politics.
The reason why many scientists won't give them the time of day is
because there is a religious type of dogma in the popular scientific
community known as naturalism. Nothing can challenge naturalism
because naturalism is a sacred part of the philosophy of modern
popular science. I suggest that you get your head out of the sand and
start thinking for yourself instead of worshiping the popular gods of
popular science.
Again, a nice "just so story", but based on absolute fancy, not any
sort of supportable, predictable, testable, science. Sequence
similarities could only be maintained over the course of billions of
years if they were beneficially functional. Neutral similarities
would be mutated out of existence. Also, I say again, similarities do
not, by themselves, necessitate a common evolutionary origin over
common design. That is the whole argument here. Did these
differences and similarities arise via a naturalistic mindless
process, or via some sort of outside intelligent input/design?
> > > As you might expect after
> > > that long they are very different proteins. If you study this system you
> > > can see just how gene duplication is responsible for the permeases, and
> > > inducer genes of the two cistrons. This is like the blood clotting
> > > system that the ID people have to acknowledge that there is a lot of
> > > evidence that it could have evolved. The proteins in the system are
> > > related to eachother and obviously were created by gene duplication.
> >
> > If given the "a priori" assumption that evolution is true, then yes,
> > this is the only logical explanation. However, just because various
> > genes look quite similar or even identical does not mean that they
> > necessarily arose via gene duplication.
>
> Give your alternative mechanism and the evidence for it.
Intelligent Design. The evidence is that there is no good rational
for explaining how such functions can arise without ID. For example,
I might ask you to explain how a broken window in a house could be
fixed outside of ID? You see, the evidence for ID is the lack of a
reason explanation for an observation outside of ID. It is an
argument of probability against any other mechanism.
> > Very similar genes may be
> > used in very different ways in different systems of function. The
> > evolution of different systems of function using the same genes is
> > still quite problematic since the assembly of any new system of
> > multiple genes would require the crossing of neutral gaps in function.
> > No such functional system of multiple genes, to my knowledge, has
> > been demonstrated to have evolved in real time.
>
> You have a problem in that you haven't been able to find a system
> where you can claim that this has occurred. Shouldn't you demonstrate
> that there is a problem before you claim it is a problem. Give
> specific examples and how you determined that the changes had to be
> neutral.
I have done this over and over again. The fact that lactase does not
evolve in E. coli over tens of thousands of generations in very large
colonies is very good evidence for the existence of such neutral gaps.
Also, any reasonable thinking person would admit that there are a lot
more neutral options than there are functional options out there and
that the neutral options expand greatly with increasing complexity of
the interacting parts… as with a language system like English. For
example, evolve the phrase, "Methinks it is like a weasel" one
mutation at a time and see how far you can go. How many different
function English phrases can you get before having to cross gaps of
neutral/non-function?
> > For example, it is
> > thought that the motility function of bacterial flagella arose via the
> > use of existing genes in new combinations so as to produce a new
> > function of motility. Well, if it is so easy, and there are few or no
> > neutral gaps to cross, the evolution of such a motility system should
> > be easy to demonstrate in short order. After all, the necessarily
> > genes to produce all the necessary parts are all there in the
> > non-motile cell. What is the problem with using these existing parts
> > to make a new function? It should be so easy, but it really runs into
> > the same problem as using the same 20 amino acids to produce new
> > functions. All the amino acids are there, but making a new function
> > using the 20 amino acids quickly runs into roadblocks of gaps of
> > neutral/non-function. The same thing happens when you try to use
> > existing proteins to make new functions. The gaps are still there and
> > are even wider than trying to cross gaps in single protein function.
>
> Demonstrate that the changes had to be neutral and what order that you
> think that they occurred in.
Why don't you demonstrate that the changes would not be neutral and
the order that such mutations would have to occur in order to follow
your hypothesized path of ever improving function. For example, what
good are 30 of the parts all in their correct places if 60 parts are
needed for flagellar function? The 30 parts might in fact be useful
in other systems of function, but for flagellar function to be
realized, they must come together in a very specific way… with another
30 parts. How do you explain this… one point mutation at a time?
> It could be easy to evolve a flagellum,
Oh really?… Please, explain how.
> but we have a problem. We
> don't know what the first one looked like.
Ok, that is not a problem… reduce the current flagellum one part at a
time so that each reduction is functional in some theoretical
environment.
> It has changed in the
> billions of years since it first evolved. Looking at the different
> flagellum we can see that they probably did evolve from some original
> one, but some have different parts. Some parts seem to have been
> lost, some may have been gained, some lost and regained. It has been
> a very long time.
This is another "Just-So-Story". Sounds lovely, but absolutely no
solid testable evidence to support it.
> What did the original flagellum look like? What
> proteins and their sequences were available as basic material that it
> evolved from? Without this basic knowledge how do you expect us to
> reproduce the evolution of flagellum?
It should be easy to start from what you know about a given bacterium
with its given genes a propose some way that that bacterium could
evolve a flagellum. Or, even better, reduce a flagellum, one part at
a time, and still have the remaining apparatus doing some beneficial
function.
Some have argued along these lines by saying that many of the parts of
the flagellum do in fact have other useful functions in the cell… such
as secretory pores, ATPases etc. Perhaps a third of the total number
of parts have been explained in this way. However, this does not
explain how these parts come together to form a new function. For
example, all 20 amino acids are there to make a flagellum in all
bacteria. All the parts are there. However, these amino acids do not
self assemble themselves to make a flagellum in all bacteria. So you
see, just because you have all the needed materials does not mean that
you have any particular function.
> Look at ebg, a billion years
> ago it's sequence may not have been able to evolve Beta gal activity
> in a single mutation, but hundreds of amino acid changes since then
> now provide a substrate for beta gal evolution.
Perhaps, but you would be able to estimate how long it would take
given a particular distance that would be required to be crossed. If
the neutral gap was in fact "hundreds" of amino acids wide, then the
odds are extremely unlikely that this gap would have been crossed in a
billion years… even given a population the size of the galaxy or even
the known universe.
> You need to know the
> sequences of the proteins like the ATPases at the time that flagella
> were evolving in order to try and figure out how hard it would be to
> get one to form the hexamer needed by the flagellum. Maybe the
> original flagellum only had a tetramer arrangement, maybe only a
> dimer. Do you know this kind of stuff? Can you recreate the
> conditions under which flagellum were evolving? You know that these
> details are very important. Different starting sequences will give
> you different results.
Actually, since I do not believe that the flagellum evolved or could
have evolved, I do not believe that these "original sequences" exist.
You cannot even hypothesize any path, even a theoretical path, that
would get you from any group of proteins to a flagellum. Try it. It
seems like quite a problematic situation for you.
> > > What design mechanism would do this? We have a mechanism that we observe
> > > to occur in nature that fits the bill very nicely, but where is your
> > > mechanism and how does it work?
> >
> > But you do not have a mechanism that you can detail as to how such
> > gaps are crossed.
>
> What was the mechanism used for ebg evolution. Random mutation,
> genetic drift and natural selection. If you have some other mechanism
> just lay it out and compare it to the mechanism that we have actual
> evidence is working in nature.
The gap in ebg evolution was extremely small… just one mutation wide.
Genetic drift works very well in such cases. However, genetic drift
is really limited with larger gaps as detailed above. You are left
without a sufficient mechanism to explain such complex functions as
bacterial motility or other multi-protein systems of function, as well
as relatively simple enzymatic functions such as the lactase function
in bacteria that are lacZ and ebg negative.
> > It is back to the "God of the Gaps" argument. If
> > you can explain how to cross the gaps using naturalistic mechanisms,
> > then I will believe you.
>
> I just did, and I used a real verfied example.
Again… your example is extremely weak in explaining much of anything.
Even Hall seems to recognize the problem more than you do. I even
believe in such evolution across small gaps. However, I see that this
gap problem is a lot bigger than you seem to realize.
> > Otherwise, you have nothing but wishful
> > thinking. For example, it is easy to explain how a window could be
> > broken using a naturalistic mechanism, but it is another thing
> > entirely to explain how a broken window can be fixed using a
> > naturalistic mechanism.
>
> Evolution isn't fixing broken windows. The window was never really
> intact it just adds pieces. Halls example is fixing a broken window,
> but real life evolution doesn't have to do that except in dire cases
> that probably usually result in extinction. All evolution has to do
> is make the window more solid than it was. If you have a better
> mechanism state it and the evidence for it.
No, evolution has to explain how the window got there to begin with.
How does a house with no windows get windows? Not via naturalism… but
via intelligent design.
> > > It is good to see you back. It has been pretty boring around here with
> > > just the willfully ignorant moron types posting on the creationist side.
> > > Read the recent posts by Glenn, McCoy, nowhereman, and Zoe but be
> > > prepared to cringe a lot. With guys like those on your side you don't
> > > need me to tell you how bad off your side is. What makes it worse is
> > > that they have been about the only ones supporting the creationist
> > > position.
> >
> > I have been very busy lately, but thanks for the compliment here.
> > Really though, telling me that I only have idiots who support me
> > really doesn't help your position. All it says is that my position is
> > unpopular and that you are strongly supported by the popular vote.
> > This means nothing since it explains nothing in a way that I can
> > understand. It is just an argument of authority, but says nothing of
> > explanatory substance.
>
> It says more than that your position is unpopular. Most or a large
> chunk of the people in the US probably side with you. The problem is
> that they do it because they are ignorant, and certain people play off
> this ignorance to get them to do stupid things.
You are talking about the majority of scientists. So am I. You are
arguing from authority. Lame.
> > > IC the way Behe uses it is bullshit. Demonstrate that it isn't using his
> > > old or new definitions if you can. He admits that IC systems can evolve,
> > > but he defines his IC systems as those IC systems that can't evolve. So
> > > IC by itself is worthless, it has to be coupled with something else. He
> > > hasn't figured out how to determine if they can't evolve, so he is stuck
> > > with a worthless concept that he can't do anything with.
> >
> > I don't agree with everything Behe says. I think that he is somewhat
> > confused in certain areas. I do agree with his basic definition of
> > IC, but I think that he limits himself in what he defines as IC. For
> > me, I consider all functions to be irreducibly complex. I don't limit
> > the definition at all.
>
> How can you say this when you can evolve function using antibodies
> that had no enzymatic function before or evolve function from random
> sequences, or evolve new fuctions for existing proteins like ebg?
> Your definition makes less sense than Behe's. Behe's first definition
> was found to be worthless because his IC defined systems could evolve
> and he acknowledged that. His new definition is just plain worthless
> because he can't demonstrate that it applies to anything.
I see every function as being IC. It is just that some functions are
more complex than other functions, like words or thoughts expressed in
the English language. Some thoughts are very simple to express, while
others are much more complex. The more simple the function or
thought, the fewer symbols or parts it takes to express that function.
With fewer parts, the odds are better that other functions with the
same degree of complexity will be found close by. It is like
three-letter words. It is easy to go from cat to hat to bat to bad to
bid to dig to dog. The gaps are generally short because a large
percentage of the potential sequences do in fact have some sort of
function. However, when the function becomes more complex, a far
lower percentage of sequences of a given length will have a function.
Like six-letter words. It is far harder to evolve six-letter words to
other six-letter words than it is to evolve three-letter words to
other three-letter words. Behe also realizes this. This is really
what his new argument is all about. Simple IC systems of function are
easier to evolve that more complex IC functions. That is the entire
argument. And, it is certainly a tough one for you and other
evolutionists to overcome.
> > This can be easily demonstrated and supported.
> > Any particular function that is dependent upon various "parts" for
> > its operation is IC. Remove certain parts and that function will
> > cease. This means that a function can be destroyed if the parts are
> > changed or "reduced". The lactase function is IC. Remove a certain
> > number of amino acids and that function will end. Obviously then, IC
> > functions can evolve. However, the problem comes with the type of
> > function in question. Some functions are very simple functions.
> > Others functions are much more complex. Simple functions may require
> > fewer parts and there may be many more arrangements of specified parts
> > that could still do a simple function. However, more complex
> > functions might require more parts and there are probably far fewer
> > relative arrangements of such parts that could produce this given
> > function. This means that random/neutral mutations would be far less
> > likely to come across a collection of parts with a more complex
> > function than a more simple function (such as the motility function
> > vs. nylonase function).
>
> This is just the same old bull of the creationist probability argument
> when you can't even begin to calculate the probabilities. Quantify
> the difference between nylonase and motility complexes. Some motility
> complexes are simpler than others. Try and calculate the
> probabilities when you don't even know what the first flagellum looked
> like.
Again, this is a ridiculous comeback. You don't have to think about
the improbabilities of your position because you already know what
happened. Therefore, you don't even try to think in detail about how
things could have evolved, you just trust that they did. What a
crock.
> > Behe makes the mistake of trying to limit the definition of IC systems
> > to those systems of function that he considers to be highly complex.
> > I feel that this is a significant mistake on his part. However, his
> > basic concept is a good one and remains as a roadblock to natural
> > selection as a reasonable mechanism for naturalistic evolution.
>
> The definition that if you take away a part then the system doesn't
> work isn't any good in determining if the system could have evolved or
> not.
Actually it is. It helps you to know or estimate how wide the gap it
is a particular part is taken way. Once the gap distance is known,
the average time required to cross this gap can be calculated quite
accurately.
> You basically admit that these systems have been observed to
> evolve.
Certainly. It is easy to evolve new functions if the gap between what
there is and what is needed is small. However, there is good evidence
that large and even gigantic gaps exist between various functions that
we see in living systems.
> You have to have something more. Just saying it is
> improbable is pretty silly since you can't even begin to calculate the
> probabilities because even if you did have all the information I'd
> like to see you deal with all the non independent variables.
LOL - Ok... there what would it take to convince you? You see various
functions and you do not understand how a functional bridge can be
made between them, yet you believe that such a bridge exists and that
such an explanation must be out there. You think that science will
one day discover these bridges. You will not believe otherwise unless
I prove a negative to you. You ask me to prove all variables and all
potential sequence changes before you will question your current
position. Well, you are asking for a scientific impossibility. No
one can prove a negative. The best that can be done is to show the
probability for a negative… which I think I have done quite well, at
least to my own current satisfaction. It seems to me that your faith
is quite amazing in light of the weakness of the evidence in your
favor. The best experiments that you have in evolving new functions
have crossed neutral gaps of only 2 point mutations. And yet, you
hold up such evidence as being more than it is, as demonstrating
significant evolution in real time. How lame.
> How improbable would it be to co-opt an ATPase for flagellar work if
> you only needed a single aminoacid substitution to do it?
It would be very probable. All you have to do is show that this is
all it takes, and then you would have a start. The problem is that a
single mutation that makes ATPase adaptable for flagellar work is not
enough. What happens if you not only need a mutation for ATPase
adaptation, but another mutation for this part and another mutation
for that part and and and…. ? Until all of these mutations are
realized via random drift, you have no motility function… period.
> What was
> the sequence of that ATPase and how many mutations were needed to get
> it to do its new function?
There is no new function without the other parts. Don't you get it?
Without all the 60+ different proteins all working together, a
"correct" ATPase part isn't going to do the job by itself.
> Maybe no mutations had to happen in the
> ATPase. Some mutation in another protein that made it interact with
> the ATPase and form a structure needed for flagellar development may
> have happened.
Certainly this might have been the case, but what if these two
proteins got together in just the right way… great… but now you have
58 more to go before the motility function is realized.
> Make up your own story, but you have to rule them all
> out before you can claim that they are impossible.
I'm not saying that your "just-so-stories" are impossible… only
extremely unlikely.
> Ron Okimoto
Sean
John Harshman
Sean Pitman wrote:
> John Harshman
>
>
>>Perhaps you shouldn't post things you aren't very interested in, then. I
>>for one would most like to discuss the evidence for and (if any) against
>>common descent. How about you?
>>
>
> I don't post things that I'm not interested in. Why would you get
> that idea?
>
> As far as the evidence for and against common descent, I think that a
> discussion of evolutionary mechanisms (or the lack thereof) is quite
> relevant to this topic.
It's somewhat relevant, but I repeat: do you have any interest in
discussing common descent directly?
>>>It seems quite obvious to me that given a particular
>>>creature, such as a bacterium, that the vast majority of possible
>>>amino acid sequences/proteins of a given length will have no
>>>beneficial function for that creature in its current environment.
>>
>>Agreed. This is obvious.
>>
>>>Only a very tiny
>>>fraction of the potential amino acid sequences will be recognized by
>>>any given bacterium or living cell in any given creature.
>>>
>>Recognized? What meaning are you using for "recognized"?
>
> Take for example the insulin protein. Not every cell in the body
> "recognizes" the insulin amino acid sequence. Other cells, having the
> proper surface receptors, do recognize the insulin protein and perform
> various functions when insulin comes around.
Not every protein (and probably a decided minority for that matter) acts
by binding with a receptor, so I'm confused about why you would bring
this up in a discussion of general protein function.
> So, for some cells the
> insulin protein really has no function or meaning while for other
> cells it does. It is like different words for different languages. A
> given word might have some meaning in Spanish, but none in English.
> The same is true for protein "words" in living cells. A given
> protein/amino acid sequence might have function or "recognition" for
> one cell, but have no function/meaning/recognition for another cell.
> If a given part performs some sort of function in a given system of
> functional parts, then that part is "recognized" by that particular
> system. The system "knows" what to do with that part. It "knows"
> what function that part has. For example, the term "recognition" is
> often used when describing the interactions of antibodies with
> antigens. When the antibody comes in contact with a particular
> antigen that it fits with, the antibody is said to "recognize" the
> antigen. Does this make sense now?
That's what I thought you meant, but it doesn't really make sense. Many
functional proteins don't "recognize" anything even under the most
liberal definition -- i.e. having a specific substrate. Functional
proteins can do all sorts of things, so I'm unsure why you are
attempting to restrict the universe of functions in this way.
>>>Take humans
>>>for example. The vast majority of human DNA does not code for any
>>>functional protein much less a beneficially functional protein. The
>>>proteins that are coded for are somewhat plastic, true, but they are
>>>also very specific. If changed or "denatured" to any significant
>>>degree, they loose all function.
>>>
>>You are confusing two forms of change. We were talking about mutation.
>>Denaturing is a loss of tertiary or quaternary structure, most often as
>>a result of heating. Nothing to do with what we are referring to. (Also,
>>I don't understand your distinction between "functional" and
>>"beneficially functional", or what you mean by "somewhat
>>
> plastic".)
>
> I mention protein "denaturing" to emphasize the idea that changes in
> protein sequence *and* structure affect protein function. We are
> talking about protein function in general here. Whatever changes a
> protein (mutation, heat, chemicals etc) can affect its function in a
> given system of function since protein function is dependent upon its
> 3D shape/structure.
In general, each protein has a unique 3D structure. In general, primary
structure determines secondary structure. So this is irrelevant to any
question you have so far attempted to discuss.
> Also, a protein can be functional without being "beneficially"
> functional. For example, a protein can have a "detrimental" function.
That's arguable. Let it go for now.
>>> This means that the vast majority of
>>>potential protein sequences and three-dimensional shapes are worthless
>>>to a given human cell.
>>>
>>This is not quite clear, at least the "vast majority" part. There are
>>lots of protein sequences that don't do exactly what we would like, but
>>it does appear that we can find function from random sequences. See
>>this: Hayashi, Y., H. Sakata, Y. Makino, I. Urabe, and T. Yomo. 2003.
>>Can an artibrary sequence evolve towards acquiring a biological
>>function? J. Mol. Evol. 56:162-168.
>
> Of course one would expect that various random sequences could be
> found that do actually have some sort of function in a given cellular
> system of function. Some of these might even have a "beneficial"
> function in a given cell and environment. However, the vast majority
> of potential sequences of a given length and 3D structure will not
> have a function at all. You admitted as much above.
Yes, but I've had second thoughts. Had you actually read the paper I
cited, you would see that the function involved is specified beforehand,
and that that function improved over time through mutation and
selection. A surprisingly high percentage of the random sequences were
useful for that specific function. This directly refutes your claim, as
far as I can see. But you will have to read the paper and address it.
> When I said, "It
> seems quite obvious to me that given a particular creature, such as a
> bacterium, that the vast majority of possible amino acid
> sequences/proteins of a given length will have no beneficial function
> for that creature in its current environment", you said, "Agreed. This
> is obvious." Well then, what are you trying to do here? You seem to
> be contradicting yourself in the same breath.
I changed my mind after reflection and a search of the literature.
Something that you would be advised to try some time.
So far all this is touchy-feely. What's the real difference, in a
protein system, between 3- and 6-letter words? What functions require
each? I have found an example of random sequences produces a previously
specified function, which seems to argue that many functions can be
performed by random sequences. After all, the function wasn't chosen
with prior intent that it be easy for random sequences to do it. And
this was a specific, chosen function. How much more likely that a random
sequence will do *something* useful to the organism?
> The average time involved becomes the problem because, with increasing
> complexity, the total number of sequences with potential function
> decreases dramatically leaving larger and still larger gaps in
> function between those sequences that would actually have function for
> a given cell in a given environment. The random drift or "selection"
> involved in getting from one sequence with function to any other
> sequence with a different function of comparable complexity requires
> greater and still greater amounts of time.
You really have to watch your use of language. Equating selection with
drift is not a good idea. You have yet to demonstrate, by the way, that
large, neutral gaps need to be crossed in evolutionary transformations.
>>And the introduction of 3-D shapes only confuses the question.
>
> Actually, the 2-D sequence of proteins really is not what does the
> job. The 3D structure is what really matters when it comes to protein
> function. The same sequence can be folded in different ways.
But almost always there is a unique folding assumed upon translation.
This is irrelevant and I don't know why you think it matters to your point.
> And,
> depending upon which way the protein is folded; function may be gained
> or lost. Proteins do not always spontaneously fold in the proper way
> to realize their function. There are other proteins that fold new
> proteins as they are made. If the 3D structure of a particular
> protein is "unfolded" and then allowed to "refold" by itself, it most
> likely will not fold properly and its function will be lost.
True for some proteins, not for many others. Some proteins need
chaperonins to fold properly, some fold properly but spontaneously only
during translation, and others fold properly and spontaneously under a
wide variety of conditions. I don't know of a case in which some major
evolutionary transformation of function is alleged to have resulted from
a change in chaperonins without any change in the primary structure of
the protein being folded. Do you?
> So,
> really, we talk about the 2D sequence because it is easier to talk
> about, but in reality, the 3D structure is very important to function
> and only compounds the problem of complexity since even more
> differences can be realized for a given amino acid sequence than a
> simple 2D sequence analysis would suggest. For a 2D sequence of 10
> amino acids, the total number of potential proteins is:
> 10,240,000,000,000 (~10 trillion). However, the total number of
> different proteins would actually be much higher than this because of
> all the added differences in 3D structures that are not being included
> in the total number. This makes for even less of a chance of picking
> those sequences/3D structures of amino acids that actually have some
> sort of function, much less beneficial function, for a given cell in a
> given environment.
All this is doubtful. Without help from chaperonins, any given protein
does have a preferred, spontaneous folding as it is translated. There is
no serious random component.
>>>As far as demonstrating a negative (ie: A lack of a functional path
>>>between two different proteins), it is impossible this side of
>>>eternity. A negative finding never means that a positive finding is
>>>impossible. However, the likelihood that a negative finding will
>>>occur can be calculated.
>>>
>>If it can, then you haven't done it yet. This remains to be seen.
>>
>
> Well, of course I disagree. Can you prove that these gaps do not
> exist or explain how they might not exist?
No. There probably are such gaps. The question is whether they are
sufficiently dense that most transitions among forms require crossing
one, and thus evolution is unlikely. I have two arguments: 1)
experimental results (cited above) show that random sequences produce
specified functions capable of being improved by selection on random
mutations, arguing against such gaps. 2) We have excellent evidence from
many sources that evolution does indeed happen, and new functions do
evolve; you cannot therefore argue that new functions don't evolve, and
are left to argue that the mechanism by which they evolve is not natural
selection. In that case, however, it would be important for you to
suggest what that mechanism might be, and present some evidence for its
existence at least.
> For example, can you show
> how a relatively complex function, such a bacterial motility (Any
> type, not necessarily flagellar motility), could evolve where no
> genetic gaps in function would need to be crossed? There are those
> who suggest that there is no goal in evolution. Therefore, the
> testing of a specific "goal" such as the evolution of a specific
> function, such as motility, is not a valid challenge of evolution
> since a given type of bacteria may evolve other equally complex
> functions before motility is ever evolved.
>
> This is a great argument. For one thing, without a goal to defend,
> there is no need to move goal posts as YECs are so often accused of
> doing. Just because a particular function does not evolve, such as
> the lactase function in certain of Hall's bacteria, does not mean that
> evolution is having problems. It only means that evolution does not
> need to travel down any particular path, regardless of the benefits
> that would be realized if that path was traversed. Well, Ok... lets
> go there. Naturalistic evolution obviously does not "know" which path
> to choose. It can go down any path in any direction and eventually
> get somewhere with some beneficial function. Sure it can. However,
> what if each starting point is completely surrounded by a huge ocean
> of neutral function or nonfunction?
In that case, evolution by natural selection wouldn't get very far,
assuming that the gaps between functional sequences were large. But I
don't think they are, and there's evidence to support that belief.
> Consider that if there were 1
> million defined 6-letter words that each word would, on average, be
> surrounded by 300 non-defined words. No matter which way evolution
> went, odds are that it would quickly run into a gap of nonfunction
> that separates current function from new function. Try it. Starting
> with a 6-letter word, how far can you go before you are blocked by a
> gap of nonfunction? Now, if that seems hard, try to evolve a larger
> sequence of letters, such as a sentence of words, one letter at a time
> and see how far you can go before you are blocked by sequences of
> nonfunction.
I will agree that one can invent systems of this sort.
>>How do you
>>know there are such gaps? For eyesight, it has certainly been shown that
>>there is a continuous series of slight morphological variants, each
>>advantageous, from a patch of light-sensitive cells to a camera eye.
>
> A series of morphologic variants that appear to follow a smooth
> evolution of very small steps is deceptive in that is covers up the
> complexity of the genetics involved. If in fact every "slight"
> morphologic variant was the result of an equivalently "slight" change
> in the genetic code then you would be correct in your statement that
> such a series of morphologic variants give convincing evidence of
> common descent. However, there are several problems with such an
> automatic assumption. One problem is that apparently small
> morphologic changes often require relatively large changes in the
> underlying genetic code.
Personal pet peeve: you are using "genetic code" as a synonym for
"sequence". But it has quite another meaning and your idiosyncratic
usage merely causes confusion. The genetic code is the mapping of 3-base
codons to amino acids, no more and no less.
But to your main point: it may indeed be that the mapping between size
of molecular and morphological changes is loose. But do you have any
examples of this? There are certainly known cases in which small genetic
changes can produce large morphological changes, and large molecular
changes producing zero morphological changes. But do you have a case in
which a small morphological change *requires* a large genetic change?
> The same is true for computer functions.
> Apparently "simple" or "small" changes in a program's function often
> require comparably large changes in the underlying code. For example,
> going from a "simple" eye spot or collection of light sensitive cells
> to a slightly concave eye cavity spot, seems morphologically simple,
> but the genetics involved are quite complex. All the cells involved in
> the formation of this cavity must be programmed to relate with the
> other cells in this area in a very specific way to form this
> concavity. This orchestration requires many very specific genetic
> changes. Gaps in beneficial function are certainly involved.
That's just a series of unsupported assertions. Do you have anything to
back it up?
> Another
> problem is that function is arbitrarily attached to code. Very
> different codes can and do code for the same or similar functions and
> very similar codes can and do code for very different functions.
> Because of this arbitrary nature of code, a change in the code will
> probably not result in an equivalent change in code function or
> "morphology". Very small changes in code can result in huge changes
> in morphology. Also, very large changes in code might not change
> morphology/function very much at all.
Are you talking about computer programs or genetics here? Your point is
exceeding muddy.
> An argument based on morphology alone might seem compelling if that is
> all that one had, but we know more now than Darwin knew. We know that
> there is an underlying code or genotype that gives rise to morphology
> or phenotype. If you can explain, genetically, how the gaps between
> these various "small" differences in morphology can be explained, then
> you would certainly win the Nobel Prize.
Actually, there is no Nobel Prize in evolutionary biology, or even in
biology. Just "medicine". And the gaps, so far, exist only by virture of
your assertion.
> As of yet, I have found no
> detailed genetic explanation or real-time experiment that explains or
> demonstrates how the evolution of morphologic variants, such as the
> morphologic eye variants or various bacterial motility systems,
> evolved or even could have evolved.
Yes, we don't know enough yet about the regulation of development to
attempt such a detailed scenario for most features. It's a complex
question. We are just beginning to understand the basics.
>>I'm
>>sure you are familiar with How would one go about demonstrating that
>>there are or are not such gaps with respect to feathers?
> Yes, try to evolve a feather or a feather-like structure or to
> estimate how long it would take based on genetic sequence analysis,
> mutations rates, functional genetic intermediates, and the length of
> the average genetic pathway to such a function in a given creature.
> Detail the genetic codes involved in coding for feathers and then
> compare these codes to the codes that are available in other
> non-feathered creatures and see if a genetic path could be detailed
> and how long it would take to cross this path.
Eventually, this should be possible. We need a lot of research before
any of this is known in sufficient detail to do such tests.
>>We do know that
>>feathers arose in a bipedal, non-flying dinosaur. That seems clear
>>enough.
>
> Oh really? How so? Is there a gradual step-by-step demonstration of
> this evolution in the fossil record?
Not gradual enough for you, perhaps, but then again every new
intermediate fossil automatically increases the number of gaps by one. I
would say that Sinosauropteryx has very nice intermediates between
feathers and non-feathers.
> Not any more than could be
> detailed various creatures all living at the same time today.
Well, no. All organisms alive today either have feathers or not, and are
either quite derived birds or not. Feathers are rarely preserved, so we
have much less an idea of feather evolution from fossils than we have of
bird evolution in general. But there are certainly a great many
feathered theropods these days. How do you explain them?
> It is
> the same argument as the evolution of simple to complex eyes. Get a
> bunch of different kinds of eyes and line them up in a morphologic
> sequence from more "simple" to more "complex". Obviously, once this
> lineup is complete, the conclusion must follow that the simple eyes
> gave rise to the more complex eyes. This might seem reasonable at
> first glance, but this is not necessarily a correct conclusion.
> Practically any collection of objects can be categorized in such a
> manner, but this does not mean that these various object arose via
> common descent... especially if the mechanism to adequately explain
> such variations is weak. For example, the various books on my
> bookshelf can be categorized in this manner, and just as convincingly,
> from more "simple" to more "complex." But, this does not mean that
> the more complex books arose via common descent from the less complex
> books even if the changes between them seem to be relatively small.
> You see, without an ability to detail a mechanism of change, the
> differences and similarities, by themselves, do not necessarily
> support the position of common descent.
You mistake the point of the exercise. It's not to prove common descent
(that's done by other means) but to refute the claim that intermediate
conditions are impossible. (e.g. "What good is half an eye?") If
intermediate conditions exist, no matter what the relationships among
the organisms, the argument of impossibility is refuted.
>>Whether they arose by natural selection, or by any naturalistic
>>pathway, is difficult to determine. I suppose you could, if you liked,
>>support some kind of theistic evolution in which God gives the
>>occasional nudge to get a genome across some functional gap. I'm not
>>sure where you would find evidence for it, as there is for selection,
>>and I'm pretty sure you would reject such a theory anyway. Right?
>
> The evidence that you have is one of morphology alone, not of
> genetics. The morphologic evidence is not compelling enough to
> adequately support the theory of common descent. You need genetic
> evidence or some way to explain how the genetic gaps can be crossed.
No you don't. You can reliably infer many phenomena without knowing the
mechanisms that produced them. There is much genetic evidence for common
descent. Your demand that the detailed mechanism be known before we can
agee on the phenomenon itself is unreasonable.
> Also, I find the standard interpretation of fossils and the geologic
> column unconvincing and quite biased or colored by the a priori
> assumptions of evolution and naturalism. I see no clear evidence that
> feathers must have evolved from featherless creatures. The fossil
> record is a static record and is thus quite limited in what it can
> tell us about the lives and changes of creatures over time. You need
> real-time examples detailing the actual genetic changes in life forms.
This is unreasonable. You are saying that in order to show common
descent, one must duplicate it in every particular. You would never
require such an unreasonable standard for any inference that doesn't
contradict your literal view of the bible.
> Relying on morphology is easy to do, but it is rather weak when it
> comes to explaining how the genetic codes themselves evolved via some
> naturalistic process.
Once again you conflate our ability to infer common descent with our
ability to infer that the mechanism of change is natural selection (or
some other naturalistic process). These ideas are independent.
>>> If you think that a neutral gap in function
>>>that requires just one protein sequence is hard to cross, try
>>>
> crossing
>
>>>a gap that requires the evolution of multiple proteins to cross where
>>>hundreds or even many thousands of neutral mutations are needed.
>>
>>I agree that this scenario sounds unlikely. I just don't agree that it
>>is necessary.
>
> Why not? What *genetic* explanation do you have to account for the
> differences then?
Natural selection?
>>>If there were such a path from scales to feathers, then we should be
>>>able to quickly demonstrate such evolution in real time.
>>>
>>I deny that there is any such expectation. Why should there be? Are you
>>saying that we should be able to demonstrate every possible occurrence
>>in the lab? Why? If we are talking about something that took millions of
>>years, why should we be able to do it in one or two? And this assumes
>>that we know what steps are necessary, which we don't, at least not yet.
>
> If it took millions of years... why did it take so long if there was a
> beneficially functional path each step (mutation) of the way?
I advance a number of possibilities below.
>>You have the kernel of an interesting point there, and it's been a
>>conundrum of evolution for some time. Why is evolution so slow over the
>>long term, when natural selection is so fast? I think there are several
>>reasons: waiting for mutations, waiting for the environment (internal
>>and external) to change so that new selective pressures are seen, and
>>following a twisty path around constraints rather than the straight path
>>you seem to think is the only possible one. It's an interesting problem,
>>but not as you seem to think a disproof of the efficacy of selection.
>
> Mutations occur quite rapidly. For humans, the average mutation rate
> is around 250 mutations per individual per generation. In a large
> population, such mutations, if a fair proportion were directed in some
> way, would result in rapid evolution along a great variety of
> evolutionary paths. Feathers, wings, eyes, legs, arms, and a host of
> potentially beneficial functions would evolve in short order.
This is your assertion only, with nothing to back it up.
> The
> problem is that the path is quite "twisty" indeed. The path is not
> straight. That is the problem. The path is very curvy because of the
> random drift problem. If each and every step is not selectively
> advantageous, then evolution starts to wander around a neutral sea of
> function. The wandering is very curvy or nonlinear. In fact, it is
> such a curvy path that millions, billions, and trillions upon
> trillions of years are simply not enough to traverse this path. The
> "efficacy of selection" is dependent upon nature's ability to select
> between different genetic changes. If the changes are "neutral" in
> function then natural cannot select between different genetic
> sequences that have the same function (or nonfunction). At this point
> the "efficacy" of natural selection is severely limited.
You merely assume what you want to prove. There are many possible
constraints on the speed of selection. One, and one that's well
supported by the fossil record, is that different intermediates fill
different functions. The gill supports of a primitive vertebrate didn't
become mammalian middle ear bones in one go. They first spent some time
as jaw supports. The path to the middle ear (quite well documented by
fossils) was quite windy, but the morphology was functional at all points.
>>>There are gaps between various functions that
>>>require a lot of time to cross. In fact, many of these gaps seem so
>>>wide that billions or even many trillions upon trillions of years are
>>>simply not enough.
>>>
>>If there are, name one and show the evidence that it is such a gap.
>
> I already have. Depending on the complexity of the function in
> question, the evidence for non-evolution can be found in comparing
> what is available with what is needed. The lactase function in E.
> coli is a good example of this non-evolution. When lacZ and ebg genes
> are deleted from E. coli, they simply do not use any other genetic
> sequence to evolve the lactase function despite being observed for
> many thousands of generations while growing on selective media that
> would benefit them if they were ever to evolve the lactase function
> again. B. G. Hall himself described such E. coli colonies as having,
> "limited evolutionary potential." Obviously these limits are there
> and they are found in the form of neutral/nonfunctional genetic gaps
> in function. All codes/language systems have these gaps. Human
> languages, computer languages, and even genetic languages/codes have
> these gaps. Natural selection cannot cross gaps in function in any
> directed way. Without direction, mutations are purely random and
> random changes wander around a very curvy path that simply takes to
> long to come across new beneficial functions.
Other people who know the subject better than I do have addressed this one.
>>>You know that naturalism is
>>>the answer... without knowing how it works?
>>>
>>Did I mention naturalism? No. In fact I mentioned divine intervention as
>>one potential mechanism. So your comments are irrelevant. I'm talking
>>about common descent. Would you care to argue about the evidence for
>>common descent?
>
> The theory of common descent is a naturalistic theory. It is an
> argument from the position that nature and naturalistic processes can
> explain the variety in living forms.
No it isn't. What is theistic evolution (a quite popular theory among
Christians) but an acceptance of common descent but a rejection of
naturalism? These two aspects of evolution are entirely separable.
> You are therefore "mentioning
> naturalism." You mentioned "divine intervention as one potential
> mechanism" but you do not believe that this is the mechanism over the
> idea that a naturalistic process is a more likely or reasonable
> explanation.
Yes, but that's just me. It serves to show that pattern and mechanism
are separate theories.
> For myself, I'm not so much arguing for the identity of
> the designer as I am for the fact that there is evidence of design,
> from some intelligent source somewhere, in living things. Humans are
> also capable of such designs in code and systems of function. Are we
> therefore "divine"? No, but we certainly are capable of
> "supernatural" activities in the sense that non-intelligent natural
> processes, such as random mutation and natural selection, are
> incapable of performing. A tree limb, as it is blown by the wind, may
> break a window without relying on deliberate design or creative
> intelligence. However, there is no naturalistic process for fixing
> the window and putting it back in its place outside of deliberate
> design/creative intelligence... regardless of where this intelligence
> came from... be it divine or human or an intelligent alien from the
> planet Zorg. Whatever the source of intelligence, the fact that
> "supernatural" intelligence (ie: above the naturalistic
> non-intelligent processes of a mindless nature) was required can be
> detected.
Unsupported assertion, but certainly a possible position. The question
I'm most interested in, however, is whether you would accept the
possibility that the designer intervened in a process involving common
descent rather than using fiat creation of unrelated kinds.
>>I didn't mention anything about random mutations. I'm talking about
>>common descent. Common descent is separable from the mechanism that
>>causes adaptation. You, as a creationist, deny common descent. I'm
>>saying that if, somehow, you were to show that natural selection is
>>insufficient as a driving mechanism, then the evidence for common
>>descent would remain untouched and conclusive.
>
> Not so. Without a knowledge of the mechanism of common descent, the
> evidence for common descent is far from "conclusive." Common descent
> is not a forgone conclusion, especially if the mechanistic explanation
> fails.
We appear to have a basic disagreement here. Would you agree that we
know things fall down, even though we don't have a clear understanding
of what gravity is? Would you agree that the existence of atoms was
established by Dalton, Lavoisier, and others long before we had any idea
of atomic structure or quantum mechanics?
>>>You obviously have a very great faith in the power of naturalism to
>>>answer all questions pertaining to the physical universe. For you,
>>>the very notion that there just might be evidence of design in the
>>>natural world/universe is simply out of the question.
>>>
>>I said nothing whatsoever either for or against design. I'm not talking
>>about design. I'm talking about common descent. Is that clear?
>
> When you are arguing in favor of common descent, you are arguing
> against design. The theory of common descent is a theory that tries
> to propose a naturalistic cause, outside of design, to the existence
> of various life forms. So, really, you are talking about design.
> Whether or not you admit it or realize it is another issue.
No it isn't. The theory of common descent proposes that all life forms
are descended from a common ancestral population through descent with
modification. How that modification was accomplished, whether through
natural or supernatural means, is another question entirely.
>>I happen to believe, based on the evidence,
>>that natural selection is a pretty good mechanism and that evolution has
>>indeed proceeded "naturally" (and there is considerable evidence
>>that evolution has no particular goal), but that's not at all what I'm
>>talking about here. Your inability to separate "darwinism" into
>>independent components is causing a communication failure.
>
> You would like to think that one component has no bearing on the other
> components of the theory, but the fact of the matter is that all the
> components of Darwinism are intimately intertwined. If one basic
> component fails, the whole thing fails. I suppose you could say that
> the theory of evolution is... "irreducibly complex." ; )
What is your logical basis for making this claim?
>>Actually, under normal conditions most mutations occur during DNA
>>replication, which I believe does occur simultaneously with cell
>>division in most prokaryotes.
>
> Yes, this is true. However, these mutations, once they occur, are
> passed on from one generation to the next.
That point was not in contention, so I have no idea why you brought it up.
>>>However, once the mutations occur, these mutations
>>>are passed on to the bacterium's clonal offspring via the
>>>division/replication/mitotic process.
>>>
>>Mitosis is something that happens in eukaryotes, not prokaryotes.
>
> True again, but prokaryotic replication/division is similar to
> eukaryotic mitosis. The offspring are "clonal" in both cases.
Right. I just want you to be careful about your terminology.
>>Once again: hypermutations are observed to occur in bacteria that are
>>not actively dividing. Generally they happen under starvation conditions
>>in which the bacteria cannot reproduce. If one bacterium experiences a
>>mutation that lets it reproduce, then the subsequent colony descends
>>from that one. Actively dividing bacteria do not experience these
>>hypermutational rates.
>
> True again. However, in my calculations I wanted to raise the
> mutation rate as much as possible in favor of the evolution of new
> traits in a reasonable amount of time. Hall also used other mutagens
> to increase the mutation rate in his colonies. In any case, the point
> of the high mutation rate is to show the difficulty in crossing
> apparently small gaps in function.
>
>>> In fact, Hall
>>>does so in his own paper. He makes his own estimations of the
>>>mutation rates for his bacterial colonies, "per generation."
>
>>Are these hypermutational rates, i.e. a response to stress? I'm afraid I
>>don't have the paper available in front of me.
>
> The mutation rates that I used in my calculations are higher than
> those used by Hall in his calculations. The mutation rates that he
> uses are increased over normal because he used various mutagens to
> increase the mutational diversity in his experiments.
So the answer would be "no", then.
I'm afraid that without empirical data, one guess is as good as another.
You pick guesses that make the numbers work for you. However the
empirical data (Hayashi et al. 2003) suggest that the proportion of
functional sequences is much higher than you claim.
[snip more repetition of large, made-up numbers]
>>>In the replacement of a particular base in a sequence of DNA, the
>>>replacement could replace the base at the position in question with
>>>the same base 1/4th of the time. Therefore, the odds that a given
>>>"change" will result in a specific base are 1 in 4.
>>>
>>If a base is replaced with the same base we don't call it a mutation. We
>>don't call it anything, except maybe "replication". A mutation rate that
>>includes "no change" would be a rate of 1 per site per generation, since
>>every site will either change or not change. You really need to fix this.
>
> Ok... I've thought about this point further and you've got me here. I
> will fix this. Thanks for pointing out this error, but it really has
> no significant bearing on the point at hand. Be the odds 1 in 4 or 1
> in 3 makes no real difference as far as the problem is concerned.
Agreed. But the difficulty I had in convincing you of one simple
mathematical error should give you pause, at least.
>>Well, it [neutral evolution] does say how neutral gaps can be crossed. With low probability,
>>getting lower as the size of the gap increases. If there is a large
>>neutral gap between two functional proteins it is unlikely to be
>>crossed. But who says that such gaps are prevalent?
>
> You are one of the more reasonable evolutionists that I have come
> across. At least you recognize the problem and seek a reasonable
> solution, such as the idea that such gaps do not exist. If such gaps
> really did not exist, then yes, evolution would not present a problem
> at all. However, it seems like you understand that if such gaps do
> exist that they would actually present a significant problem for your
> theory.
Not quite. Such gaps must not only exist, they must be overwhelmingly
prevalent, such that few separate functions are connected without such gaps.
[snip repetition of matters discussed at length above]
Ron Okimoto
> roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.0304...@posting.google.com>...
>
> > > For example, the odds of getting one, two, or even three necessary
> > > mutations "right" in a reasonable amount of time, even in a gene some
> > > 3,500 base pairs in length, is not unimaginable . . . since this gene
> > > is starting very close to the "goal" to begin with.
> >
> > Why is it starting very close to the goal? You acknowledge that it is
> > a very different protein. Why should this matter? Was it present by
> > design or just chance?
>
> Even though the ebg gene produces a very different protein from the
> one produced by the lacZ gene, this protein was only one point
> mutation away from the lactase function. A single point mutation was
> all that was required to realize a beneficial lactase function. At
> this point, purely random chance is all that is needed to gain the
> beneficial function in short order.
So what? It was one of around 2000 proteins in the cell. A couple of
mutations in antibody genes can produce a wide range of enzymatic
functions that the original protein did not have, so it doesn't look
like such a big deal.
>
>
> > I don't know if I agree with your numbers, but all they indicate is
> > that we are more on the right track than you are. You have to keep
> > these mutations from happening. We observe them to happen. What is
> > your problem?
>
> You just don't seem to get it do you? I'm not trying to "keep these
> mutations from happening." I am well aware that they do happen. The
> problem is that as the neutral gaps in function get wider, the time
> required to cross these gaps gets exponentially longer and longer
> until zillions of years are needed.
No, by your own calculations you can span up to 20 mutations in just 2
years with a population of only a trillion bacteria. Beats me if this
calculation is correct. This would seem to be an over estimate
because Hall spanned 3 and probably did it in a couple of weeks. You
have around 10^12 E. coli in your guts on any given day. There are
around 6 or 7 billion people, so an event like this must be occuring a
lot more than once a day. Just think the population would be at
equilibrium and that last mutation must be plunking down somewhere
quite often.
>
> > > But, what if the starting sequence was two mutations away from the
> > > desired lactase function? Would that make any difference? The odds of
> > > getting either one of the two needed mutations with the first mutation
> > > are 1 in 8.2 million mutations. The odds of getting the second
> > > mutation right are 1 in 16.4 million mutations. So, the odds of
> > > getting both mutations right are 1 in 134,480,000,000,000 (~1.34
> > > trillion) mutations. With these odds, the correct mutation will occur
> > > in about 315 bacteria in the first generation.
> >
> > How does this help you out? These calculations just make our model
> > look better.
>
> Not really? Although I have since revised the numbers significantly in
> keeping with my new understanding of the probabilities involved (with
> the help of the binomial equation), the statistics certainly don't
> help you out of the gap-crossing problem.
You must be joking. You have switched your criteria from 3 to 30 and
I bet that you can't come up with a single example of where it takes 5
or even 4 neutral mutations to cross a barrier to function.
If you have such an example present it.
>
> > > If the starting sequence was three mutations away from the desired
> > > function, the odds of getting all three mutations right shoots up to 1
> > > in 735,157,333,333,333,333,333 (~735 million trillion) mutations. With
> > > these odds, the correct mutation will occur in one bacterium in
> > > 1,792,682 generations. With a generation time of 20 minutes, that's a
> > > bit over 68 years.
> >
> > You can't calculate the probabilities like that because they aren't
> > independent. You have to calculate the probabilities based on the
> > actual situation. Once you have one mutation, you don't have to get
> > it again. You can as often as you like, but the second mutation would
> > occur in a bacterium that already had the mutation. Like you
> > indicated by your own calculations 315 bacteria would have any one of
> > the three. Close to 1000 in just the first generation would have one
> > of the three. How many in the second generation? The 100th? The
> > chance of two is the mutation rate in those bacteria that already have
> > one. Your numbers collapse dramatically, and even more dramatically
> > if the mutations were not neutral, but had some selective advantage
> > that allowed them to increase in frequency in the population.
>
> First off, by definition a "neutral" mutation has no selective
> advantage. This is the point. Because of this, nature does not
> preferentially select to increase their frequency in a population.
> This is the basis of my whole point? you understand.
>
>
Snip explanation of calculations:
>
> So, what does this mean? As it turns out, a population of a trillion
> bacteria can cross a neutral gap of 3 or 4 point mutations in a few
> weeks, not hundreds or thousands of years as I had previously
> calculated. In fact, a population of a trillion E. coli bacteria
> could cross a neutral gap of 20 mutations in around 2 years.
Does this give you some clue that you might be wrong?
Snip some strange calculations:
>
> So you see, the problem continues to stand. A gap of 30 or 40 is
> nothing compared to the complexity of the functions that exist in
> living things. A sequence of 30 base pairs would only code for an
> amino acid sequence of 10. Consider that the lacZ and ebg genes are
> over 1,500 base pairs in length? and this is what is needed to code
> for the relatively simple enzymatic lactase function of a single
> protein. It turns out that populations of bacteria forming a ball the
> size of the galaxy or even the known universe would not be enough to
> keep up with the time required to cross neutral gaps of even 100 or
> 200 base pairs.
Since you have yet to shown that more than 3 are needed this seems to
be pretty pathetic to invoke 30 or 40. How are you going to make sure
that all 30 or 40 are really neutral? How do you know that groups of
4 or 5 won't be selected for for some other reason? Until you can
demonstrate that gaps like this really exist you don't have an
argument. You have effectively killed your own argument. You
acknowledge this by pushing the goal posts back from 3 to 30 when you
don't have an example of even 4 or 5 being necessary.
>
> http://faculty.vassar.edu/lowry/binom_stats.html
>
> Interestingly enough, Hall himself discusses this problem:
>
> "Given a gene of 1000 base pairs there are over 10e34 sequences that
> differ from the wild-type sequences by 10 or fewer mutations. Not
> only can we not explore all of those possible variants, life itself
> has barely had sufficient time to explore all of those possibilities.
> The mass of the earth's oceans is about 1.4 x 10e24g. Even if living
> cells constituted a 10e-4 of the mass of the oceans, given about 10e12
> bacterial cells per gram, a reproduction rate of about 1 cell
> generation per day and a mutation rate of about 10e-9 per cell
> generation and 4 billion years of life there has been sufficient time
> to explore only 1.6 x 10e34 variants of a single 1000-bp sequence.
> However, evolution does not proceed by exploring all possible variants
> but by incorporating single mutations, selecting the fittest of those
> variants, expanding the population of the fittest variants, and
> incorporating additional single changes."
The point that you continually miss is that the entire sequence space
does not have to be sampled to create these functions. They happen so
often that only a small fraction of the sequence space has to be
sampled before function is identified. In the antibody example you
can evolve new enzyme functions in less than 10^12 molecular events.
This is such an absurdly small sampling of the possible antibody
sequences that why are you still complaining about this? Isn't it
obvious that you can get specific enzyme functions so easily that you
don't have to sample the entire sequence space to get what you want?
Do you understand what you argue? By your own calculations the
mutations do not have to be fixed, but can just be at equilibrium
drifting neutrally in the population, to get the desired results.
Your arugment is bogus. The mutations do not have to be fixed to have
the final one be selected for. Fixation rate would be mutation rate
which would be around 10^7 or 10^8. If Hall had had to wait for
fixation of the first two mutations before he was able to select for
the third one it would have taken him longer than a couple of weeks to
do it.
>
> http://www.eeb.uconn.edu/Courses/EEB449/Hall%20FEMS.pdf
>
> So you see, even Hall admits that even relatively small neutral gaps
> of three mutations might be enough to "limit" further evolution.
> Thus, such functions that are isolated from other functions by neutral
> gaps might be quite difficult for a theory of purely naturalistic
> evolution to explain.
You still have to demonstrate that these difficult gaps exist.
This is a plate assay and you would miss all the mutations that
occured after the bacteria was plated. This is even worse for you
than the previous single step selection because this is a single step
selection. If 2 or more mutations are needed to get lactase function
you will always see red colonies unless you got extremely lucky and
got the one in a what? 10^24 bacterium that had 3 mutations before it
was plated. You are talking about plating on the order of 1000
bacteria per plate so that you can score them for white or red. Is it
any wonder that Hall didn't find a protein that took 3 mutations to
get lactase function? You can plate until dooms day and never see it.
You can plate a much higher density of bacteria in a Cairns type
experiment because all you are screening for is the bacteria that can
grow.
>
> > The way
> > that these selection experiments work (by researchers like Cairns and
> > Campbell) is to plate the bacterium out on a plate where they have
> > minimal metabolic capability. They have to work their DNA repair
> > mechanism and be able to transcribe the new mutations in the DNA to
> > mRNA or they will not express the new mutations, but they do not grow
> > well or divide very well. After a period of time in this semi stasis
> > most of them die on the plate. You can't revive them even if you add
> > medium that they can grow on. I don't know when you call a bacteria
> > dead, but if it never divides again that gets my vote.
> >
> > What did Hall do and would it be considered to be the way things
> > usually work in nature?
>
> Other researchers may have done things differently, but Hall used a
> non-lethal selective media in his experiments, closely simulating real
> life non-lethal situations where the gain of a particular function
> would enhance survival and reproduction.
Do you see what is wrong with Hall's experiment from the point of view
of your argument? It obviously did not reproduce natural conditions.
> Exactly? but the environments in both cases were non-lethal. In other
> words, they allowed for the build up of additional mutations.
Even though the medium was non lethal the detection scheme makes the
point moot. The bacteria were not allowed to build up additional
mutations because the colony would have bacteria making red pigment
unless all or most of the bacteria produced lactase activity.
>
> > > > It looks like Hall has met your
> > > > challenge with the system you are trying to say supports your contention
> > > > that it is impossible.
> > >
> > > I never said that a neutral gap of 3 mutations was "impossible." I
> > > said that depending on function complexity that certain gaps of such
> > > lengths or larger would be impossible for neutral evolution to cross
> > > in a reasonable amount of time. Where has Hall demonstrated this to
> > > be incorrect?
> >
> > Yes, by any standard. How many man hours do you think the experiment
> > took. Probably less than 6 months worth of experiments, and more
> > likely just a couple of weeks. He may have been working on this
> > problem since the 1970s but his bacteria were probably in the freezer
> > most of that time.
>
> Still, 10s or even hundreds of thousands of generations were in fact
> observed? still with no evolution of certain specific functions.
> Also, there are many other types of bacteria out there that have not
> been in any freezers since the 1970s (ie: Salmonella, Proteus, etc)
> that still do not have lactase ability, despite its relative
> simplicity of function, and despite having experience over a million
> generations with huge populations sizes under selection pressures that
> would benefit such bacteria if they ever did evolve the lactase
> function.
Hall observed the span of 3 mutations to get better function in the
span of those few weeks. Do you think that the reason that other
bacteria haven't evolved rudimentary lactase activity is because E.
coli and some other bugs beat them to it and do it much more
effectively. Have you heard of natural selection?
>
> > > He still hasn't demonstrated the evolution of the
> > > lactase function in E. coli lacking both the lacZ as well as the ebg
> > > genes. Why is this?
> >
> > He doesn't do the experiments like they would happen in nature? He
> > never lets the bacterium have a chance to evolve the number of
> > mutations that are needed to get activity using some other protein?
>
> Yes, Hall does in fact do the experiments as they would be expected to
> happen in nature. This is a non-argument. The reason why the
> bacteria aren't given a chance to evolve the number of mutations that
> are needed is because the time required to evolve such specified
> mutations is more time that Hall has left in his life? even if he were
> to live thousands or millions of years.
No he didn't do the experiments like you would do them in nature. You
wouldn't detect neutral mutations needed for function using Hall's
method unless you got very lucky and plated the bacteria with all or
most of the mutations you needed. Just think of if you needed three
mutations to get lactase function and you happened to plate the a
bacteria that already by chance had two of the needed mutations
(pretty improbable on its own), with a mutation rate of 10^7 what is
the probability that you would detect the third mutation as being a
white colony or even a pink colony?
>
> > > The only logical reason for such a limitation to
> > > the evolution of the lactase function in such bacterial colonies
> > > (despite the potential benefits if they were able to evolve this
> > > function) is that there is a gap in function between the lactase
> > > function and the collective genomic real estate potential of Hall's E.
> > > coli colonies... even given hundreds of thousands of generations.
> >
> > This is pretty bogus because you have to admit that it happened once
> > in only 2000 proteins found in E. coli. From the couple of other
> > bacteria that he has been able to do this with it has happened in them
> > too, and different proteins were involved in those activities. So
> > what is your problem. It seems like it isn't so special. Demonstrate
> > that it is. If it is so hard, why was he able to do it again in other
> > species?
>
> The reason why it is a problem is that when you remove the egb gene,
> it never happens again? nor does it happen in many other bacterial
> species despite 50+ years of observation and selective pressures.
> Granted, the lactase function does appear to be a rather simple
> enzymatic function that can be performed by a single protein sequence
> working alone. The fact that such a relatively simple function is
> difficult to evolve in various types of bacteria is quite interesting.
> If a simple enzymatic function is so difficult to evolve, what about
> more complex functions that require multiple proteins all working
> together simultaneously? The gaps rapidly get quite enormous as the
> complexity of function increases. If you think it is fortunate for 1
> out of 2000 proteins to be able to evolve a relatively simple function
> like the lactase function, try figuring out the odds of getting a more
> complex multi-protein function to evolve? such as bacterial motility.
You have to demonstrate that the changes have to be neutral, and Hall
didn't do the experiments the way you need to do them to cross your
gaps. He was able to cross your gaps when he selected for better
growth on lactose. What does that tell you?
>
> > > > Why don't you research the work more carefully
> > > > before making these types of mistakes?
> > >
> > > LOL - Why don't you? You evidently do not understand the experiments
> > > that you are trying to use to support your position.
> >
> > Demonstrate that you understand the experiments, and that they tell
> > you what you think that they are telling you.
>
> See above?
You seem to have botched another one.
I'd agree with Hall that under his conditions I wouldn't expect to see
a gap of three mutations crossed, but this is due to the selection and
identification criteria.
>
> > As long as you use creationist
> > literature, expect to be wrong about 100% of the time.
>
> That's bogus. There are in fact many creationists that are well
> educated, honest, and insightful in their thinking and writings.
> Outlandish statements such as this only speak against your
> credibility. I don't say such things about evolutionists. I think
> that there are many brilliant evolutionists who are very well
> educated, brilliant, honest, as well as insightful. I have found the
> same to be true of many, though certainly not all or even most,
> creationists.
Put up a single creationist argument that you can defend from one of
these honest and insightful creationists. You haven't been able to
come up with one so far. It kind of looks like 100%, but I always
qualify my arguments. What you mean to say is that you are ignorant
enough to be fooled by the scams these creationist put on you, and
that you haven't crosschecked the data or the arguments so that you
don't know it is a scam yet, in some cases. Demonstrate that this
isn't true. Present an honest creationist with a valid scientific
argument. We aren't talking articles of faith, here, but science.
>
> > That is just a
> > fact that you know and have run into so many times that it must hurt.
> > The "evolutionist" that matter are the professional biologist. Joe
> > Blow down the street doesn't carry much weight in science, but for
> > some reason he carries the weight of creationism on his shoulders.
>
> You evidently do not understand that there are many well educated
> professional biologists and other scientists who are in fact
> creationists or design theorists. To make such generalizations that
> all creationists are poorly educated idiots is simply ridiculous.
Name one that publishes creationist material in their scientific
publications. Lots of religious people are scientists, but that
doesn't make their religious beliefs rational. They run into the same
problem. Name one of these creationists or design theorists that
claim to have scientific reasons for their belief and that have
published these verified claims in the scientific literature. They
all know that these beliefs do not measure up. Every single one of
these creationists scientists understand this or they are too out to
lunch to be consider as scientists. The guys that you should really
be upset about are the guys that realize this, but lie to the general
public about it.
>
> > That is the difference between science and creationism. You know
> > this, I shouldn't have to tell you that. Why try and make it look
> > like the guys that don't matter, matter? If you don't know what you
> > are talking about, you don't get much attention in science. Look at
> > all the ID supporters, until they come up with something to evaluate,
> > science wouldn't give them the time of day. They only get attention
> > because of the dishonest things that they are doing in politics.
>
> The reason why many scientists won't give them the time of day is
> because there is a religious type of dogma in the popular scientific
> community known as naturalism. Nothing can challenge naturalism
> because naturalism is a sacred part of the philosophy of modern
> popular science. I suggest that you get your head out of the sand and
> start thinking for yourself instead of worshiping the popular gods of
> popular science.
There is this little problem that the supernatural has a 100 percent
failure rate in explaining anything that we can study in nature. 100
percent is 100 percent, if you have an exception present it. All the
god did it explanations that we have been able to test have failed.
100 percent of the ones we have been able to test. Don't you think
that before ID deserves notice that they should come up with at least
one example where their basic premise accounts for something in
nature? What is the difference between saying that some god makes
babies, from saying that some god makes flagellum? Just the level of
ignorance.
If you come up with some evidence of a designer capable of doing this
we could consider it. Where is this designer? When did he do this
designing, and how do you think that he did it?
We have solid reproducible results demonstrating how genes change with
time. We have comparative sequences from thousands of species. What
do you have?
In your model what do you predict to find in another species of
bacteria distantly related to E coli for proteins that do the normal
function of ebg? What do you expect to find in the sequence of a more
closely related bacteria like salmonella? Why will the ebg gene be so
different in the two when they do the same thing? Present your better
explanation and make it consistent across all species. Just think of
cytochrome C, why would a protein that does the same thing in all
those organisms reflect common descent if it didn't happen?
>
> > > > As you might expect after
> > > > that long they are very different proteins. If you study this system you
> > > > can see just how gene duplication is responsible for the permeases, and
> > > > inducer genes of the two cistrons. This is like the blood clotting
> > > > system that the ID people have to acknowledge that there is a lot of
> > > > evidence that it could have evolved. The proteins in the system are
> > > > related to eachother and obviously were created by gene duplication.
> > >
> > > If given the "a priori" assumption that evolution is true, then yes,
> > > this is the only logical explanation. However, just because various
> > > genes look quite similar or even identical does not mean that they
> > > necessarily arose via gene duplication.
> >
> > Give your alternative mechanism and the evidence for it.
>
> Intelligent Design. The evidence is that there is no good rational
> for explaining how such functions can arise without ID. For example,
> I might ask you to explain how a broken window in a house could be
> fixed outside of ID? You see, the evidence for ID is the lack of a
> reason explanation for an observation outside of ID. It is an
> argument of probability against any other mechanism.
Unfortunately, your example is nonbiological and irrelevant. If ID
explains these things in biology, why don't they have a scientific
theory of ID? ID isn't a mechanism it is political propaganda. If
you think that it is more than that present the scientific theory and
mechanisms of ID. ID has no theory or mechanisms. The ID supporters
state it very clearly that they aren't interested in mechanisms. This
is very plainly due to the fact that they can't support any
mechanisms. ID obviously is not an alternative mechanism.
This is getting too long. I'll pick it up later.
Snip:
Ron Okimoto
Ron Okimoto
> roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.0304...@posting.google.com>...
>
> Intelligent Design. The evidence is that there is no good rational
> for explaining how such functions can arise without ID. For example,
> I might ask you to explain how a broken window in a house could be
> fixed outside of ID? You see, the evidence for ID is the lack of a
> reason explanation for an observation outside of ID. It is an
> argument of probability against any other mechanism.
>
> > > Very similar genes may be
> > > used in very different ways in different systems of function. The
> > > evolution of different systems of function using the same genes is
> > > still quite problematic since the assembly of any new system of
> > > multiple genes would require the crossing of neutral gaps in function.
> > > No such functional system of multiple genes, to my knowledge, has
> > > been demonstrated to have evolved in real time.
> >
> > You have a problem in that you haven't been able to find a system
> > where you can claim that this has occurred. Shouldn't you demonstrate
> > that there is a problem before you claim it is a problem. Give
> > specific examples and how you determined that the changes had to be
> > neutral.
>
> I have done this over and over again. The fact that lactase does not
> evolve in E. coli over tens of thousands of generations in very large
> colonies is very good evidence for the existence of such neutral gaps.
> Also, any reasonable thinking person would admit that there are a lot
> more neutral options than there are functional options out there and
> that the neutral options expand greatly with increasing complexity of
> the interacting parts? as with a language system like English. For
> example, evolve the phrase, "Methinks it is like a weasel" one
> mutation at a time and see how far you can go. How many different
> function English phrases can you get before having to cross gaps of
> neutral/non-function?
The assay system is wrong. You can't claim this from the data. What
is the probability that you will see a color change in the colony if
the last mutation you need does not occur within the first 5 or 6
generations. You blew it. That should be enough of this bullshit.
Enzymes are not phrases in the English language. If this argument
were valid why would we be able to evolve enzyme function in
antibodies in less than 10^12 trials? Give it up. You must realize
by now that there is something very wrong with this argument. Can you
tell us what it is?
>
> > > For example, it is
> > > thought that the motility function of bacterial flagella arose via the
> > > use of existing genes in new combinations so as to produce a new
> > > function of motility. Well, if it is so easy, and there are few or no
> > > neutral gaps to cross, the evolution of such a motility system should
> > > be easy to demonstrate in short order. After all, the necessarily
> > > genes to produce all the necessary parts are all there in the
> > > non-motile cell. What is the problem with using these existing parts
> > > to make a new function? It should be so easy, but it really runs into
> > > the same problem as using the same 20 amino acids to produce new
> > > functions. All the amino acids are there, but making a new function
> > > using the 20 amino acids quickly runs into roadblocks of gaps of
> > > neutral/non-function. The same thing happens when you try to use
> > > existing proteins to make new functions. The gaps are still there and
> > > are even wider than trying to cross gaps in single protein function.
> >
> > Demonstrate that the changes had to be neutral and what order that you
> > think that they occurred in.
>
> Why don't you demonstrate that the changes would not be neutral and
> the order that such mutations would have to occur in order to follow
> your hypothesized path of ever improving function. For example, what
> good are 30 of the parts all in their correct places if 60 parts are
> needed for flagellar function? The 30 parts might in fact be useful
> in other systems of function, but for flagellar function to be
> realized, they must come together in a very specific way? with another
> 30 parts. How do you explain this? one point mutation at a time?
This is so much bullshit and you know it. You are the one making the
assertion. I make no claim that I could do this. The only claim that
I make is that you can't do it so it makes your argument worthless.
If you can't determine that the changes had to be neutral what good is
your argument? Give it up, you only look stupid trying to make claims
that you can't support. It is not up to me to support your claims.
>
> > It could be easy to evolve a flagellum,
>
> Oh really?? Please, explain how.
If you told me the intial conditions and the genes present it could be
pretty straight forward. Since you can't do this you can't make any
claims as to how hard it would be, can you? How many mutations were
needed to create the first flagellum if you don't know what the first
one looked like and you don't know what the starting material was?
>
> > but we have a problem. We
> > don't know what the first one looked like.
>
> Ok, that is not a problem? reduce the current flagellum one part at a
> time so that each reduction is functional in some theoretical
> environment.
You obviously don't know what you are talking about. If it were this
easy Dembski would have done it by now. Think for 5 minutes and see
where it gets you on this one. You'd have to be pretty naive to think
that you can do it this way. Why hasn't Behe or Dembski done this by
now?
>
> > It has changed in the
> > billions of years since it first evolved. Looking at the different
> > flagellum we can see that they probably did evolve from some original
> > one, but some have different parts. Some parts seem to have been
> > lost, some may have been gained, some lost and regained. It has been
> > a very long time.
>
> This is another "Just-So-Story". Sounds lovely, but absolutely no
> solid testable evidence to support it.
Just the facts as they stand. Ask the ID people. They know that this
is the problem or they would be doing something along the lines that
you claim is possible. If you have a better explanation of the data
let's see it.
>
> > What did the original flagellum look like? What
> > proteins and their sequences were available as basic material that it
> > evolved from? Without this basic knowledge how do you expect us to
> > reproduce the evolution of flagellum?
>
> It should be easy to start from what you know about a given bacterium
> with its given genes a propose some way that that bacterium could
> evolve a flagellum. Or, even better, reduce a flagellum, one part at
> a time, and still have the remaining apparatus doing some beneficial
> function.
Why hasn't someone done it? Why hasn't Dembski proposed an
evolutionary mechanism so that he can test it with his filter. If it
was as easy as you claim then maybe Dembski has done it and found that
his filter doesn't work? You should ask him how many of these simple
pathways that he has checked out. One reason that it wouldn't do him
any good is because we don't think that evolution of such biological
systems is that easy. Behe admits that it is possible to evolve IC
systems he just thinks that some IC systems are too complex to evolve.
Ask him how simple it is to try and figure out evolutionary paths.
Since he hasn't given a single pathway for the evolution of the
flagellum it doesn't look like they are very serious about testing
their assertions.
>
> Some have argued along these lines by saying that many of the parts of
> the flagellum do in fact have other useful functions in the cell? such
> as secretory pores, ATPases etc. Perhaps a third of the total number
> of parts have been explained in this way. However, this does not
> explain how these parts come together to form a new function. For
> example, all 20 amino acids are there to make a flagellum in all
> bacteria. All the parts are there. However, these amino acids do not
> self assemble themselves to make a flagellum in all bacteria. So you
> see, just because you have all the needed materials does not mean that
> you have any particular function.
Like I said if you tell us what genes were available when the
flagellum were evolving we could answer some of those questions.
Please don't keep us in suspense if you know something that we don't.
2 billion years ago ebg probably couldn't evolve lactase function in a
single step, but hundreds of random amino acid substitutions since
then seem to have provided an extant template that could do it. The
20 amino acids don't have to self assemble from scratch. They are
already doing something in the cell. The evidence that we have says
that this scenario is possible. What evidence do you have that it
didn't happen?
>
> > Look at ebg, a billion years
> > ago it's sequence may not have been able to evolve Beta gal activity
> > in a single mutation, but hundreds of amino acid changes since then
> > now provide a substrate for beta gal evolution.
>
> Perhaps, but you would be able to estimate how long it would take
> given a particular distance that would be required to be crossed. If
> the neutral gap was in fact "hundreds" of amino acids wide, then the
> odds are extremely unlikely that this gap would have been crossed in a
> billion years? even given a population the size of the galaxy or even
> the known universe.
The data indicates that a very small fraction of any sequence space
has to be tested in order to get enzyme function. There is absolutely
no evidence that hundreds of changes have to be crossed or tried. You
keep forgetting that the trials sample sizes are so small to produce
these activities that claiming that hundreds are necessary is
ludicrous. Explain the antibody data or just the random assembly of
RNAs to get function. Just due to expense and available manpower only
a small number of sequences are tried in these experiments, but they
still work. If you were right, would we be able to generate enzyme
activities by random assembly? Yes or no?
>
>
> > You need to know the
> > sequences of the proteins like the ATPases at the time that flagella
> > were evolving in order to try and figure out how hard it would be to
> > get one to form the hexamer needed by the flagellum. Maybe the
> > original flagellum only had a tetramer arrangement, maybe only a
> > dimer. Do you know this kind of stuff? Can you recreate the
> > conditions under which flagellum were evolving? You know that these
> > details are very important. Different starting sequences will give
> > you different results.
>
> Actually, since I do not believe that the flagellum evolved or could
> have evolved, I do not believe that these "original sequences" exist.
> You cannot even hypothesize any path, even a theoretical path, that
> would get you from any group of proteins to a flagellum. Try it. It
> seems like quite a problematic situation for you.
But to test your assertion you have to be able to tell us this data
don't you. If you claim that it is impossible for these systems to
evolve, you must be able to test that assertion, right? If you can't
test the assertion, what good is it? I make no claim that I can do
this, in fact, I claim that we can't do it at this time. You need to
be able to do it, not me. Your argument is bogus until you can
demonstrate that you can test your assertions.
>
> > > > What design mechanism would do this? We have a mechanism that we observe
> > > > to occur in nature that fits the bill very nicely, but where is your
> > > > mechanism and how does it work?
> > >
> > > But you do not have a mechanism that you can detail as to how such
> > > gaps are crossed.
> >
> > What was the mechanism used for ebg evolution. Random mutation,
> > genetic drift and natural selection. If you have some other mechanism
> > just lay it out and compare it to the mechanism that we have actual
> > evidence is working in nature.
>
> The gap in ebg evolution was extremely small? just one mutation wide.
> Genetic drift works very well in such cases. However, genetic drift
> is really limited with larger gaps as detailed above. You are left
> without a sufficient mechanism to explain such complex functions as
> bacterial motility or other multi-protein systems of function, as well
> as relatively simple enzymatic functions such as the lactase function
> in bacteria that are lacZ and ebg negative.
ebg was able to span your challenge of 3 mutations to get function.
Hall was able to find a bacteria that had 3 mutations to improve
lactase activity. 3 used to be too many for you, now it is 30 or
hundreds, when you can't demonstrate that it takes even 4 or 5.
>
> > > It is back to the "God of the Gaps" argument. If
> > > you can explain how to cross the gaps using naturalistic mechanisms,
> > > then I will believe you.
> >
> > I just did, and I used a real verfied example.
>
> Again? your example is extremely weak in explaining much of anything.
> Even Hall seems to recognize the problem more than you do. I even
> believe in such evolution across small gaps. However, I see that this
> gap problem is a lot bigger than you seem to realize.
The example was your example. It happened, you can't deny it. How
did it happen that 3 mutations were found? Hall would have required
the fixation of the first two mutations before the 3rd in his red
plate assay because all the bacteria plated would need to have at
least two of the three so that only a single mutation would be needed
to see a difference on the plates. Hall's argumment was valid for his
red plate system, but you demonstrated that in nature you don't have
to rely on fixation, just neutral drift. You destroyed your own
argument.
>
> > > Otherwise, you have nothing but wishful
> > > thinking. For example, it is easy to explain how a window could be
> > > broken using a naturalistic mechanism, but it is another thing
> > > entirely to explain how a broken window can be fixed using a
> > > naturalistic mechanism.
> >
> > Evolution isn't fixing broken windows. The window was never really
> > intact it just adds pieces. Halls example is fixing a broken window,
> > but real life evolution doesn't have to do that except in dire cases
> > that probably usually result in extinction. All evolution has to do
> > is make the window more solid than it was. If you have a better
> > mechanism state it and the evidence for it.
>
> No, evolution has to explain how the window got there to begin with.
> How does a house with no windows get windows? Not via naturalism? but
> via intelligent design.
There is no window is there? Why do we have to explain where
something that doesn't exist came from? All that is claimed is that
existing lifeforms can change over time and that these changes don't
have to be fixing broken windows. Lifeforms are dividing happily. We
only have to claim that certain changes make them reproduce just as
well (neutral) or even a little better compared to their competition.
Bacteria with out flagellum do OK. Some lucky bug developed a means
to move that obviously helped it. It didn't have to evolve a
flagellum did it? So it doesn't really matter how impossible it looks
it just has to be like winning the lottery. The bug didn't have to
win the lottery it just did. Your own calculation make it possible to
happen by known mechanisms. So what is your problem?
>
> > > > It is good to see you back. It has been pretty boring around here with
> > > > just the willfully ignorant moron types posting on the creationist side.
> > > > Read the recent posts by Glenn, McCoy, nowhereman, and Zoe but be
> > > > prepared to cringe a lot. With guys like those on your side you don't
> > > > need me to tell you how bad off your side is. What makes it worse is
> > > > that they have been about the only ones supporting the creationist
> > > > position.
> > >
> > > I have been very busy lately, but thanks for the compliment here.
> > > Really though, telling me that I only have idiots who support me
> > > really doesn't help your position. All it says is that my position is
> > > unpopular and that you are strongly supported by the popular vote.
> > > This means nothing since it explains nothing in a way that I can
> > > understand. It is just an argument of authority, but says nothing of
> > > explanatory substance.
> >
> > It says more than that your position is unpopular. Most or a large
> > chunk of the people in the US probably side with you. The problem is
> > that they do it because they are ignorant, and certain people play off
> > this ignorance to get them to do stupid things.
>
> You are talking about the majority of scientists. So am I. You are
> arguing from authority. Lame.
It doesn't matter how lame it is if it is true. My statement was true
wasn't it? Just answer yes or no? Who is being lame?
This is just the old creationist probability argument and you know it,
even if you can't admit it to yourself. You don't need the system to
be IC for this argument do you, you just need it to be so complex that
you can't imagine how it could have evolved. Is God or nature limited
by your imagination?
It is true. Your statement about it is ridiculous. Demonstrate that
it is not a probability argument. Just try.
>
> > > Behe makes the mistake of trying to limit the definition of IC systems
> > > to those systems of function that he considers to be highly complex.
> > > I feel that this is a significant mistake on his part. However, his
> > > basic concept is a good one and remains as a roadblock to natural
> > > selection as a reasonable mechanism for naturalistic evolution.
> >
> > The definition that if you take away a part then the system doesn't
> > work isn't any good in determining if the system could have evolved or
> > not.
>
> Actually it is. It helps you to know or estimate how wide the gap it
> is a particular part is taken way. Once the gap distance is known,
> the average time required to cross this gap can be calculated quite
> accurately.
It tells you that there is a possible gap, but perhaps you can tell us
how wide the gaps are when you can't even tell us that they are there.
Behe acknowledges that there is the possiblity that systems could
have evolved from existing systems and that due to further evolution
they are IC now, but they didn't have to be when they first evolved.
Tell us what the first flagellum looked like so that we can determine
if it was IC from its first appearance, and that it could not have
evolved from other systems.
ID proponents admit that type III secretory systems may have evolved
from flagellum. They are complex and IC. What is to keep the
flagellum from evolving from preexisting systems. If you could tell
us the systems available at the time we could test your idea.
>
> > You basically admit that these systems have been observed to
> > evolve.
>
> Certainly. It is easy to evolve new functions if the gap between what
> there is and what is needed is small. However, there is good evidence
> that large and even gigantic gaps exist between various functions that
> we see in living systems.
What is this evidence and what are these systems? Demonstrate that
the gaps and changes had to be neutral. Your problem is that you
can't back up your assertions.
>
> > You have to have something more. Just saying it is
> > improbable is pretty silly since you can't even begin to calculate the
> > probabilities because even if you did have all the information I'd
> > like to see you deal with all the non independent variables.
>
> LOL - Ok... there what would it take to convince you? You see various
> functions and you do not understand how a functional bridge can be
> made between them, yet you believe that such a bridge exists and that
> such an explanation must be out there. You think that science will
> one day discover these bridges. You will not believe otherwise unless
> I prove a negative to you. You ask me to prove all variables and all
> potential sequence changes before you will question your current
> position. Well, you are asking for a scientific impossibility. No
> one can prove a negative. The best that can be done is to show the
> probability for a negative? which I think I have done quite well, at
> least to my own current satisfaction. It seems to me that your faith
> is quite amazing in light of the weakness of the evidence in your
> favor. The best experiments that you have in evolving new functions
> have crossed neutral gaps of only 2 point mutations. And yet, you
> hold up such evidence as being more than it is, as demonstrating
> significant evolution in real time. How lame.
The only lame bit is your inability to realize that your own
calculations pretty much end this debate if they are accurate. You
have to hope that they aren't accurate because you can't come up with
a single system where 20 neutral changes have to be bridged. Present
such a system and your evidence for the necessity of neutral changes.
>
> > How improbable would it be to co-opt an ATPase for flagellar work if
> > you only needed a single aminoacid substitution to do it?
>
> It would be very probable. All you have to do is show that this is
> all it takes, and then you would have a start. The problem is that a
> single mutation that makes ATPase adaptable for flagellar work is not
> enough. What happens if you not only need a mutation for ATPase
> adaptation, but another mutation for this part and another mutation
> for that part and and and?. ? Until all of these mutations are
> realized via random drift, you have no motility function? period.
You have to demonstrate that these changes had to be neutral and that
the new ATPase didn't have some function in the cell. Can you do
this?
>
> > What was
> > the sequence of that ATPase and how many mutations were needed to get
> > it to do its new function?
>
> There is no new function without the other parts. Don't you get it?
> Without all the 60+ different proteins all working together, a
> "correct" ATPase part isn't going to do the job by itself.
Demonstrate that this is true. Since you can't, why make such a
statement? All you have is what flagellum look like now, and there
are different types with different parts.
>
> > Maybe no mutations had to happen in the
> > ATPase. Some mutation in another protein that made it interact with
> > the ATPase and form a structure needed for flagellar development may
> > have happened.
>
> Certainly this might have been the case, but what if these two
> proteins got together in just the right way? great? but now you have
> 58 more to go before the motility function is realized.
How many proteins did the first flagellum have and what was the
function of that flagellum. Was it motility or was the tube used as
an anchor or did it have some other function? Did it function as a
protein secretion unit before it formed the tube or did the tube come
first? If you can't reason through how stupid your argument is I
can't help you.
>
> > Make up your own story, but you have to rule them all
> > out before you can claim that they are impossible.
>
> I'm not saying that your "just-so-stories" are impossible? only
> extremely unlikely.
>
> > Ron Okimoto
>
> Sean
We don't need just so stories we have real data and actual mechanisms.
You need more than just so stories or you can't test your assertions.
Your argument is bogus until you can do more than put up wishful
thinking. We have evidence that it could happen, you have no evidence
that it couldn't because you can't tell us what happened and why it is
impossible.
Ron Okimoto
John Harshman
Ron Okimoto wrote:
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03050...@posting.google.com>...
>
>>roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.0304...@posting.google.com>...
[snip everything]
I just had an interesting thought for a metaphor that might help
illuminate the question to Dr. Sean (in my dreams, that is), and I am
randomly attaching it to Ron's recent post.
Let's imagine gene sequence space (or protein sequence space if you
like) as a plane. It's really multi-multi-dimensional, but try
visualizing in that many, and 2 will do for the point. We can envisage
sequences following a mutational path through this space, and let's
pretend that all mutations are point mutations that move the sequence
one step in some direction. Neutral evolution follows a random walk. Dr.
Sean contends that the space is flat, and the chance that any sequence's
random walk will ever reach a particular, selected point depends on the
distance between the starting point and the target point, with the
probability decreasing to as close to zero as we like as distance goes
up. (Ron has argued that these probabilities are much higher than Dr.
Sean likes for much larger distances than he likes, but forget that for
now.) I would contend, however, that the surface is not flat, but that
around each sequence that is maximally functional for some task, there
is a depression of some size. Deepness of depression corresponds to
fitness, and due to selection, a sequence is more likely to move down a
slope than up it, with probabilities depending on the steepness of the
slope. Under such conditions, sequences that enter the edges of a
depression will be attracted toward the center. My contention would be
that a high proportion of sequence space does have a discernible slope.
Moreover, sequence space is not static. Fitness depends on environment,
both genetic (other sequences in the organism) and external. Depressions
move, coalesce, and separate, taking sequences with them. A sequence can
end up very far from its starting point just through rolling down
ephemeral slopes. (This is more or less stealing Sewall Wright's concept
of adaptive landscapes; and why not?)
H,R.Gruemm
roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.03050...@posting.google.com>...
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03050...@posting.google.com>...
> > roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.0304...@posting.google.com>...
> >
> SniP
>
> > Intelligent Design. The evidence is that there is no good rational
> > for explaining how such functions can arise without ID. For example,
> > I might ask you to explain how a broken window in a house could be
> > fixed outside of ID?
We know that humans exist and can fix windows. Thus "Joe fixed it"
becomes a rational explanation.
You see, the evidence for ID is the lack of a
> > reason explanation for an observation outside of ID. It is an
> > argument of probability against any other mechanism.
For a probability argument, you need a comparison of *two*
probabilities: the (alleged) probability of a non-ID explanation
versus the probability of the existence of a sufficiently powerful and
suitably motivated designer.
I await with great curiosity Dr.Pitman's reasoned estimate for the
latter probability.
Regards,
HRG.
TomS
<5662bb3.03050...@posting.google.com>, psych...@xpoint.at
stated..."
And then there is the argument of Jefferys and Ikeda, which tends
to show that the Argument From Design is an argument *against* a
"sufficiently powerful and suitably motivated" designer. By an
analysis of the probabilities involved.
<http://quasar.as.utexas.edu/anthropic.html>
>
>I await with great curiosity Dr.Pitman's reasoned estimate for the
>latter probability.
I still have a problem with understanding these intelligent
designers.
Whatever they are, they are clearly something quite different
from the God of conventional monotheistic faith.
Letting aside for a while the question of just how many of them
there are, as indicated by their need to construct conflicting
designs. Rather, I am puzzled by what the existence of *complex*
solutions to design problems shows.
To me, complex solutions are an indication of complex problems.
Difficult solutions are an indication of difficult problems. Simple
solutions may be an indication of simple problems, or an indication
of a very good problem-solver.
So, if we have an "irreducibly complex" design, it is complex,
and that indicates that there is some problem that the designer(s)
found complex -- *for* *them* (her/him/it).
But I cannot imagine the Creator of the universe finding any
problem complex.
Surely not so complex that the Creator would find it necessary
to make such a complex solution as the immune system. (Particularly
when I can think of a simpler solution: don't design bacterial
flagella so as to make bacteria so virulent.)
Oh, perhaps the immune system is not really all that complex,
and maybe us mortals just don't appreciate its elegance and simplicity.
But the whole point of the "irreducibly complex" argument is that it
*is* complex (irreducibly so, indeed). If it "really" is not complex
(or if we just aren't able to tell), then there is no point to the
argument that "irreducible complexity" points to a designer.
If "irreducible complexity" is a sound argument, it points to
designers who were confronted with a problem that they found complex.
Tom S.
Ron Okimoto
I like Wright's fitness landscape idea. Thinking of protein function
is more complex than that. Each specific protein sequence would have
a landscape for a particular function, and there would be a near
infinite number of different functional landscapes for each specific
protein sequence. For any given protein there are a very large number
of related sequences that can do the same function well enough to pass
for an equivalent sequence, but each of these equivalent sequences has
a different functional landscape for each of the near infinite
possible functions for the protein. There was a fellow in the late
70's that calculated that just for the short protein like cytochrome C
(104 amino acide residues) using just the sequence variation known at
that time, that there were 10^45 possible functional cyt c sequences
confined to the 104 sequence limit. We have more variation known now,
so the number would probably be higher. If you asked how many 110,
150, 200, etc. amino acid sequences would do the same function you get
the idea that the number of sequences of a reasonable length that
could do what cyt c does is an unimaginably large number.
These would mostly be potential functional landscapes as you say. One
or a few changes in any protein sequence could facilitate selection
for that new function.
Combining these notions it could be a way to reason why it seems to be
so easy to evolve different functional sequences from antibody motifs.
A prediction could be that there were some peaks (possible paths to
function) for any given sequence for any given function, and that
sequence evolution was likely to go along that path to get that
function most of the time. For a sequence that didn't have that
function one key mutation may lead to this peak and channel future
mutations up that peak. Your model would predict that the peak with
mutations with the selectable phenotype or that facilitates evolution
to that function by altering the potential functional landscape of the
protein, would be the path followed even though there were functional
peaks that would lead to more efficient function possible for a given
starting sequence. If the mutations were selectable you would see
them as raised topology, but I don't know what you would visualize the
facilitating mutations as. They aren't selectable, but they do make
it possible that later mutations are selectable. Alternative
functional peaks that are not chosen as frequently would require more
of these facilitating mutations before selectable function was
observed so you might see them as divots around the peaks. Those
peaks that needed no facilitating mutations would rise from a flat
surface and those that needed facilitating mutations would have a
trench around them of varying depth.
You might not be able to model it in 2D or 3D, because you are talking
about a linear sequence that has a 3D shape and the amino acids
involved in functional peaks are spread around the molecule. It would
be more of an inaccurate graphic to get people to think about what was
going on. Each change would alter the functional landscape, so to be
accurate you need a temporal axis too. One landscape picture probably
won't do it.
Ron Okimoto
Sean Pitman
> > As far as the evidence for and against common descent, I think that a
> > discussion of evolutionary mechanisms (or the lack thereof) is quite
> > relevant to this topic.
>
> It's somewhat relevant, but I repeat: do you have any interest in
> discussing common descent directly?
Although I am interested in your views on what you consider to be
convincing evidence of common descent I am more interested in
discussing the mechanism or lack thereof for common descent. As I see
it, similarities and differences in morphology and even genetics are
all fine and good as far as proposing this or that phylogenetic
relationship, but all that is pretty much hot air if there is no good
mechanism to explain such stories about how things "must have
happened." The theory of evolution is not like other theories or laws
such as the law of gravity where we see the effects of gravity working
on a daily basis without fully knowing the mechanism. The theory of
evolution is different in that we do not see things evolving beyond a
certain point in real time. The best real time examples of evolution
that we have are very feeble indeed. Almost all are based on a single
point mutation, or at best 2 or 3 point mutations. These are easily
explainable as the result of random chance working alone to cross the
bridge between functions so that natural selection can take over on
the other side. Beneficial functions that are only 1, 2 or even a few
mutations away from what is currently present are statistically likely
to come around by sheer random chance. This is not so when gaps start
increasing in size.
Because of a general lack of real time observation of evolution in
action, the evidence in favor of evolution requires a great deal of
subjective interpretation that cannot be directly tested. Then, when
it seems like there are significant barriers to genetic evolution in
the form of neutral gaps, the evidence in favor of evolution becomes
flimsy indeed.
> >>> It seems quite obvious to me that given a particular
> >>>creature, such as a bacterium, that the vast majority of possible
> >>>amino acid sequences/proteins of a given length will have no
> >>>beneficial function for that creature in its current environment.
> >>
> >>Agreed. This is obvious.
> >>
> >>>Only a very tiny
> >>>fraction of the potential amino acid sequences will be recognized by
> >>>any given bacterium or living cell in any given creature.
> >>>
> >>Recognized? What meaning are you using for "recognized"?
> >
> > Take for example the insulin protein. Not every cell in the body
> > "recognizes" the insulin amino acid sequence. Other cells, having the
> > proper surface receptors, do recognize the insulin protein and perform
> > various functions when insulin comes around.
>
> Not every protein (and probably a decided minority for that matter) acts
> by binding with a receptor, so I'm confused about why you would bring
> this up in a discussion of general protein function.
Every functional protein is part of a larger system of function within
a cell. This system is able to incorporate a given protein into a
particular place to do a particular job or function. Can it be said
then that that system "recognizes" that particular protein? Ascribing
human-like abilities, such as the ability to recognize something, to
non-living things is done all the time to help us in our descriptions
of ideas or concepts. The word "recognize" need not be limited to a
receptor's ability to interact with a protein in the production of a
particular function. However, if my use of the term "recognized"
confuses you, replace it with the term, "beneficial function." For
example, only a very tiny fraction of the potential amino acid
sequences of a given length will be "beneficially functional" in a
given bacterium or living cell in a given environment. There, is that
better?
> > So, for some cells the
> > insulin protein really has no function or meaning while for other
> > cells it does. It is like different words for different languages. A
> > given word might have some meaning in Spanish, but none in English.
> > The same is true for protein "words" in living cells. A given
> > protein/amino acid sequence might have function or "recognition" for
> > one cell, but have no function/meaning/recognition for another cell.
> > If a given part performs some sort of function in a given system of
> > functional parts, then that part is "recognized" by that particular
> > system. The system "knows" what to do with that part. It "knows"
> > what function that part has. For example, the term "recognition" is
> > often used when describing the interactions of antibodies with
> > antigens. When the antibody comes in contact with a particular
> > antigen that it fits with, the antibody is said to "recognize" the
> > antigen. Does this make sense now?
>
> That's what I thought you meant, but it doesn't really make sense. Many
> functional proteins don't "recognize" anything even under the most
> liberal definition -- i.e. having a specific substrate. Functional
> proteins can do all sorts of things, so I'm unsure why you are
> attempting to restrict the universe of functions in this way.
It is not the protein that does the "recognizing", but the system of
function that does the recognizing. The system of function is what
"recognizes" the protein. Given a particular system of function, such
as a flagellar system, only 60 or so proteins would be "recognized" by
that system as having some sort of beneficially functional part to
play in the operation of that system. True, particular proteins that
do one job in the flagellar system of function might also be
"recognized" by other systems of function and used in different ways
to do different jobs. However, for that particular system of function
a particular protein is recognized as doing a particular job. The same
is true for many different parts used in mechanical systems. Various
parts can be used to build either a car or a house, but each system
will use a given part in a particular way, and some parts will not be
useful to a particular system of function at all. For example, if you
throw an insulin protein into the mix of flagellar proteins, the
flagellar apparatus will not know what to do with the insulin protein.
The insulin protein is thus "functionless" or "not recognized" from
the perspective of the flagellar system of function. The same can be
said for all the systems of function within a given cell. Most
proteins have absolutely no function, much less beneficial function,
in a given cell in a given environment . . . although they may have
some function somewhere in some other cell or system of function. But
what good is it if some other cell could use a particular protein if
the current cell in question cannot?
> >>>Take humans
> >>>for example. The vast majority of human DNA does not code for any
> >>>functional protein much less a beneficially functional protein. The
> >>>proteins that are coded for are somewhat plastic, true, but they are
> >>>also very specific. If changed or "denatured" to any significant
> >>>degree, they loose all function.
> >>>
> >>You are confusing two forms of change. We were talking about mutation.
> >>Denaturing is a loss of tertiary or quaternary structure, most often as
> >>a result of heating. Nothing to do with what we are referring to. (Also,
> >>I don't understand your distinction between "functional" and
> >>"beneficially functional", or what you mean by "somewhat plastic".)
> >
> > I mention protein "denaturing" to emphasize the idea that changes in
> > protein sequence *and* structure affect protein function. We are
> > talking about protein function in general here. Whatever changes a
> > protein (mutation, heat, chemicals etc) can affect its function in a
> > given system of function since protein function is dependent upon its
> > 3D shape/structure.
>
> In general, each protein has a unique 3D structure. In general, primary
> structure determines secondary structure. So this is irrelevant to any
> question you have so far attempted to discuss.
Even though primary structure generally determines secondary and even
tertiary protein structure, it is the final tertiary 3D structure that
really counts. We talk about the linear sequence of proteins because
it is easier to do, but we shouldn't forget that the 3D structure is
what really does the job. The reason why this is relevant, as
mentioned before, is that a particular 3D structure is not always an
automatic default given a particular amino acid sequence. Cells can
and often do put together different 3D structures with the use of the
same amino acid sequence.
> > Also, a protein can be functional without being "beneficially"
> > functional. For example, a protein can have a "detrimental" function.
>
> That's arguable. Let it go for now.
No, it's not arguable. Where the heck do you get that? Proteins
certainly can have detrimental functions. What do you call the effect
of botulism toxin on a human cell if not detrimental? What about
snake venom from the perspective of the one who got bitten? Proteins
can be quite detrimental to the function of a given cell or life form.
What about prions when they infect the brains of cows, sheep, and
even humans to cause spongiform encephalopathy? Or, what about the
mutated chloride channel protein that causes cystic fibrosis in
humans? Please. . . where is the argument? You try to be so picky
and precise in your language, to a fault, so why do you say, "Let it
go for now"? Really, if you have a point here, explain your
"argument". It is not a mute point from my perspective. It has a lot
to do with my position.
> >>> This means that the vast majority of
> >>>potential protein sequences and three-dimensional shapes are worthless
> >>>to a given human cell.
> >>>
> >>This is not quite clear, at least the "vast majority" part. There are
> >>lots of protein sequences that don't do exactly what we would like, but
> >>it does appear that we can find function from random sequences. See
> >>this: Hayashi, Y., H. Sakata, Y. Makino, I. Urabe, and T. Yomo. 2003.
> >>Can an artibrary sequence evolve towards acquiring a biological
> >>function? J. Mol. Evol. 56:162-168.
> >
> > Of course one would expect that various random sequences could be
> > found that do actually have some sort of function in a given cellular
> > system of function. Some of these might even have a "beneficial"
> > function in a given cell and environment. However, the vast majority
> > of potential sequences of a given length and 3D structure will not
> > have a function at all. You admitted as much above.
>
> Yes, but I've had second thoughts. Had you actually read the paper I
> cited, you would see that the function involved is specified beforehand,
> and that that function improved over time through mutation and
> selection. A surprisingly high percentage of the random sequences were
> useful for that specific function. This directly refutes your claim, as
> far as I can see. But you will have to read the paper and address it.
Actually, it doesn't refute my claim. Many functions, such as certain
enzymatic functions that require a single protein, are in fact
relatively simple functions, comparable to a 3-letter word in the
English language. Such functions may and often do have many different
amino acid sequences of a given length that can perform them. This is
certainly true with the lactase function. Although very much
different (only about 30-40% sequence identity), the ebg gene
(produces a hexamer protein) and the lacZ gene (produces a tetramer
protein) perform the same lactase function. I wouldn't be surprised
if there are a very large number of proteins that have some sort of
lactase function. However, it certainly seems that there is a
significantly greater number of proteins of comparable length and that
do not have the lactase function. This assertion is beautifully
demonstrated by the work of B.G. Hall. When Hall deleted both the
lacZ and ebg genes from his E. coli colonies, they never evolved any
other gene or genetic sequence to produce any other protein with
lactase function despite a large population size growing over tens of
thousands of generations and over 4 million base pairs of DNA to work
with. I find it quite interesting that only 2 genes had the potential
to produce the lactase function out of all the proteins produced over
this span of time by all of these E. coli. It seems to me that this
experiment proves that the lactase function is not coded for by
anything close to a "surprisingly high percentage of random sequences"
when the total number of potential sequences (~ 3e+1951) are taken
into account. Wouldn't you agree?
In any case, since I have not yet had a chance to read the particular
reference that you sited, please quote the relevant points here so I
can see what is so convincing about the evidence sited in this paper
you speak of. I will try to local and read it in the meantime, but
since you already have the paper and have read it, others following
this thread might be interested in its relevant findings and points as
well. I predict though that these previously specified functions that
you speak of were all relatively simple, mostly enzymatic type
functions, that the experiments were not done from the perspective of
a given cell or life form (ie: What a particular cell would see as
"beneficial"), and that the functional sequences were still a small
minority of the total number of sequences analyzed.
For example, I have read certain studies which showed that in a given
collection of antibodies produced by a given animal, many of these
antibodies have other functional activities, such as various enzymatic
functions. For example, some of these antibodies might be able to
break down lactose. This is expected, but how does this help the
creature that produced this antibody? The antibody's function in its
environment is not enhanced by its lactase ability. The creature that
made this antibody is not benefited by antibodies that have other
potential functions. Why? Because that antibody was not made by the
correct cell to be useful as a lactase enzyme. It is still only
useful as an antibody for the creature that produced all of these
various antibodies. Also, those antibodies that happen to have a
lactase function still make up a tiny fraction of the total number of
antibodies produced, even though their lactase function is a
relatively simple single protein enzymatic type function.
But how does this relate to the evolution of various functions in a
creature such as a single celled bacterium or colony of bacteria?
Well, it has a lot to do with such potential evolution. A bacterial
genome has a certain degree of flexibility or potential for change.
Such potential for change allows the bacterium to search through the
pile of potential protein sequences for something that might benefit
it in its current environment. If it is looking for a particular
function, such as a lactase function, the time needed for the
bacterium to find this lactase function depends on a few questions:
How common is this lactase function in the pile of options? How much
genetic real estate does the bacterium have available to search this
pile? And, how rapidly does this real estate search for new
sequences?
> > When I said, "It
> > seems quite obvious to me that given a particular creature, such as a
> > bacterium, that the vast majority of possible amino acid
> > sequences/proteins of a given length will have no beneficial function
> > for that creature in its current environment", you said, "Agreed. This
> > is obvious." Well then, what are you trying to do here? You seem to
> > be contradicting yourself in the same breath.
>
> I changed my mind after reflection and a search of the literature.
> Something that you would be advised to try some time.
Interesting that you changed your mind within two paragraphs. You
write one thing in one paragraph, go do some reading, come back, and
write something very contradictory in the next paragraph without
bothering to change the paragraph above? But, no matter . . . The
point is that you changed your mind based on something you read.
Please, quote what you read that explains how there is a significant
percentage of genetic sequences of a given length that would be of
some sort of beneficial function for a particular living cell in a
particular environment. Please . . . I do in fact read quite a bit of
scientific "literature", but I have never come across any study or
article detailing this sort of estimate. You actually found an
article that proposed that a significant percentage of genetic
sequences and/or proteins would be beneficial for a particular living
cell in a particular environment? Where did you read this? Pardon
me, but I am quite skeptical.
Take for example the lactase function. Both the ebg and lacZ genes
code for proteins over 1,000aa in length (for each subunit). It seems
like the lactase function requires at least several hundred amino
acids in a protein before a protein can have this particular function.
In other words, no sequence of 100 amino acids or less could be found
that has the lactase function. The lactase function seems to have a
significant degree of required amino acid sequence complexity. What
does this mean? It means that the lactase function is "irreducibly
complex". It also means that given a pile of sequences of 100aa or
smaller, only a tiny fraction of the 1e130 potential sequences in this
pile would have the lactase function.
> I have found an example of random sequences produces a previously
> specified function, which seems to argue that many functions can be
> performed by random sequences.
Certainly random sequences can quickly be sorted out to come up with
one or several sequences that produce a previously specified function.
. . especially if that function is relatively simple, such as a
simple enzymatic function. The same could be done with three letter
words. Random three-letter sequences could be sorted through until a
one was chosen with a certain specified function, such as "cat". Of
course, since there are only 17,576 possible three letter English
sequences out there, the desired previously specified function of
"cat" can be isolated in a relatively short time. And, if our
previously specified function had 1,000 representatives in the pile of
17,576, the sorting process would go that much faster. However, many
functions are not that simple and only have a relatively few sequences
that can perform them out there in the pile of random sequences. A
given cell with a limited amount of genetic real estate might take a
long long time to search through the pile to find even one of the
relatively few sequences out there that given a previously specified
function.
You, no doubt, will ask once more for evidence of this. And, one
again, I will point you back to Hall's work with E. coli and the
evolution of the lactase function. The previously specified function
for these E. coli is the lactase function. Each of these E. coli has
over 4 million base pairs of DNA to work with as well as around 2,000
proteins to work with. Without the lacZ and the ebg genes, these
mutant E. coli never evolved this previously specified lactase
function back. You see the problem here? A given population has a
limited amount of options to work with. It can only sort through the
pile of random sequences so fast and no faster. This random sorting
takes time. And, at least for the previously specified lactase
function the sorting takes quite a while. It is obviously not a fast
search in any case even if there were millions of potential lactase
enzymes out there in that pile somewhere. The problem is that that
pile has relatively few lactase sequences in it compared with its
total size. There seems to be no other logical explanation. But,
maybe you can think of a reason why these E. coli can't seem to sort
through the pile effectively when it comes to the previously specified
lactase function?
> After all, the function wasn't chosen
> with prior intent that it be easy for random sequences to do it. And
> this was a specific, chosen function. How much more likely that a random
> sequence will do *something* useful to the organism?
Tell me what, exactly, this specified function was? Was it a simple
enzymatic function? If so, how many different proteins with this
function where isolated from the pile of options? What was the
percentage of those sequences with this function as compared to the
total number of sequences available? Given these numbers, one could
estimate the time needed for a given living cell or colony of cells,
like E. coli, to evolve such a sequence. I am betting that it is not
easy as you would like to think. I am betting that the specified
function in this experiment was a relatively simple enzymatic function
and that even this function is still relatively rare given the total
number of proteins in this experiment that did not have this
particular enzymatic function.
> > The average time involved becomes the problem because, with increasing
> > complexity, the total number of sequences with potential function
> > decreases dramatically leaving larger and still larger gaps in
> > function between those sequences that would actually have function for
> > a given cell in a given environment. The random drift or "selection"
> > involved in getting from one sequence with function to any other
> > sequence with a different function of comparable complexity requires
> > greater and still greater amounts of time.
>
> You really have to watch your use of language. Equating selection with
> drift is not a good idea.
Come on now, I was not "equating" random drift with directed *natural*
selection. I was equating random drift with *random* selection. I
select one sequence. . . It isn't right so I have to select another
sequence, it isn't right, so I select another an another . . . and so
on. Random selection takes time. There is a random drift involved if
the selection or sorting process of neutral sequences.
> You have yet to demonstrate, by the way, that
> large, neutral gaps need to be crossed in evolutionary transformations.
What do you call the "limited evolutionary potential" of the E. coli
in Hall's experiment then? What was it that "limited" their ability
to evolve the lactase function? If not a large gap between what they
have and what they need, then what is the limiting force here? What
kind of demonstration are you asking for? For these particular E.
coli to gain the lactase function, it seems as though some sort of gap
must in fact be crossed, but how is it done? Please . . . explain.
> > And,
> > depending upon which way the protein is folded; function may be gained
> > or lost. Proteins do not always spontaneously fold in the proper way
> > to realize their function. There are other proteins that fold new
> > proteins as they are made. If the 3D structure of a particular
> > protein is "unfolded" and then allowed to "refold" by itself, it most
> > likely will not fold properly and its function will be lost.
>
> True for some proteins, not for many others. Some proteins need
> chaperonins to fold properly, some fold properly but spontaneously only
> during translation, and others fold properly and spontaneously under a
> wide variety of conditions. I don't know of a case in which some major
> evolutionary transformation of function is alleged to have resulted from
> a change in chaperonins without any change in the primary structure of
> the protein being folded. Do you?
See Below
> > So,
> > really, we talk about the 2D sequence because it is easier to talk
> > about, but in reality, the 3D structure is very important to function
> > and only compounds the problem of complexity since even more
> > differences can be realized for a given amino acid sequence than a
> > simple 2D sequence analysis would suggest. For a 2D sequence of 10
> > amino acids, the total number of potential proteins is:
> > 10,240,000,000,000 (~10 trillion). However, the total number of
> > different proteins would actually be much higher than this because of
> > all the added differences in 3D structures that are not being included
> > in the total number. This makes for even less of a chance of picking
> > those sequences/3D structures of amino acids that actually have some
> > sort of function, much less beneficial function, for a given cell in a
> > given environment.
>
> All this is doubtful. Without help from chaperonins, any given protein
> does have a preferred, spontaneous folding as it is translated. There is
> no serious random component.
Depending on which way the chaperonins fold the protein is very
significant seeing as how it is possible to fold the protein in many
different ways besides that in which it would fold spontaneously.
This is significant in that the potential for variety is greatly
increased by this potential.
> >>>As far as demonstrating a negative (ie: A lack of a functional path
> >>>between two different proteins), it is impossible this side of
> >>>eternity. A negative finding never means that a positive finding is
> >>>impossible. However, the likelihood that a negative finding will
> >>>occur can be calculated.
> >>>
> >>If it can, then you haven't done it yet. This remains to be seen.
> >>
> >
> > Well, of course I disagree. Can you prove that these gaps do not
> > exist or explain how they might not exist?
>
> No. There probably are such gaps. The question is whether they are
> sufficiently dense that most transitions among forms require crossing
> one, and thus evolution is unlikely. I have two arguments: 1)
> experimental results (cited above) show that random sequences produce
> specified functions capable of being improved by selection on random
> mutations, arguing against such gaps.
These experiments are extremely limited to very simple functions.
Hall also did such experiments with the evolution of the ebg gene
sequence. He demonstrated the evolution of lactase as well as a
number of other closely related enzymatic functions, each requiring a
single point mutation from the previous step for a total of 3 steps.
The problem is, such evolutionary sequences are quite limited. They
quickly come to walls that cannot be crossed by single point
mutations. Random drift must take over at this point. And, random
drift takes a lot longer to reach new functions, as detailed
previously. The specified functions that have been shown to evolve
have always been simple functions that arise via 1 or 2 point
mutations, such as the enzymatic functions of lactase or nylonase or
single point mutations that change target sequences that result in
bacterial antibiotic resistance. Really, these aren't the problem.
The problems come when the complexity of functions increases and there
are fewer and fewer sequences in the random pile that can perform such
functions.
> 2) We have excellent evidence from
> many sources that evolution does indeed happen, and new functions do
> evolve; you cannot therefore argue that new functions don't evolve, and
> are left to argue that the mechanism by which they evolve is not natural
> selection.
Where the heck do you get this notion? Obviously new functions have
and do evolve and this is via single point mutations/short random
drifts and natural selection. Random mutations and natural selection
are very powerful and real forces of nature. However, they become
very much limited as the complexity of function increases. Natural
selection doesn't work when all options are equal. Random drift takes
over but random drift takes a long time before it comes across
something that is selectable by nature. This is the problem you see.
The only way I know of to speed up this process is with the use of
intelligent guidance or "design".
> In that case, however, it would be important for you to
> suggest what that mechanism might be, and present some evidence for its
> existence at least.
What have I been doing? Where have you been? I have been suggesting
the mechanism of intelligent design all along. The evidence for ID is
the lack of a reasonable explanation of how neutral gaps between
various functions can be crossed without intelligent input from an
outside source. I have provided the experimental evidence that seems
to demonstrate that such gaps do in fact exist between what there is
in a given creature/colony and new specified functions, such as the
lactase function, in various bacterial strains (ie: Certain of Hall's
mutant E. coli strains, among many others). What more do you need?
> > For example, can you show
> > how a relatively complex function, such a bacterial motility (Any
> > type, not necessarily flagellar motility), could evolve where no
> > genetic gaps in function would need to be crossed? There are those
> > who suggest that there is no goal in evolution. Therefore, the
> > testing of a specific "goal" such as the evolution of a specific
> > function, such as motility, is not a valid challenge of evolution
> > since a given type of bacteria may evolve other equally complex
> > functions before motility is ever evolved.
> >
> > This is a great argument. For one thing, without a goal to defend,
> > there is no need to move goal posts as YECs are so often accused of
> > doing. Just because a particular function does not evolve, such as
> > the lactase function in certain of Hall's bacteria, does not mean that
> > evolution is having problems. It only means that evolution does not
> > need to travel down any particular path, regardless of the benefits
> > that would be realized if that path was traversed. Well, Ok... lets
> > go there. Naturalistic evolution obviously does not "know" which path
> > to choose. It can go down any path in any direction and eventually
> > get somewhere with some beneficial function. Sure it can. However,
> > what if each starting point is completely surrounded by a huge ocean
> > of neutral function or nonfunction?
>
> In that case, evolution by natural selection wouldn't get very far,
> assuming that the gaps between functional sequences were large. But I
> don't think they are, and there's evidence to support that belief.
Where? Where is this evidence to support your belief? It simply
isn't out there as far as anything I have come across so far. You
think that a significant percentage of potential amino acid sequences
of say, 500 or less, would be of some benefit to a particular colony
of E. coli? Please! Where do you get this notion? The total number
of possible proteins of this length boggles the mind. It is around
3e+650 (That's a 3 with 650 zeros after it). This is zillions of
times bigger than the total number of particles in the universe
(~1e+80). And, you think that a significant portion of this total
number of potential protein sequences of 500aa or less (take one at a
time) would benefit a particular E. coli bacterium in a given
environment? How so?
> > Consider that if there were 1
> > million defined 6-letter words that each word would, on average, be
> > surrounded by 300 non-defined words. No matter which way evolution
> > went, odds are that it would quickly run into a gap of nonfunction
> > that separates current function from new function. Try it. Starting
> > with a 6-letter word, how far can you go before you are blocked by a
> > gap of nonfunction? Now, if that seems hard, try to evolve a larger
> > sequence of letters, such as a sentence of words, one letter at a time
> > and see how far you can go before you are blocked by sequences of
> > nonfunction.
>
> I will agree that one can invent systems of this sort.
This is not an invention. This is really what is happening. It
happens not only in the English language system, but other coded
language systems as well, such as in computer language code or the
coded information contained in the DNA of living things. How is this
an invention? Where is the flaw in this parallel?
> >>How do you
> >>know there are such gaps? For eyesight, it has certainly been shown that
> >>there is a continuous series of slight morphological variants, each
> >>advantageous, from a patch of light-sensitive cells to a camera eye.
> >
> > A series of morphologic variants that appear to follow a smooth
> > evolution of very small steps is deceptive in that is covers up the
> > complexity of the genetics involved. If in fact every "slight"
> > morphologic variant was the result of an equivalently "slight" change
> > in the genetic code then you would be correct in your statement that
> > such a series of morphologic variants give convincing evidence of
> > common descent. However, there are several problems with such an
> > automatic assumption. One problem is that apparently small
> > morphologic changes often require relatively large changes in the
> > underlying genetic code.
>
>
> Personal pet peeve: you are using "genetic code" as a synonym for
> "sequence". But it has quite another meaning and your idiosyncratic
> usage merely causes confusion. The genetic code is the mapping of 3-base
> codons to amino acids, no more and no less.
There is a difference between THE Genetic Code (The code that defines
3-base codons), and the coded information contained by the order of
these codons, which is also a type of "genetic code". The sequence of
codons also "codes" for a sequence of amino acids. This information
is symbolic or "coded" via the order of codon sequence. Please, get
off your high horse. You know perfectly well what I am talking about
here.
> But to your main point: it may indeed be that the mapping between size
> of molecular and morphological changes is loose. But do you have any
> examples of this? There are certainly known cases in which small genetic
> changes can produce large morphological changes, and large molecular
> changes producing zero morphological changes. But do you have a case in
> which a small morphological change *requires* a large genetic change?
The burden of proof is really on you. You are the one who says that
the morphologic steps between various types of eyes from "simple" to
more "complex" are small. The point is that you cannot say this based
on morphology alone. You have to demonstrate that the *genetic* steps
between the various types of eyes are small. Even you understand and
agree that morphology can be deceptively simple, covering up a lot of
underlying complexity. What you think is a "small morphologic change"
may not be small at all when it comes to the genetics required. The
same is true for computer programming. A very small change in program
function may require quite a lot of change in underlying computer
code. You are the one who has to show that the "small" morphologic
steps are based on equally small genetic steps. Behe does a great job
in his book, "Darwin's Black Box" on explaining many of the underlying
genetic complexities involved in some apparently "small" morphologic
steps in certain evolutionary scenarios. These are the details that
Behe is talking about when he says that there are no detailed
evolutionary pathways in literature showing how something as complex
as a simple eye spot or a flagellum or even a cascade like the
glycolytic pathway or the blood clotting pathway could have evolved
(or even certain single protein enzymatic functions in a given
creature). Many have laughed at this saying that the evolutionary
pathways of such systems have been described in great detail, but
really, they have not been described in great genetic detail, mutation
by mutation, where there are no significant genetic gaps in advancing
beneficial function. Many suggested pathways are mainly based on
morphologic intermediates and those that do use amino acid sequences
make large leaps between various functional intermediates.
> > The same is true for computer functions.
> > Apparently "simple" or "small" changes in a program's function often
> > require comparably large changes in the underlying code. For example,
> > going from a "simple" eye spot or collection of light sensitive cells
> > to a slightly concave eye cavity spot, seems morphologically simple,
> > but the genetics involved are quite complex. All the cells involved in
> > the formation of this cavity must be programmed to relate with the
> > other cells in this area in a very specific way to form this
> > concavity. This orchestration requires many very specific genetic
> > changes. Gaps in beneficial function are certainly involved.
>
> That's just a series of unsupported assertions. Do you have anything to
> back it up?
Again, you are the one saying that morphology is all that is needed to
show that the steps are small. Well, since morphology is based on
genetics the steps you really need to be demonstrating are genetic
steps. What I am saying is that the burden of proof is with you. I
have given you many reason for my serious doubt concerning your
ability to demonstrate that the genetic gaps are small enough to
cross, but you have continually come back with morphologic arguments
and weak assertions that the genetic gaps must be small. But, you
really have no evidence to support yourself. You have no clue on how
to support the notion that random mutations combined with a mindless
nature can create such diversity as we find in living things. You and
other scientists have made a very bold claim that a mindless nature
can create even more fabulous things than we humans, with all our
creativity, brilliance, and imagination have been able to come up
with. This is quite a bold and counterintuitive assertion and it
requires impressive evidence for its support.
The evidence for my opinions here comes from everything that I have
learned about genetics, mechanical systems of function, and
language/coded systems of function. Many functions are deceptively
simple in appearance but require a large amount of informational input
in the form of code or individual interacting parts. Living things
are no different. Even "simple" eyespots are made up of a rather
large number of interacting parts. Any time you have multiple
interacting parts, a simple change such as the formation of a
concavity, requires many different changes in many different parts and
therefore genes. All of these changes must be complimentary or the
concavity will not form properly. The information for this concavity
must also be beneficial for the organism in its current environment
and then this information must be passed on to the offspring. Really,
the genetic complexity of something this simple is far more complex
than the required morphologic change would seem to suggest. I
challenge you to explain how the genetics involved in such a "simple"
morphologic change really are more simple than I am suggesting here.
I mean, Dawkins and others make up stories about how single cells in
the early oceans started clustering together in groups of cells and
then formed a cavity in the middle of the cells and then started
folding into this cavity . . . on an embryological type road to higher
complexity. However, these stories, although visually appealing, fail
not only in explaining how each morphologic step is beneficial, but
how each of these morphologic variants could be achieved genetically,
one mutation at a time where each change of a base in the DNA was
beneficial. It is very very complicated to "program" a cell to
cluster with other cells. This is not a simple thing to do. Once
this clustering activity is programmed, it is a very difficult thing
to program these cells to form a central cavity. Again, it seems
simple that once this cavity is there that it would be easy to program
the cells to fold into it, but this is also very complex. The order
of folding has to be established. Each cell has to be programmed as
to where it will be when the folding begins and ends and how it will
relate with the other cells around itself. This is incredibly
complicated stuff. Anyone who has studied the complexity of
embryology will be able to begin to appreciate this. In fact, it is
so complex that one marvels that any baby is ever born "normal".
Really truly, most "simple" morphologic changes or "intermediates" are
not at all simple.
> > Another
> > problem is that function is arbitrarily attached to code. Very
> > different codes can and do code for the same or similar functions and
> > very similar codes can and do code for very different functions.
> > Because of this arbitrary nature of code, a change in the code will
> > probably not result in an equivalent change in code function or
> > "morphology". Very small changes in code can result in huge changes
> > in morphology. Also, very large changes in code might not change
> > morphology/function very much at all.
>
> Are you talking about computer programs or genetics here? Your point is
> exceeding muddy.
Both. The above statement holds true for both computers as well as
the coded information in the DNA of living things. It also holds true
for other coded systems of information, such as the English language
system. Very small changes in the spelling of words may result in
huge changes in word or sentence meaning, and very large changes or
differences may not result in any significant change at all. All of
these coded systems work in a very similar way.
> > An argument based on morphology alone might seem compelling if that is
> > all that one had, but we know more now than Darwin knew. We know that
> > there is an underlying code or genotype that gives rise to morphology
> > or phenotype. If you can explain, genetically, how the gaps between
> > these various "small" differences in morphology can be explained, then
> > you would certainly win the Nobel Prize.
>
> Actually, there is no Nobel Prize in evolutionary biology, or even in
> biology. Just "medicine". And the gaps, so far, exist only by virture of
> your assertion.
Why do you think Watson and Crick won the Nobel Prize for their work
in detailing the structure of DNA? If you were able to detail the
mechanism of naturalistic evolution, you would certainly win the Nobel
Prize in something, even medicine . . . I have no doubt.
> > As of yet, I have found no
> > detailed genetic explanation or real-time experiment that explains or
> > demonstrates how the evolution of morphologic variants, such as the
> > morphologic eye variants or various bacterial motility systems,
> > evolved or even could have evolved.
>
> Yes, we don't know enough yet about the regulation of development to
> attempt such a detailed scenario for most features. It's a complex
> question. We are just beginning to understand the basics.
That's an understatement! ; ) All this confidence in the "truth" of
naturalistic evolution and yet hardly anything to base it on.
> >>I'm
> >>sure you are familiar with How would one go about demonstrating that
> >>there are or are not such gaps with respect to feathers?
>
> > Yes, try to evolve a feather or a feather-like structure or to
> > estimate how long it would take based on genetic sequence analysis,
> > mutations rates, functional genetic intermediates, and the length of
> > the average genetic pathway to such a function in a given creature.
> > Detail the genetic codes involved in coding for feathers and then
> > compare these codes to the codes that are available in other
> > non-feathered creatures and see if a genetic path could be detailed
> > and how long it would take to cross this path.
>
> Eventually, this should be possible. We need a lot of research before
> any of this is known in sufficient detail to do such tests.
Yeah . . . a LOT of research I am betting. In fact, I am betting
that it will never happen. The evidence is already overwhelming that
significant neutral gaps do in fact exist and that there is no
naturalistic explanation for how they were crossed or even could have
been crossed.
> >>We do know that
> >>feathers arose in a bipedal, non-flying dinosaur. That seems clear
> >>enough.
> >
> > Oh really? How so? Is there a gradual step-by-step demonstration of
> > this evolution in the fossil record?
>
> Not gradual enough for you, perhaps, but then again every new
> intermediate fossil automatically increases the number of gaps by one. I
> would say that Sinosauropteryx has very nice intermediates between
> feathers and non-feathers.
See Below . . .
> > Not any more than could be
> > detailed various creatures all living at the same time today.
>
> Well, no. All organisms alive today either have feathers or not, and are
> either quite derived birds or not. Feathers are rarely preserved, so we
> have much less an idea of feather evolution from fossils than we have of
> bird evolution in general. But there are certainly a great many
> feathered theropods these days. How do you explain them?
Of course, I explain them with the use of Intelligent Design. There
is no need to rely on any naturalistic process to explain the arrival
of feathers from non-feathered creatures. It seems to me that the
neutral gap is simply too wide to cross.
> > It is
> > the same argument as the evolution of simple to complex eyes. Get a
> > bunch of different kinds of eyes and line them up in a morphologic
> > sequence from more "simple" to more "complex". Obviously, once this
> > lineup is complete, the conclusion must follow that the simple eyes
> > gave rise to the more complex eyes. This might seem reasonable at
> > first glance, but this is not necessarily a correct conclusion.
> > Practically any collection of objects can be categorized in such a
> > manner, but this does not mean that these various object arose via
> > common descent... especially if the mechanism to adequately explain
> > such variations is weak. For example, the various books on my
> > bookshelf can be categorized in this manner, and just as convincingly,
> > from more "simple" to more "complex." But, this does not mean that
> > the more complex books arose via common descent from the less complex
> > books even if the changes between them seem to be relatively small.
> > You see, without an ability to detail a mechanism of change, the
> > differences and similarities, by themselves, do not necessarily
> > support the position of common descent.
>
> You mistake the point of the exercise. It's not to prove common descent
> (that's done by other means) but to refute the claim that intermediate
> conditions are impossible. (e.g. "What good is half an eye?") If
> intermediate conditions exist, no matter what the relationships among
> the organisms, the argument of impossibility is refuted.
This is ridiculous. Given any three objects, one of them can be
classed as an "intermediate" in some aspect or another between the
other two. That is how many phylogenetic trees are drawn up. Pick
any particular trait, and three objects will fall on some sort of
classifiable continuum. Of course, such classification systems need
not say anything whatsoever about origins or any other actual
relationship between the objects.
The argument of, "What good is half an eye?" is also lame in that it
does not detail exactly what half an eye is. Are we talking about
half a human eye? You know, it is easy to point out various types of
eyes and to declare that this type of eye is an "intermediate" or
"half way there" between two other types of eyes. But the fact of the
matter is that all eye types in all creatures are "all the way there."
There are no "simple" eyes or "half eyes" out there.
However, depending on your definition, "half an eye", as pointed out
by Dawkins many times, can be quite good indeed depending on what you
mean by the term "half". However, all eye types found in various
creatures are fully formed and quite complex. The question is, "What
good is each *genetic* step in getting from one type of eye to the
other?" That is the question. The question is not, "Can a
morphologic intermediate be found that could be classed between this
eye and that eye?" The question is, "Can I get from this eye to the
next eye with each genetic mutation being functionally beneficial?"
With this question in mind, I highly doubt it. Nothing even close has
ever been demonstrated. According to popular science, eyes should be
rather easy to evolve. After all, they have been successfully evolved
in different creatures some 40+ independent times . . . or so it is
said. The paths between different eyes should be well established.
We should see this eye evolution progressing at a very rapid rate
right before us. Why is it then that such demonstrations are lacking?
> >>Whether they arose by natural selection, or by any naturalistic
> >>pathway, is difficult to determine. I suppose you could, if you liked,
> >>support some kind of theistic evolution in which God gives the
> >>occasional nudge to get a genome across some functional gap. I'm not
> >>sure where you would find evidence for it, as there is for selection,
> >>and I'm pretty sure you would reject such a theory anyway. Right?
> >
> > The evidence that you have is one of morphology alone, not of
> > genetics. The morphologic evidence is not compelling enough to
> > adequately support the theory of common descent. You need genetic
> > evidence or some way to explain how the genetic gaps can be crossed.
>
> No you don't. You can reliably infer many phenomena without knowing the
> mechanisms that produced them. There is much genetic evidence for common
> descent. Your demand that the detailed mechanism be known before we can
> agee on the phenomenon itself is unreasonable.
Actually, if there is evidence that a mechanism is highly unlikely,
then the other evidences that you have that seems to indicate common
descent are rather weak and more easily and rationally explained by
the intelligent design of a common designer. To say that the designer
may have created over long periods of time does not take away from the
evidence for design. Design is design regardless of when or how it
happens, and the workings of intelligent, deliberate activity can be
detected with the use of the scientific method.
For example, lets say that I have a bucked of snails, some jars of
white, red, yellow, and blue paint, and a white canvas. I put the
snails, jars of paint, and canvas in a room and leave for the day.
When I come back the next day I see that the canvas has been painted
with a beautiful picture of my wife. I look and see the snails each
covered with a different color of paint wandering randomly around the
room. There is certainly evidence that the snails could have painted
this picture in front of me. It could have happened. But, given my
knowledge about the workings of snails and the statistics of "random
walk" to produce such a specified work as a painting of my wife, what
conclusion is most reasonable for me to come to?
You see, without a naturalistic mechanism evident to explain the
phenomena that I see before me, I must assume that the only other
mechanism that can perform such works was present sometime along the
way. . . Intelligent Design. That is my only other reasonable
option. If there is evidence of a need for random walk in the
evolution of new functions of various complexities, this evidence
speaks for a need for Intelligent Design, just as it spoke for a need
for higher intelligent input in my snail illustration. The gaps
themselves are positive evidence for design. That is Behe's whole
point and it seems like a very reasonable point to me.
> > Also, I find the standard interpretation of fossils and the geologic
> > column unconvincing and quite biased or colored by the a priori
> > assumptions of evolution and naturalism. I see no clear evidence that
> > feathers must have evolved from featherless creatures. The fossil
> > record is a static record and is thus quite limited in what it can
> > tell us about the lives and changes of creatures over time. You need
> > real-time examples detailing the actual genetic changes in life forms.
>
> This is unreasonable. You are saying that in order to show common
> descent, one must duplicate it in every particular. You would never
> require such an unreasonable standard for any inference that doesn't
> contradict your literal view of the bible.
What I am saying is that in order to convincingly show evidence for
common descent, you must explain how the neutral gaps between various
functions in living systems can be crossed via some naturalistic
process. Of course, you argue that common descent and naturalism are
different things. You argue that an intelligent agent could have been
involved with common descent and it would still be common descent.
But this is ridiculous. If an intelligent agent was involved with
changing creatures over time, then this is not common descent, but
slow creation. This would be slow creation using intelligent design.
This would not be anything at all like Darwinian evolution. Slow
creation is still creation via common design, not a naturalistic
common descent. The similarities and differences, in such a scenario,
would have been deliberately, intelligently created over time.
It also seems to me that your mention of the Bible here is quite
interesting. The theory of evolution, as with science in general, is
a statement of faith. No theory or even law of science, since it
concerns the subjective concepts of humans in our relation to an
external world outside of ourselves and our ultimate control, is
absolute. Truth concerning the external world can be approached but
never fully realized. No one ever discovers absolute truth about
anything concerning the external world. There always remains a degree
of faith that a particular understanding is in fact "true." The
movie, "The Matrix" does quite well in playing off of this concept.
Because of this, religion can be approached in a scientific manner.
All beliefs require testable evidence in their support if they are to
be believed to be more "true" than any other position or statement of
truth. Some beliefs have more evidence than others. The theory of
evolution certainly has evidence in its support, but it seems to me
that the weight of testable evidence and predictability (ie: the
scientific method) in clearly on the side of intelligent design when
it comes to the topic of origins.
> > Relying on morphology is easy to do, but it is rather weak when it
> > comes to explaining how the genetic codes themselves evolved via some
> > naturalistic process.
>
> Once again you conflate our ability to infer common descent with our
> ability to infer that the mechanism of change is natural selection (or
> some other naturalistic process). These ideas are independent.
No, they are not independent. Common descent implies a naturalistic
explanation. So far, the only viable choice is natural selection
combined with random mutation. All other viable choices involve some
sort of outside intelligent input/design.
> >>> If you think that a neutral gap in function
> >>>that requires just one protein sequence is hard to cross, try
> >>>
> > crossing
> >
> >>>a gap that requires the evolution of multiple proteins to cross where
> >>>hundreds or even many thousands of neutral mutations are needed.
> >>
> >>I agree that this scenario sounds unlikely. I just don't agree that it
> >>is necessary.
> >
> > Why not? What *genetic* explanation do you have to account for the
> > differences then?
>
> Natural selection?
Again, natural selection cannot work if all the different genetic
sequences/options are functionally neutral. Natural selection is
blind while neutral gaps are being crossed. What you are left with is
random chance/drift . . . and what can that do for ya? That is the
whole point of this argument. . . that natural selection is limited
by neutral gaps.
Actually, there is plenty to back it up. If each mutation were
beneficially functional between various functions such as feathers,
wings, eyes, legs, arms etc, then with a mutation rate of 250+
mutations per human per generation, such functions would be realized
in short order. There is no doubt about it. The statistical
calculations are clear.
> > The
> > problem is that the path is quite "twisty" indeed. The path is not
> > straight. That is the problem. The path is very curvy because of the
> > random drift problem. If each and every step is not selectively
> > advantageous, then evolution starts to wander around a neutral sea of
> > function. The wandering is very curvy or nonlinear. In fact, it is
> > such a curvy path that millions, billions, and trillions upon
> > trillions of years are simply not enough to traverse this path. The
> > "efficacy of selection" is dependent upon nature's ability to select
> > between different genetic changes. If the changes are "neutral" in
> > function then natural cannot select between different genetic
> > sequences that have the same function (or nonfunction). At this point
> > the "efficacy" of natural selection is severely limited.
>
> You merely assume what you want to prove. There are many possible
> constraints on the speed of selection. One, and one that's well
> supported by the fossil record, is that different intermediates fill
> different functions. The gill supports of a primitive vertebrate didn't
> become mammalian middle ear bones in one go. They first spent some time
> as jaw supports. The path to the middle ear (quite well documented by
> fossils) was quite windy, but the morphology was functional at all points.
Actually, if the different intermediates did different functions in
different environments, the new functions would rapidly arise as soon
as the environment changed. The environment is the only limiting
factor in this little scenario of yours. Change the environment where
ears become advantageous, and presto, the bridge between gill supports
and middle ear bones can be crossed in short order. If the next
mutation would lead to jaw bone supports, but the fish needed middle
ear bones, then this would be a detrimental gap in function. This
would be a block to evolution. However, if each step was beneficially
advantageous, then evolution would proceed extremely rapidly.
Of course, this is again an argument of morphology. It says nothing
about the underlying complexity of the changes in coded genetic
information that would be required to change the morphology of "gill
supports" into middle ear bones.
> >>>There are gaps between various functions that
> >>>require a lot of time to cross. In fact, many of these gaps seem so
> >>>wide that billions or even many trillions upon trillions of years are
> >>>simply not enough.
> >>>
> >>If there are, name one and show the evidence that it is such a gap.
> >
> > I already have. Depending on the complexity of the function in
> > question, the evidence for non-evolution can be found in comparing
> > what is available with what is needed. The lactase function in E.
> > coli is a good example of this non-evolution. When lacZ and ebg genes
> > are deleted from E. coli, they simply do not use any other genetic
> > sequence to evolve the lactase function despite being observed for
> > many thousands of generations while growing on selective media that
> > would benefit them if they were ever to evolve the lactase function
> > again. B. G. Hall himself described such E. coli colonies as having,
> > "limited evolutionary potential." Obviously these limits are there
> > and they are found in the form of neutral/nonfunctional genetic gaps
> > in function. All codes/language systems have these gaps. Human
> > languages, computer languages, and even genetic languages/codes have
> > these gaps. Natural selection cannot cross gaps in function in any
> > directed way. Without direction, mutations are purely random and
> > random changes wander around a very curvy path that simply takes to
> > long to come across new beneficial functions.
>
> Other people who know the subject better than I do have addressed this one.
Such as? Who are these people? No one that I have talked to has
explained this issue very well from my perspective. It seems to me
that if you are not very familiar with this subject that it would be
to your benefit for you to familiarize yourself with it as this is
where the rubber meets the road. . . in my opinion at least.
> >>>You know that naturalism is
> >>>the answer... without knowing how it works?
> >>>
> >>Did I mention naturalism? No. In fact I mentioned divine intervention as
> >>one potential mechanism. So your comments are irrelevant. I'm talking
> >>about common descent. Would you care to argue about the evidence for
> >>common descent?
> >
> > The theory of common descent is a naturalistic theory. It is an
> > argument from the position that nature and naturalistic processes can
> > explain the variety in living forms.
>
> No it isn't. What is theistic evolution (a quite popular theory among
> Christians) but an acceptance of common descent but a rejection of
> naturalism? These two aspects of evolution are entirely separable.
Theistic evolution is nothing more than slow creation. It is still a
theory of intelligent design . . . only spread out over a longer time.
Theistic evolution really isn't a theory of evolution at all. Every
new step was "created" or "designed". How is this evolution? It is
basically a theory of common design. If anything is evolving in this
theory, it is the imagination of the designer and the designer only .
. . not the creatures. No no, there are really only two theories.
One is the truly naturalistic theory of common descent, and the other
is the theory of intelligent design. Any time intelligence is
required, that is not evolution, but design.
> > You are therefore "mentioning
> > naturalism." You mentioned "divine intervention as one potential
> > mechanism" but you do not believe that this is the mechanism over the
> > idea that a naturalistic process is a more likely or reasonable
> > explanation.
>
> Yes, but that's just me. It serves to show that pattern and mechanism
> are separate theories.
No, it isn't just you. Pattern and mechanism go hand in hand. That
is why many scientists claim that the theory of evolution has allowed
them to be, "intellectually fulfilled atheists."
> > For myself, I'm not so much arguing for the identity of
> > the designer as I am for the fact that there is evidence of design,
> > from some intelligent source somewhere, in living things. Humans are
> > also capable of such designs in code and systems of function. Are we
> > therefore "divine"? No, but we certainly are capable of
> > "supernatural" activities in the sense that non-intelligent natural
> > processes, such as random mutation and natural selection, are
> > incapable of performing. A tree limb, as it is blown by the wind, may
> > break a window without relying on deliberate design or creative
> > intelligence. However, there is no naturalistic process for fixing
> > the window and putting it back in its place outside of deliberate
> > design/creative intelligence... regardless of where this intelligence
> > came from... be it divine or human or an intelligent alien from the
> > planet Zorg. Whatever the source of intelligence, the fact that
> > "supernatural" intelligence (ie: above the naturalistic
> > non-intelligent processes of a mindless nature) was required can be
> > detected.
>
> Unsupported assertion, but certainly a possible position.
Unsupported? You think that deliberate design is impossible to
detect? Please . . . it happens all the time. It is in fact a part
of science. For example, what do you think forensic science is all
about?
> The question
> I'm most interested in, however, is whether you would accept the
> possibility that the designer intervened in a process involving common
> descent rather than using fiat creation of unrelated kinds.
Again, any time a designer is involved, the changes that result can't
be called evolution or common descent. The changes that require a
designer are not the result of "common descent" but are instead the
result of common design.
> >>I didn't mention anything about random mutations. I'm talking about
> >>common descent. Common descent is separable from the mechanism that
> >>causes adaptation. You, as a creationist, deny common descent. I'm
> >>saying that if, somehow, you were to show that natural selection is
> >>insufficient as a driving mechanism, then the evidence for common
> >>descent would remain untouched and conclusive.
> >
> > Not so. Without a knowledge of the mechanism of common descent, the
> > evidence for common descent is far from "conclusive." Common descent
> > is not a forgone conclusion, especially if the mechanistic explanation
> > fails.
>
> We appear to have a basic disagreement here. Would you agree that we
> know things fall down, even though we don't have a clear understanding
> of what gravity is? Would you agree that the existence of atoms was
> established by Dalton, Lavoisier, and others long before we had any idea
> of atomic structure or quantum mechanics?
Yes, many things are believed to happen without knowing how they
happen. This is what Behe refers to as Darwin's black box. Darwin
saw that changes happen so he made a very logical link to think that
perhaps such changes could add up over time to allow for all life
forms to have a common ancestor. Given the information at hand, this
seemed like a very reasonable prediction even without knowing anything
about the mechanism. Of course, Darwin did in fact propose the
mechanism of random change and natural selection. This also seemed
quite reasonable given the information at the time. However, now we
know about genetics and the appearance of more complexity than Darwin
could ever have imagined. What once seemed like a relatively short
morphologic step now because a rather huge genetic step to cross.
You see, the evidence that once was so compelling is being challenged
by new evidence that is even more compelling against a previous
understanding. We are now able to look into the black box that Darwin
wasn't able to see into. In this box we see that the mechanism
proposed by Darwin fails. With a failed mechanism as well as an
ability to explain the changes that Darwin saw with the use of
Mendelian genetics as well as certain small changes in function that
arise via point mutations and short drifts of random chance, we must
conclude that some other force is at work besides natural selection
that explains the diversity of life forms and functions that we see
all around us.
The complexity of genetics puts a significant block in the way of
thinking that such changes were really the result of random mutation
and natural selection. Something else must have been involved. The
other evidences of the fossil record and genetic similarities are
rather weak in comparison, especially considering that much about the
fossil record is incomplete, inconclusive, subjectively interpreted,
contradictory, and more easily interpreted in other ways besides the
standard ways of modern science. For example, there is good evidence
for the relatively rapid formation of the geologic column. Also,
phylogenetic trees and other subjective classification models are
often inconclusive or even contradictory. Many things can be classed
according to various similarities and differences, which have nothing
at all to do with their common origin. But there are some better
evidences for common descent. Perhaps the best independent evidence
in genetics for common descent are the shared "mistakes" and
pseudogenes within widely differing morphologic groups. However, it
is being learned that many so called pseudogenes are not really pseudo
at all, but do in fact have function and that certain shared
"mistakes" are also functional or are located in mutational "hot
spots." This all puts more weight on the idea that neutral gaps
really are a significant problem for the theory of evolution.
> >>>You obviously have a very great faith in the power of naturalism to
> >>>answer all questions pertaining to the physical universe. For you,
> >>>the very notion that there just might be evidence of design in the
> >>>natural world/universe is simply out of the question.
> >>>
> >>I said nothing whatsoever either for or against design. I'm not talking
> >>about design. I'm talking about common descent. Is that clear?
> >
> > When you are arguing in favor of common descent, you are arguing
> > against design. The theory of common descent is a theory that tries
> > to propose a naturalistic cause, outside of design, to the existence
> > of various life forms. So, really, you are talking about design.
> > Whether or not you admit it or realize it is another issue.
>
> No it isn't. The theory of common descent proposes that all life forms
> are descended from a common ancestral population through descent with
> modification. How that modification was accomplished, whether through
> natural or supernatural means, is another question entirely.
Not it isn't. If an outside source of intelligence was responsible
for the changes over time, then all live forms did not arise from the
evolutionary potential of an ancestral life form. They arose through
intelligent design over time. The common source was not an ancestral
population, but a common designer who chose which way various
creatures would change. You do understand this I hope. The modern
theory of common descent really has nothing at all to do with the idea
of any sort of outside input of intelligence or deliberate design. To
say otherwise is really heresy according to popular science today.
> >>I happen to believe, based on the evidence,
> >>that natural selection is a pretty good mechanism and that evolution has
> >>indeed proceeded "naturally" (and there is considerable evidence
> >>that evolution has no particular goal), but that's not at all what I'm
> >>talking about here. Your inability to separate "darwinism" into
> >>independent components is causing a communication failure.
> >
> > You would like to think that one component has no bearing on the other
> > components of the theory, but the fact of the matter is that all the
> > components of Darwinism are intimately intertwined. If one basic
> > component fails, the whole thing fails. I suppose you could say that
> > the theory of evolution is... "irreducibly complex." ; )
>
> What is your logical basis for making this claim?
I've already detailed my "logical basis" above. In short though,
intelligent design is intelligent design if it be long or short in the
process and cannot be called "evolution" except if it be in the sense
of the evolution of the thoughts of the designer. Darwinian evolution
is purely naturalistic. There is no room for any sort of deliberate
intelligence to be involved in the process . . . only a mindless
nature.
> >>Actually, under normal conditions most mutations occur during DNA
> >>replication, which I believe does occur simultaneously with cell
> >>division in most prokaryotes.
> >
> > Yes, this is true. However, these mutations, once they occur, are
> > passed on from one generation to the next.
>
> That point was not in contention, so I have no idea why you brought it up.
Only a point of clarification.
> >>>However, once the mutations occur, these mutations
> >>>are passed on to the bacterium's clonal offspring via the
> >>>division/replication/mitotic process.
> >>>
> >>Mitosis is something that happens in eukaryotes, not prokaryotes.
> >
> > True again, but prokaryotic replication/division is similar to
> > eukaryotic mitosis. The offspring are "clonal" in both cases.
>
> Right. I just want you to be careful about your terminology.
Please . . . give me a break.
I haven't had the time yet to read Hayashi et al. 2003. Please, fill
me in on the details. Until then, I will try to find and read his
paper. I highly doubt though that he found what you say he found.
The proportion of beneficially functional sequences must be studied
from the perspective of a given cell in a given environment. I highly
doubt this was done by Hayashi.
> [snip more repetition of large, made-up numbers]
>
> >>>In the replacement of a particular base in a sequence of DNA, the
> >>>replacement could replace the base at the position in question with
> >>>the same base 1/4th of the time. Therefore, the odds that a given
> >>>"change" will result in a specific base are 1 in 4.
> >>>
> >>If a base is replaced with the same base we don't call it a mutation. We
> >>don't call it anything, except maybe "replication". A mutation rate that
> >>includes "no change" would be a rate of 1 per site per generation, since
> >>every site will either change or not change. You really need to fix this.
> >
> > Ok... I've thought about this point further and you've got me here. I
> > will fix this. Thanks for pointing out this error, but it really has
> > no significant bearing on the point at hand. Be the odds 1 in 4 or 1
> > in 3 makes no real difference as far as the problem is concerned.
>
> Agreed. But the difficulty I had in convincing you of one simple
> mathematical error should give you pause, at least.
Oh, it did cause me a second or so of pause, but it wasn't significant
to my argument. Also, I wouldn't call your convincing me of this
error "difficult". It only took two tries and it took even that long
because I thought it such a minor point that I really didn't even
consider it when you first mentioned it. So, how difficult was that?
In any case, it doesn't seem like you are all that easy to convince of
error yourself ; ) But, it does seem to me that at least you are
trying to be honest with me and with yourself, so I do give you credit
for that. Other's in this forum are not generally like that.
> >>Well, it [neutral evolution] does say how neutral gaps can be crossed. With low probability,
> >>getting lower as the size of the gap increases. If there is a large
> >>neutral gap between two functional proteins it is unlikely to be
> >>crossed. But who says that such gaps are prevalent?
> >
> > You are one of the more reasonable evolutionists that I have come
> > across. At least you recognize the problem and seek a reasonable
> > solution, such as the idea that such gaps do not exist. If such gaps
> > really did not exist, then yes, evolution would not present a problem
> > at all. However, it seems like you understand that if such gaps do
> > exist that they would actually present a significant problem for your
> > theory.
>
> Not quite. Such gaps must not only exist, they must be overwhelmingly
> prevalent, such that few separate functions are connected without such gaps.
Exactly. . . but the fact that you at least recognize this is still
saying something. Many evolutionists that I talk to never get this
far.
Sean
Von Smith
Well said! I have pointed out before that design as we humans know it
is a response to constraints. IDers like to dodge issues like these
by saying that they don't "speculate as to the nature of the
designer", apparently not realizing (or not wanting to acknowledge)
that the whole point is that the mere assumption of design implicitly
requires all sorts of such speculations.
Von Smith
Fortuna nimis dat multis, satis nulli.
> Tom S.
zoe_althrop
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
<snipping excellent but lengthy material, because my brief post would
be lost in it.>
Thanks, Sean, for another impressive post that reveals your erudition
and wisdom. I understood your points, and can learn a lot from you.
Thanks, too, John, for being the kind of mature and reasoned poster
that Dr. Pitman can have a reasonable discussion with. It was a
pleasure watching two minds sharpen off of each other.
----
zoe
Frank J
> keeping with my new understanding of the probabilities involved (with
> the help of the binomial equation), the statistics certainly don't
> help you out of the gap-crossing problem.
>
> > > If the starting sequence was three mutations away from the desired
> > > function, the odds of getting all three mutations right shoots up to 1
> > > in 735,157,333,333,333,333,333 (~735 million trillion) mutations. With
> > > these odds, the correct mutation will occur in one bacterium in
> > > 1,792,682 generations. With a generation time of 20 minutes, that's a
> > > bit over 68 years.
> >
> > You can't calculate the probabilities like that because they aren't
> > independent. You have to calculate the probabilities based on the
> > actual situation. Once you have one mutation, you don't have to get
> > it again. You can as often as you like, but the second mutation would
> > occur in a bacterium that already had the mutation. Like you
> > indicated by your own calculations 315 bacteria would have any one of
> > the three. Close to 1000 in just the first generation would have one
> > of the three. How many in the second generation? The 100th? The
> > chance of two is the mutation rate in those bacteria that already have
> > one. Your numbers collapse dramatically, and even more dramatically
> > if the mutations were not neutral, but had some selective advantage
> > that allowed them to increase in frequency in the population.
>
> First off, by definition a "neutral" mutation has no selective
> advantage. This is the point. Because of this, nature does not
> preferentially select to increase their frequency in a population.
> words, they allowed for the build up of additional mutations.
>
> > > > It looks like Hall has met your
> > > > challenge with the system you are trying to say supports your contention
> > > > that it is impossible.
> > >
> > > I never said that a neutral gap of 3 mutations was "impossible." I
> > > said that depending on function complexity that certain gaps of such
> > > lengths or larger would be impossible for neutral evolution to cross
> > > in a reasonable amount of time. Where has Hall demonstrated this to
> > > be incorrect?
> >
> > Yes, by any standard. How many man hours do you think the experiment
> > took. Probably less than 6 months worth of experiments, and more
> > likely just a couple of weeks. He may have been working on this
> > problem since the 1970s but his bacteria were probably in the freezer
> > most of that time.
>
> Still, 10s or even hundreds of thousands of generations were in fact
> been in any freezers since the 1970s (ie: Salmonella, Proteus, etc)
> that still do not have lactase ability, despite its relative
> simplicity of function, and despite having experience over a million
> generations with huge populations sizes under selection pressures that
> would benefit such bacteria if they ever did evolve the lactase
> function.
>
> > > He still hasn't demonstrated the evolution of the
> > > lactase function in E. coli lacking both the lacZ as well as the ebg
> > > genes. Why is this?
> >
> > He doesn't do the experiments like they would happen in nature? He
> > never lets the bacterium have a chance to evolve the number of
> > mutations that are needed to get activity using some other protein?
>
> Yes, Hall does in fact do the experiments as they would be expected to
> happen in nature. This is a non-argument. The reason why the
> bacteria aren't given a chance to evolve the number of mutations that
> are needed is because the time required to evolve such specified
> to live thousands or millions of years.
>
> > > The only logical reason for such a limitation to
> > > the evolution of the lactase function in such bacterial colonies
> > > (despite the potential benefits if they were able to evolve this
> > > function) is that there is a gap in function between the lactase
> > > function and the collective genomic real estate potential of Hall's E.
> > > coli colonies... even given hundreds of thousands of generations.
> >
> > This is pretty bogus because you have to admit that it happened once
> > in only 2000 proteins found in E. coli. From the couple of other
> > bacteria that he has been able to do this with it has happened in them
> > too, and different proteins were involved in those activities. So
> > what is your problem. It seems like it isn't so special. Demonstrate
> > that it is. If it is so hard, why was he able to do it again in other
> > species?
>
> The reason why it is a problem is that when you remove the egb gene,
> species despite 50+ years of observation and selective pressures.
> Granted, the lactase function does appear to be a rather simple
> enzymatic function that can be performed by a single protein sequence
> working alone. The fact that such a relatively simple function is
> difficult to evolve in various types of bacteria is quite interesting.
> If a simple enzymatic function is so difficult to evolve, what about
> more complex functions that require multiple proteins all working
> together simultaneously? The gaps rapidly get quite enormous as the
> complexity of function increases. If you think it is fortunate for 1
> out of 2000 proteins to be able to evolve a relatively simple function
> like the lactase function, try figuring out the odds of getting a more
>
> > > > Why don't you research the work more carefully
> > > > before making these types of mistakes?
> > >
> > > LOL - Why don't you? You evidently do not understand the experiments
> > > that you are trying to use to support your position.
> >
> > Demonstrate that you understand the experiments, and that they tell
> > you what you think that they are telling you.
>
But ID is not itself a mechanism, so it has nothing to offer but
incredulity. Perhaps if you were to offer a molecular organization,
molecular drive, or genomic potential mechanism, all of which have
been postulated (and mostly ignored by anti-evolutionists), then you
might have something worth pursuing.
(snip)
Ron Okimoto
zoe_althrop wrote:
Sean, if you see Zoe's post it should give you a chill instead of a warm
fuzzy feeling. If you read her posts you know that Zoe has trouble
working through arguments. To be blunt she can't seem to think her way
out of a paper bag. This is one of the worst things about creationist
clap trap. It sucks people like you in and you just spread it around,
without verifying it. It is slick propaganda, but have you found a
single argument that you are proud to put forward? If you have what is
it?
I was appalled the first time that I saw Gish give a presentation. I
couldn't imagine that someone that claimed to be a scientist could be
that dishonest, but that wasn't the worst. They had some Bible
conference using our university basketball arena and he spoke to
Christian High School students and he was even more dishonest. He could
have told them anything, and they would have gone away thinking that
their beliefs were supported, but he chose to give even a worse speel
than he had for the university audience. Shouldn't he have been more
careful with the ignorant than he was with the audience that knew
better? These are the types of people that you are getting your
arguments from. You know it, but for some reason you want to believe
them more than your own sense of self respect.
Have you found a single honest creationist scientific argument? What is
it? Is it really worth anything? Isn't it strange that the arguments
that sound the best aren't honest arguments? What kind of people
present arguments that only have value if the audience is made to
misunderstand what is being argued?
Ron Okimoto
John Harshman
Sean Pitman wrote:
> John Harshman pontificated:
[snip the whole thing]
This post is becoming way too unwieldy. I printed it out so as to make
an attempt at seeing the whole thing, and it came to 26 pages of small
type. I will attempt to respond more at some later point, but here I'm
trying to deal with two small goals: 1) to convince you that common
descent and intelligent design are not mutually exclusive propositions
and 2) to acquaint you with the gist of Hayashi et al.
First, common descent and intelligent design. I take the first to mean
that all species alive today are descended from one (or at any rate a
very few) ancestral species by a continuous (and in sexual organisms,
reticulating) series of invidual parents and offspring. I take the
second to mean that the origins of major features of living species were
guided by some intelligent being(s).
As evidence that they are not mutually exclusive, I offer you examples
of people who believe in both: 1) Alfred Russell Wallace, though he
believed that natural selection could account for most features of
organisms, believed that divine intervention was necessary to explain
the origin of human intelligence; that is, he believed that we are
related to apes by descent, but that our transition to intelligence must
have been guided. 2) Charlie Wagner, fairly frequent poster to TO,
believes in common descent, but also believes like you that natural
selection is impotent; he thinks that all the subsequent diversity of
life was pre-programmed into the first unicellular organisms. 3) Michael
Behe, whom you cite so often, believes in common descent. It's not
entirely clear what view he has of how the intelligent design was
accomplished; at times, like Charlie, he seems to suggest
pre-programming. The other obvious alternative would be the occasional
directed mutation(s) of whatever size was necessary.
Further, many creationists believe in common descent within limits. That
is, they believe that a single kind, created as a single original
species, can develop over time into multiple species. So a single
"horse" kind can include not only horses (Equus caballus) but donkeys,
zebras, quaggas, and the various extinct horses. If you go with that,
our argument is not about common descent, which we both agree on, but on
the original number of kinds. I go with one, and you with many. (How
many would you estimate, by the way?)
Add to that the millions of Christians who are, according to polls,
theistic evolutionists, which means they accept common descent but
believe that God guided the course of evolution in some fashion. Some of
these believe he just set up the initial conditions so that evolution,
proceeding naturally, would end up where he wanted; that would be
contrary to your views. But others believe, as did Wallace, in direct
intervention at various stages.
If you reject the possibility of common descent combined with
intelligent design (let's call it CD/ID), I would be interested to know
why. What evidence can you present that argues against the CD/ID theory?
And now, on to Hayashi, Y., H. Sakata, Y. Makino, I. Urabe, and T. Yomo.
2003. Can an arbitrary sequence evolve towards acquiring a biological
function. J. Mol. Evol. 56:162-168.
Here, typed in at great personal cost, is the abstract:
To explore the possibility that an arbitrary sequence can evolve towards
acquiring functional role when fused with other pre-existing protein
modules, we replaced the D2 domain of the fd-tet phage genome with the
soluble random polypeptide RP3-42. The replacement yielded an fr-RP
defective phage that is six-order magnitude lower infectivity than the
wild-type ft-tet phage. The evolvability of RP3-42 was investigated
through iterative mutation and selection. Each generation consists of a
maximum of ten arbitrarily chosen clones, whereby the clone with highest
infectivity was selected to be the parent clone of the generation that
followed. The eperimental evolution attested that, from an initial
single random sequence, there will be selectable variation in a property
of interest and that the property in question was able to improve over
several generations. fd-7, the clone with highest infectivity at the end
of the experimental evolution, showed a 240-fold increase in infectivity
as compared to its origin, fd-RP. Analysis by phage ELISA using anti-M13
antibody and anti-T7 antibody revealed that about 37-fold increase in
the infectivity of fd-7 was attributed to changes in the molecular
property of the single polypeptide that replaced the D2 domain of the
g3p protein. This study therefore exemplifies the process of a random
polypeptide generating a functional role in rejuvenating the infectivity
of a defective baceteriophage when fused to some preexisting protein
modules, indicating that an arbitrary sequence can evolve toward
acquiring a functional role. Overall, this study could herald the
conception of new perspective regarding primordial polypeptides in the
field of molecular evolution.
A few more facts: RP3-42 (the replacement domain) is an ORF that
produces a polypeptide 139 residues long that has no secondary
structure. g3p is the "minor coat protein" with, obviously, an essential
role in getting the phage genome into bacterial cells. The replaced
domain is the middle one of three, and when it's working, it "functions
for the adsorption of g3p to the tip of the host F-pilus at the initial
stage of the infection process". fd-tet is a phage containing a
tetracycline-resistance gene, and thus only infected bacteria would grow
colonies in a tetracycline-containing medium. Infectivity was assayed by
counting colonies. The 250-fold increase in activity was achieved in 7
"generations". I use the quotes becase mutation was not done in the
phage itself, but by "error-prone PCR", in vitro, and the mutated
sequences inserted into fresh phage. In this way they insured that all
evolution that occurred was occurring in the random sequence. The
sequence was then snipped out of chosen phage clones after each
infectivity assay, subjected to more error-prone PCR, and stuck back
into fresh phage. By the 7th generation, the most infective phage had
experienced 26 replacement substitutions (as well as 11 silent
substitutions).
Would you agree that infectivity is a complex function?
Sean Pitman
In reply to your comments from the following links:
1: http://groups.google.com/groups?q=g:thl617408433d&dq=&hl=en&lr=&ie=UTF-8>&
selm=3EB6F5D8.4060000%40pacbell.net
2: http://groups.google.com/groups?q=g:thl591091078d&dq=&hl=en&lr=&ie=UTF-8>&
selm=3EB44CA6.9070808%40pacbell.net
> This post is becoming way too unwieldy. I printed it out so as to make
> an attempt at seeing the whole thing, and it came to 26 pages of small
> type. I will attempt to respond more at some later point, but here I'm
> trying to deal with two small goals: 1) to convince you that common
> descent and intelligent design are not mutually exclusive propositions
> and 2) to acquaint you with the gist of Hayashi et al.
Yes, this post is becoming quite lengthy. I thought about writing a
summary response to your last comments, but I was in too much of a
hurry to take the time to summarize everything, so I ended up
responding line by line. I do hope though that you at least read my
previous comments before making this summary reply.
> First, common descent and intelligent design. I take the first to mean
> that all species alive today are descended from one (or at any rate a
> very few) ancestral species by a continuous (and in sexual organisms,
> reticulating) series of individual parents and offspring. I take the
> second to mean that the origins of major features of living species were
> guided by some intelligent being(s).
I agree pretty much with your definitions here. Obviously common
descent of living things has happened and does happen. Changes, both
genotypic and phenotypic, certainly do occur. Our discussion is one of
the degree of change that can happen over time. If the degree of
change is greater than can be explained by a purely naturalistic
process, then the only other reasonable option that I know involves
some sort of outside intelligent agent who adds some creative input.
Of course, you are arguing that the concepts of common descent and
intelligent design are not mutually exclusive. It depends upon what
you mean when you try to combine these two ideas. If you are
proposing a scenario where a designer created an original life form
and then over time modified that original life form with the use of
deliberate design/creativity, to produce other life forms, then yes,
that could have happened. But, what would you call such tampering or
intelligent modification by an outside intelligent force? Would you
call that, "change by the process of evolution" or would you call
that, "change by the process of design"? For example, if a scientist
takes a clonal bacterial colony and inserts genetic information into
members of that bacterial colony, which makes them more "fit" in a
given environment, can it be said that these bacteria "evolved" from
those bacteria that came before? Do their similarities explain the
differences? No. Obviously not. Proving similarity does not in any
way rule out the possibility of common design. Similarities do not
necessitate a common evolutionary origin over a common deliberate or
designed origin. So, how can one tell the differences between the
creations of a mindless or "natural" process and the workings of
deliberate, intelligent, design? Only by looking at the differences.
The similarities do not provide an adequate answer since both
naturalistic processes as well as deliberate design can explain the
maintenance of similarities over time. Therefore, it is in the
differences where the questions of origins really must be answered.
If the differences can be explained without the use of intelligent
design, then the naturalistic theory of evolution is the only logical
default. Obviously then, in our hypothetical example of a scientist
deliberately inserting genetic information into bacteria, the new
genetic material was created and inserted via *intelligent design*. I
think we would both agree on this. No "evolution" took place here.
Creation via intelligent purposeful design took place here. You see,
there is a difference between the ideas of evolution and intelligent
design. The theory of evolution is certainly a naturalistic theory
based on the workings and creative potential of a mindless nature
while the theory of intelligent design proposes that there are simply
some differences that exist between various life forms that simple
cannot be explained by the workings of a mindless nature, even given
googles of years of time.
Someone might say that the naturalistic theory of evolution explains
"many" of the differences. But, as soon as they say that design is
required to explain even one difference they become creationists at
that point. Theistic "evolutionists" are really creationists . . .
to one degree or another. They just don't like to use that nasty word
"creationists" when they describe themselves. They like to think of
themselves as evolutionists, but really, they are, at some point,
creationists trying to fit in with the popular views and terminology
of the popular scientific community. I mean, come on now, even I
could call myself a theistic evolutionist. I believe in common
descent as well as the power of a mindless nature to produce certain
limited functional changes over time. I just do not believe that a
great many of the differences that do exist between various life forms
can be explained by the workings of a mindless nature. Because of
this, I believe that it is far more honest for me to call myself a
creationist.
You see, in order to use the term "evolution" to explain a particular
change over time, intelligent design cannot be involved in the
process. Any time intelligent design is required for a change to
occur, the correct description of that even is "creation", not
"evolution."
So, when you argue that the theory of "common descent" can explain all
the differences in the various life forms that exist today, you are in
fact proposing a naturalistic process of change. You cannot speak of
common descent in the context of change over time without invoking
some explanation or mechanism for that change. You must either use a
mindless naturalistic explanation or the explanation of higher
purposeful intelligence. There is no other option. The proposal of
one or the other of these mechanisms as well as evidence to support
one of these two views is vital to one's own understanding of origins.
So, in reality, you are proposing that a naturalistic mechanism did
in fact give rise to the differences that we see between various life
forms. And, in fact, you do believe that such a naturalistic process
produced all the various life forms starting from a single "primitive"
bacterial-type ancestor life form. So, do not try and tell me that
the theories of evolution and design are not mutually exclusive,
because, fundamentally, they really are. The moment intelligent
design is used to explain the existence of a particular change is the
moment evolution dies . . . at least for that moment or during that
particular process of change. Evolution cannot exist where
intelligence is required. Why? Because the processes of naturalistic
mindless evolution and the processes of intelligent design are in fact
mutually exclusive concepts.
> As evidence that they are not mutually exclusive, I offer you examples
> of people who believe in both: 1) Alfred Russell Wallace, though he
> believed that natural selection could account for most features of
> organisms, believed that divine intervention was necessary to explain
> the origin of human intelligence; that is, he believed that we are
> related to apes by descent, but that our transition to intelligence must
> have been guided. 2) Charlie Wagner, fairly frequent poster to TO,
> believes in common descent, but also believes like you that natural
> selection is impotent; he thinks that all the subsequent diversity of
> life was pre-programmed into the first unicellular organisms. 3) Michael
> Behe, whom you cite so often, believes in common descent. It's not
> entirely clear what view he has of how the intelligent design was
> accomplished; at times, like Charlie, he seems to suggest
> pre-programming. The other obvious alternative would be the occasional
> directed mutation(s) of whatever size was necessary.
Fast creation or slow step-by-step creation . . . it doesn't really
matter as both concepts/theories require intelligent design. Both
positions are really positions that invoke or require the input of
some source of higher intelligence and deliberate creativity. As such,
both creationists and theistic evolutionists hold the same basic
position.
From your description of his position, Charlie Wagner's view that the
first life form was pre-programmed with the ability to produce all the
variety that we see around us, is a very strange notion, especially if
he believes that natural selection is lacking as an adequate mechanism
for change. Without natural selection, what would cause the first life
form to produce such a variety of other forms? Also, what evidence
would Wagner provide to support his idea that natural selection is
weak if he still believes that all current life forms have a common
ancestor? If all current life forms do in fact have a common ancestor,
then what is there to challenge the idea that natural selection did in
fact play a prominent role in the diversification of life forms even
if the very first life form was pre-programmed for diversity? After
all, Mendelian genetics allows for a huge amount of phenotypic
variation without the need for mutations. The ability for great
variation has been proven to be "pre-programmed" into many creatures
without any need for reliance on random mutations at all. However,
natural selection still plays a significant role in the expression of
certain variations that are based on Mendelian inheritance. So, it
seems to me that Wagner's position has either been misrepresented or
that it is inconsistent with itself.
Alfred Russell Wallace's view that common descent made everything
except for human intelligence still requires the input of intelligent
design. He sees a limit whereby random mutations and natural selection
cannot account for something. Thus, he employs the power of
intelligent design to help him out. He is in fact a creationist at
that point.
Now, a person may believe that evolution proceeds normally "to a
point", but then requires some sort of help after that point. This
point may be different for different people. Behe, for example, thinks
that help is needed far before many other scientists (such as certain
theistic evolutionists) think that help may be needed. Behe believes
in common descent . . . to a point. He is not really all that clear on
exactly where that point is, but clearly he sees the existence of many
functions as being beyond the capabilities of purely mindless
naturalistic mechanisms.
I am in a similar boat. I obviously believe in common descent to a
point. I believe that purely naturalistic mechanisms do have the power
to give rise to many functional variations over time, but that the
creative power of purely mindless naturalistic mechanisms is
significantly limited. For example, I think that there is very good
evidence that donkey's and horses, among other such creatures, share a
common ancestor. I have even put together a paper explaining my views
on this at:
http://naturalselection.0catch.com/Files2/donkeyshorsesmules.html
However, I also think that there is very good evidence that many
functions are beyond the abilities of mutation and natural selection
to achieve. Like Behe, I believe that such functions show clear
evidence of intelligent design.
> Further, many creationists believe in common descent within limits. That
> is, they believe that a single kind, created as a single original
> species, can develop over time into multiple species. So a single
> "horse" kind can include not only horses (Equus caballus) but donkeys,
> zebras, quaggas, and the various extinct horses. If you go with that,
> our argument is not about common descent, which we both agree on, but on
> the original number of kinds. I go with one, and you with many. (How
> many would you estimate, by the way?)
Yes, we are really talking about the original number of "kinds." You
believe that just one kind of life form was needed to produce the
variety that we see all around us, while I believe that no single life
form could have had the potential to give rise to the variety that we
see around us.
It is true that some people believe that the original life form was
extremely advanced, containing all the potential for the genetic
variability of all life forms. However, not only do I see no evidence
for such a position, I see no method or logic means by which such a
"super ancestor" could have produced the variations in life forms that
we see today via some naturalistic process.
For me, I do believe in common descent within limits. I believe in
fairly static although somewhat plastic or flexible "kinds". But what
is my definition of "kind"? For me, a "kind" is basically made up of a
fairly "static" or "unchanging" gene pool of options. This gene pool
can give rise to a huge number of different phenotypic forms. But,
the options (potential functions contained in the gene pool)
themselves do not significantly increase in number or evolve to new
types of functions. There is limited allelic evolution that does in
fact produce novel beneficial functions in certain situations, but, as
described earlier, these new functions are universally simple, almost
always requiring a single protein, often with enzymatic type functions
that arise from one or two point mutations.
These original kinds or gene pools obviously could and did produce
many different phenotypic forms, often quite dramatically different,
over time. Some would classify many of these different forms into
different species or genus groups, or even higher. Now, I do take some
issue with the current classification systems in that it is often used
to imply that when different creatures are classed in different
species groups or higher, that completely separate gene pools,
functions, and breeding capabilities are involved. It seems to me that
this classification system is often quite subjective and that it says
little about the actual gene pool differences. Often various creatures
have been classed in different species, genus or even higher groups,
based on morphologic differences alone, only to find out later that
they where capable of interbreeding and producing viable, even
fertile, offspring. Also, as is the case between horses and donkeys,
the offspring need not be fertile in order for horses and donkeys to
share the same genetic information.
Now, I am not capable of listing off an exact number of original
"kinds" or gene pools that I think would have had to be initially
created, but I am thinking it was a lot more than you are thinking it
was. But, I will give you something more to chew on than most
creationists would give you. . .
The big issue for most creationists is the proposed evolutionary link
between humans and apes. Even though I personally believe that humans
did not evolve from apes, I also believe that conclusive evidence to
support my opinion in this particular case, is lacking. There is no
good functional genetic distinction, that I currently know of, between
the genetics of humans and apes, to rule out the possibility that
humans and apes share a common evolutionary ancestor. Of course, the
evolutionists are in the same boat with all their fossil and even
genetic evidence. The evidence is vague at best yielding many
inconclusive and even contradictory theories. Basically, from my
perspective at least, the evidence for or against the relationship of
humans and apes is far from conclusive either way one looks at it.
However, this is not what I am most concerned about. I am concerned
about the gaps between the genetic functions of many other creatures
that are clearly wider than what any known naturalistic process could
overcome.
> Add to that the millions of Christians who are, according to polls,
> theistic evolutionists, which means they accept common descent but
> believe that God guided the course of evolution in some fashion.
Again, if God guided anything, then that is slow creation (to some
degree or another), not pure evolution . . . regardless of what anyone
calls it. To quote a common cliche, "A rose by any other name is still
the same." Of course, if slow creation occurred with the occasional
input of information from some intelligent source, then this
intelligent activity should give evidence of itself in some detectable
form. It is my opinion that this evidence of intelligent activity
comes in the form of neutral genetic gaps that do in fact exist
between various functions in all life forms.
> Some of
> these believe he just set up the initial conditions so that evolution,
> proceeding naturally, would end up where he wanted; that would be
> contrary to your views. But others believe, as did Wallace, in direct
> intervention at various stages.
Direct intervention is the same as intermittent creation or
intelligent design. In other words, naturalistic evolution needed
help.
> If you reject the possibility of common descent combined with
> intelligent design (let's call it CD/ID), I would be interested to know
> why. What evidence can you present that argues against the CD/ID theory?
I do not reject this idea of mixed CD/ID as a possibility at all. The
fact is though, any time ID is included, common descent fails at that
point. If one believes that ID was needed just one time along the way,
then one must have evidence for this belief. This evidence must be
such that the naturalistic *requirements* of common evolutionary type
descent are not powerful enough to overcome some obstacle that blocks
the way to some sort of change. At this point, creationism takes over.
> And now, on to Hayashi, Y., H. Sakata, Y. Makino, I. Urabe, and T. Yomo.
> 2003. Can an arbitrary sequence evolve towards acquiring a biological
> function. J. Mol. Evol. 56:162-168.
>
> Here, typed in at great personal cost, is the abstract:
Great personal cost? Two paragraphs almost did you in eh? Sorry to put
you out like that ; )
> To explore the possibility that an arbitrary sequence can evolve towards
> acquiring functional role when fused with other pre-existing protein
> modules, we replaced the D2 domain of the fd-tet phage genome with the
> soluble random polypeptide RP3-42. The replacement yielded an fd-RP
> defective phage that is six-orders of magnitude lower in infectivity than the
> wild-type fd-tet phage. The evolvability of RP3-42 was investigated
All functions are complex functions. In fact, all functions are
"irreducibly complex". And yes, novel, new, beneficial, irreducibly
complex functions can evolve, if the neutral gaps are small enough.
And, when they do, the evolution is usually quite rapid, as in this
case of fd-RP (infectious protein) evolution.
Basically, this is the same type of experiment performed by Barry Hall
with his E. coli lactase evolution experiments. It is nothing at all
like I thought it would be. What Hayashi did was to decrease the
function of a given gene (a gene that allowed a bacterial phage to be
infective), with the splicing in of a random DNA sequence that
interfered with the original gene's infective function. However this
splicing of the random sequence did not completely destroy the
function of the original gene. In fact, the original gene produced a
protein that was still able to allow its host to infect the target
bacteria. In other words, it still maintained some of its former
function despite the interference of this random sequence of DNA. Some
mutations, in the interfering DNA sequence, *reduced* the interference
of this sequence in each generation. In fact, as I would have
predicted, without knowing the outcome in such a setup, it seems as
though just about every change in the random DNA sequence (that
resulted in a change in the coded amino acid sequence) caused a
change in the function of the original gene.
Don't you see what you have here? You have a starting point, the
fd-RP, which produces significant interference with the original gene
function. Odds are that a random starting point will not give either
maximum nor minimum gene function interference. The odds also are that
each amino acid change in an interfering amino acid sequence will most
likely NOT be a neutral change. This means that all along the way
toward "improved function" are steps that are only one mutation wide.
Each step results in either a detrimental or a beneficial change in
function. Such changes can be detected by the force of natural
selection and "directed" toward improved function in a very rapid
manner (Only 7 generations in this case).
You do understand why Hayashi's experiment worked so well and so
quickly don't you? Hayashi did not randomly pick a genetic sequence,
insert it into a bacteria, and come up with a brand new function at
all. The insertion of his random sequence only interfered with the
operation of an existing function. The sequence itself had no
independent function of its own. Mutations to it made it less and less
of an interference, but this would only seem likely. Stick in a random
sequence of amino acids into any protein and odds are that it will
decrease the performance of the original protein's original function.
However, it seems only reasonable that certain sequences will be less
of an interference than other sequences of a given length. Because of
this, each sequence is very likely to be just one or two mutations
away from another sequence with either "more" or "less" interference.
This experiment is not surprising or new and the results are not
unexpected at all. Even I would have predicted this outcome. It's
easy. Success was virtually certain given this scenario. And, as in
this case, the changes are expected to be rapidly realized. The reason
for this is that just about every single change in an amino acids
sequence (of the interfering sequence) is likely to result in some
sort of change in function (either increased or decreased function).
The ability to cause a detectable change in function is all-important
for natural selection to be able to preferentially select between
sequences. With just about every single amino acid substitution
resulting in some sort of detectable change in function, natural
selection is able to quickly pick out the most beneficial change out
of the pile of options in every round.
This scenario is a complete setup for success. I am quite surprised
that you even tried to use it as an example to support your point of
view because it does nothing of the sort. This is not the challenge
that evolutionary scenarios need to overcome. Evolution needs to
explain the existence of functions that are separated from all
available genetic real estate by NEUTRAL gaps in function that are
wider than one or two or even a few mutations. Neutral gaps are the
problem because natural selection cannot function if all options are
neutral in function.
This experiment by Hayashi is not at all like you described it. You
indicated that this experiment demonstrated the picking out of
specified functional proteins from a random selection of amino acid
sequences. This experiment does not demonstrate anything even close to
that. There are in fact experiments that do demonstrate this sort of
thing (often done with antibodies having other functions, such as
various enzymatic functions), but Hayashi's experiment here is not one
of them.
You really need to come up with something much much better. Hall's
experiments showed that neutral gaps do in fact exist between various
genetic functions and the what is available in the genetic real estate
at hand. In Hall's experiments these gaps did in fact result in the
"limited evolutionary potential" of certain colonies of E. coli. These
are the gaps that must be explained. How are they crossed outside of
deliberate intelligent design?
Part 2: Written in reply to comments by Ron Okimoto (linked above)
> I just had an interesting thought for a metaphor that might help
> illuminate the question to Dr. Sean (in my dreams, that is), and I am
> randomly attaching it to Ron's recent post.
>
> Let's imagine gene sequence space (or protein sequence space if you
> like) as a plane. It's really multi-multi-dimensional, but try
> visualizing in that many, and 2 will do for the point. We can envisage
> sequences following a mutational path through this space, and let's
> pretend that all mutations are point mutations that move the sequence
> one step in some direction. Neutral evolution follows a random walk. Dr.
> Sean contends that the space is flat, and the chance that any sequence's
> random walk will ever reach a particular, selected point depends on the
> distance between the starting point and the target point, with the
> probability decreasing to as close to zero as we like as distance goes
> up. (Ron has argued that these probabilities are much higher than Dr.
> Sean likes for much larger distances than he likes, but forget that for
> now.)
Note: Ron didn't do the math here, he only suggested a concept that
was in fact quite a valid concept. I did the calculations myself based
on this concept and it turns out that the statistics do change
somewhat in favor of the crossing of larger gaps than I had previously
imagined (but not really . . . relatively speaking). However, this
change in my calculations did not turn out to be a significant change
at all. The mutation rates and population sizes that are required to
keep up with increasing gaps sizes exponentially expands so that in
relatively short order the required population size is well beyond the
size and mass of the known universe. With a fixed population size,
such as the total number of bacteria of all types currently living on
this entire planet, the time required to travel across a neutral gap
of just 20 or so amino acid changes requires trillions upon trillions
of years. This is a bit longer distance that I had previously
suggested, but it really changes nothing as far as the problems that
it causes for the theory of evolution. Ron suggests that I have
shifted my goal posts some huge distance. But really, relatively
speaking, they have barely budged. The problem not been solved in the
least by such a minor change the statistical calculations.
> I would contend, however, that the surface is not flat, but that
> around each sequence that is maximally functional for some task, there
> is a depression of some size. Deepness of depression corresponds to
> fitness, and due to selection, a sequence is more likely to move down a
> slope than up it, with probabilities depending on the steepness of the
> slope. Under such conditions, sequences that enter the edges of a
> depression will be attracted toward the center. My contention would be
> that a high proportion of sequence space does have a discernible slope.
> Moreover, sequence space is not static. Fitness depends on environment,
> both genetic (other sequences in the organism) and external. Depressions
> move, coalesce, and separate, taking sequences with them. A sequence can
> end up very far from its starting point just through rolling down
> ephemeral slopes. (This is more or less stealing Sewall Wright's concept
> of adaptive landscapes; and why not?)
What a fine idea . . . but it only works for relatively simple
functions that require relatively short amino acid sequences. Sure, it
seems very reasonable to me that just about every maximally functional
sequence (DNA or protein), will have a depression, so to speak, like a
gravity field of sorts, around it where variations in the sequence
will still be functional, but less so as one moves outward from the
center. Obviously many proteins can change a great deal without a
complete loss of function. I like to call this ability for change
without a complete loss of function a "plastic" ability. Many
proteins are somewhat plastic or flexible in their sequencing.
However, all proteins have certain amino acids that cannot change at
all without a complete loss of protein function. For example, consider
the hemoglobin protein. Richard Dawkins himself estimates that at
least a third of the amino acids in hemoglobin are not changeable or
are "invariant" without a complete loss of hemoglobin function. Many
others can only be changed within the same class or type of amino
acids (ie: hydrophobic or hydrophilic).
So, it is true that many if not most proteins have a degree of
plasticity, but generally speaking, proteins are quite rigid or
specific in their sequencing. If changed beyond a certain point, they
loose ALL function. At this point, further changes to the sequence of
a non-functional protein are, yes, functionally neutral. Your
hypothetical plane of function becomes perfectly flat at this point.
Random walk takes over and further mutations are lost on an almost
endless sea of random drift.
You and Ron like to think that these depressions or islands of
functional land that surround maximal protein function are almost
infinite, but clearly they aren't even close. If they were just about
"infinite" as Ron has suggested, then why did Hall's E.coli, who
lacked the ebg and lacZ genes, have such a difficult time evolving the
lactase function back again? Despite a high mutation rate, a large
population size, and thousands upon thousands of generations, they
never did evolve the lactase function back again. The same thing
happens with many other types of bacteria. Our hospital logs have
records on many types of bacteria going back over 40 years and many of
these have never tested lactase positive over this entire time
(representing over a million generations for many of them). If the
depression around this function were truly close to infinite in scope,
then just about any other gene or genetic sequence in the E. coli
genome would be expected to have at least *some* beneficial lactase
type function . . . wouldn't you think? And, given this "slope", one
would expect a more rapid tendency to slide down toward the middle . .
. right? So then, where did our hypothesis go wrong with Hall's mutant
E. coli bacteria? Hmmmmmm?
The problem is that, relatively speaking, these islands of function
are quite small indeed. When compared to the total number of
completely non-functional sequences out there in the ocean of
non-function, those sequences that have any function whatsoever (from
the perspective of a given life form in a given environment), make up
only the tiniest of fractions, especially when you start talking about
functions that require amino acid sequences that average more than one
enzymatic-type protein in length. When functions require multiple
proteins totaling several hundred, thousand, or even tens or hundreds
of thousands of amino acids in length, then your little islands with
their little impressions don't come near close enough to avoid the
random drift problem.
But, there is something hopeful about your hypothetical suggestion.
The very fact that you proposed such a hypothetical solution to the
problem means that you might actually recognize the problem, which is
a significant step. In any case, I remain most interested in your
thoughts and struggles with this issue.
Sean
Sean Pitman
> But ID is not itself a mechanism, so it has nothing to offer but
> incredulity. Perhaps if you were to offer a molecular organization,
> molecular drive, or genomic potential mechanism, all of which have
> been postulated (and mostly ignored by anti-evolutionists), then you
> might have something worth pursuing.
This is ridiculous. ID certainly is a mechanism. The use of ID can
also be recognized by the scientific method without a need to know the
identity of the designer ahead of time. For example, forensic science
is all about the detection of design in the assessment of the evidence
without knowing the identity of the designer ahead of time. For
example, was a person deliberately killed or did they die of "natural"
causes? If they were deliberately killed, then the investigators look
for evidence of deliberate intelligent design that might give some
backing for the charge of murder.
Also, many scientists, such as those spending millions on the SETI
projects, suggest the possibility of intelligent beings living
elsewhere in the universe. These scientists think that they can
detect the activity of intelligent design without having ever met
these proposed intelligent alien life forms. Now, what do you propose
that they are looking for? They are looking for evidence of phenomena
that cannot be explained via any known mindless naturalistic process.
In other words, they are looking for phenomena that require a
thoughtful, purposeful, intelligent mind.
The lame argument is often used that we can assume design in certain
cases, such as in a case of murder or in the workings of a wristwatch,
because we have seen intelligent human designers create such works
before. However, since we have never seen any designer create living
things, we cannot therefore present any evidence to support any theory
that proposes such a designer of life. Now, this is just about the
most mysterious and lame argument that I have every heard, but it is
used all the time by many very intelligent people. Just because we
have never seen a particular object created before does not mean that
it will not give us conclusive evidence of its origin in intelligent
design. If I were to go off traveling through the universe and end up
in some far distant galaxy on the planet Zorg, would I not be able to
assume deliberate intelligent design if I were to find a rock on that
planet with strange hieroglyphic-like symbols on it, or a collection
of large rocks shaped like a local starry constellation? . . .
something on the order of Stonehenge which any alien visiting earth
would instantly recognize as being intelligently designed? I mean,
without a logical naturalistic explanation for a given phenomenon, ID
is the only logical recourse to explain its existence even without
having ever met the designer or ever seeing such a phenomenon created
before.
So, for you to claim then that ID is not a mechanism that explains any
sort of phenomena is quite misinformed. ID obviously explains many
phenomena quite well. So, for you to suggest that only mindless
naturalistic mechanisms that involve, "molecular organization,
molecular drive, or genomic potential mechanisms" need be considered
in a discussion of the origin of life is quite narrow minded and even
non-scientific. The scientific method requires no "a priori"
assumptions such as a the idea that only mindless naturalistic
processes can be considered when considering potential theories on the
origin of life. Such mindless mechanisms are certainly not an
automatic default especially when the naturalistic mechanisms, which
have been proposed so far, fall far short of explaining the diversity
of genetic functions that we find in all life forms. No proposed
mechanism in literature has adequately explained how neutral gaps that
do exist between different genetic functions can be crossed in a
reasonable amount of time. Darwinian evolution relies on the power of
random mutation as well as natural selection to guide changes over
time. Both of these forces for change are required for evolution to
work. Without either one of them, evolution fails. Gaps of neutral
function do in fact eliminate one of these forces, the force of
natural selection. Without a change in detectable function, a change
in a sequence of DNA or protein cannot be selected for or against by
the force of natural selection. Such a gap blinds natural selection
so that it becomes worthless. At this point the only force for change
that is left is random mutation. And, by itself, random mutation is
extremely weak as an evolutionary force. This is a real problem and
this problem is exactly what has not been explained by popular
science.
So please, try and suggest something that actually makes rational
sense instead of falling for that old weak dogma of modern scientific
philosophy that "ID offers nothing but incredulity" and that
"Naturalism must explain everything concerning origins . . . no matter
how counterintuitive." Such positions are really not logical or
scientific, but are more akin to the dogmatism of religious doctrine
and fervor.
Sean
Mark VandeWettering
> Frank J wrote in message news:<38c5d0dd.03050...@posting.google.com>...
>
>> But ID is not itself a mechanism, so it has nothing to offer but
>> incredulity. Perhaps if you were to offer a molecular organization,
>> molecular drive, or genomic potential mechanism, all of which have
>> been postulated (and mostly ignored by anti-evolutionists), then you
>> might have something worth pursuing.
>
> This is ridiculous. ID certainly is a mechanism. The use of ID can
> also be recognized by the scientific method without a need to know the
> identity of the designer ahead of time. For example, forensic science
> is all about the detection of design in the assessment of the evidence
> without knowing the identity of the designer ahead of time. For
> example, was a person deliberately killed or did they die of "natural"
> causes? If they were deliberately killed, then the investigators look
> for evidence of deliberate intelligent design that might give some
> backing for the charge of murder.
Forensics has an advantage that ID does not have: it doesn't have to deal
with the actions of all conceivable entities, merely humans and other
animals whose properties are well known to us through observation.
Forensics cannot (and indeed specifically discounts) actions by supernatural
agents of undefined powers. Yes, it might be true that the gun shot residue
fairy sprinkled gunshots on your shirt, but forensics doesn't include this
idea in its considerations because nothing resembling a gunshot residue
fairy has ever been observed.
In the absence of the properties of intelligent agents, forensics can
conclude nothing. In particular, since God is omnipotent, all possible
evidence could be claimed to be consistent with Intelligent Design, which
clearly shows that it has no real explanatory power. Ultimately all
questions are answered by "because God _did_ it that way", which is
unfalsifiable.
> Also, many scientists, such as those spending millions on the SETI
> projects, suggest the possibility of intelligent beings living
> elsewhere in the universe. These scientists think that they can
> detect the activity of intelligent design without having ever met
> these proposed intelligent alien life forms. Now, what do you propose
> that they are looking for? They are looking for evidence of phenomena
> that cannot be explained via any known mindless naturalistic process.
> In other words, they are looking for phenomena that require a
> thoughtful, purposeful, intelligent mind.
But SETI researchers will tell you quite clearly that they have made
assumptions (and perhaps unwarranted assumptions) that other intelligent
beings will act in the same way we do. The universe may be chocked full
of intelligent dolphins who somehow never bothered to invent the radio
telescope. SETI researchers simply will never find such beings.
> The lame argument is often used that we can assume design in certain
> cases, such as in a case of murder or in the workings of a wristwatch,
> because we have seen intelligent human designers create such works
> before. However, since we have never seen any designer create living
> things, we cannot therefore present any evidence to support any theory
> that proposes such a designer of life. Now, this is just about the
> most mysterious and lame argument that I have every heard, but it is
> used all the time by many very intelligent people. Just because we
> have never seen a particular object created before does not mean that
> it will not give us conclusive evidence of its origin in intelligent
> design. If I were to go off traveling through the universe and end up
> in some far distant galaxy on the planet Zorg, would I not be able to
> assume deliberate intelligent design if I were to find a rock on that
> planet with strange hieroglyphic-like symbols on it, or a collection
> of large rocks shaped like a local starry constellation? . . .
> something on the order of Stonehenge which any alien visiting earth
> would instantly recognize as being intelligently designed? I mean,
> without a logical naturalistic explanation for a given phenomenon, ID
> is the only logical recourse to explain its existence even without
> having ever met the designer or ever seeing such a phenomenon created
> before.
It seems vastly more strange that in the absence of any evidence that
any intelligent being has ever created a living thing as a concious
design act as evidence that _all_ living things are just so designed.
Your examples are hand tailored to demonstrate things that are familiar
to us as designed objects. Suppose I hand you a rock, and ask you
whether it was designed or not. How could you tell? Suppose you'd
observed similar rocks scattered all over the place, seemingly the
result of erosion processes and weathering. How could you tell if _this
particular_ rock was the result of these natural forces, or the result
of somebody intelligently working to create a rock of this precise
shape?
We recognize design in writing because we have observed other intelligent
beings using writing. We recognize design in rock temples because we have
observed intelligences creating rock temples.
We have never observed any intelligence consciously creating living
things. It seems perverse to conclude that this is evidence that they
must have been so designed.
ID is not a mechanism, it's a catch phrase. It doesn't tell us anything
about the process or method by which supposedly deisgned systems came into
being.
More than that, ID doesn't even give us a glimpse into what objects were
designed _for_. When we design objects, they are usually designed to
fufill some purpose. What is the purpose of life forms? Why so many
beetles? Why the platypus? Why parasites? Why so many turtle eggs,
and so few turtles? ID gives us no insights into these questions.
> So please, try and suggest something that actually makes rational
> sense instead of falling for that old weak dogma of modern scientific
> philosophy that "ID offers nothing but incredulity" and that
> "Naturalism must explain everything concerning origins . . . no matter
> how counterintuitive." Such positions are really not logical or
> scientific, but are more akin to the dogmatism of religious doctrine
> and fervor.
Mark
> Sean
TomS
<slrnbbl6a6.v...@keck.vandewettering.net>, Mark stated..."
[...snip...]
>ID is not a mechanism, it's a catch phrase. It doesn't tell us anything
>about the process or method by which supposedly deisgned systems came into
>being.
>
>More than that, ID doesn't even give us a glimpse into what objects were
>designed _for_. When we design objects, they are usually designed to
>fufill some purpose. What is the purpose of life forms? Why so many
>beetles? Why the platypus? Why parasites? Why so many turtle eggs,
>and so few turtles? ID gives us no insights into these questions.
Let's suppose that ID *did* give us some hint about what the things
were designer for, or what kind of beings did the designing.
Let's see ... we'd find that humans had these various design features
(like eyes, immune system, blood clotting system, cilia, DNA code) that
were very much like nearly all of the Subphylum Vertebrata; and still
more like the Superfamily Hominoidea. That would tell us that, if the
human body plan were designed, it was obviously designed to perform very
much like other vertebrates, and very, very much like other apes. What
kind of implications that has for what we humans ought to be doing with
our bodies, I leave for the pious to tell us.
Let's see ... and then, we see that a feature like the vertebrate
immune system was obviously designed to oppose invaders like bacteria;
and that the bacterial flagella were designed to help bacteria be
virulent. That would tell us that there was some kind of conflict
between the designers of these two designed systems.
Let's see ... another thing, we'd see that a lot of the systems
which are intelligently designed are complex (irreducibly complex, but
that's just an added layer of complexity). That would tell us that the
designers were giving complex solutions to problems that they themselves
found to be complex to them. That tells us that the designers are
beings that must operate under external constraints.
Let's see ... finally, we'd see that the designers stopped doing
their designing some many millions of years ago. Maybe as far back
as the Cambrian, some hundreds of millions of years ago.
So, what we would infer about the designers would be that they
were, several different finite designers who are no longer doing their
designing, nor have they ever shown any particular interest in humans
(either as a species, but especially not as individuals). That is, if
"intelligent design" actually did propose to offer something of
substance.
I suggest that when ID comes up for a debate, that these answers
be pointed out to the legislators, school boards, courts, churches, and
voters. It should be interesting to find out how many people are in
favor of teaching this as the alternative to evolution. Of course, I
am not suggesting that the legislators, school boards, courts, churches,
and voters are necessarily the most authoritative judges as to what the
scientific facts are. Political/legal processes are not necessarily
the way to get to the truth.
But it would be interesting to find out what the reaction would be.
If ID did have something to say, that is.
Tom S.
Tracy P. Hamilton
turn on. Mark VandeWettering <wett...@attbi.com> said:
>In article <80d0c26f.03050...@posting.google.com>, Sean Pitman wrote:
[snip]
>> Also, many scientists, such as those spending millions on the SETI
>> projects, suggest the possibility of intelligent beings living
>> elsewhere in the universe. These scientists think that they can
>> detect the activity of intelligent design without having ever met
>> these proposed intelligent alien life forms. Now, what do you propose
>> that they are looking for? They are looking for evidence of phenomena
>> that cannot be explained via any known mindless naturalistic process.
>> In other words, they are looking for phenomena that require a
>> thoughtful, purposeful, intelligent mind.
>
>But SETI researchers will tell you quite clearly that they have made
>assumptions (and perhaps unwarranted assumptions) that other intelligent
>beings will act in the same way we do. The universe may be chocked full
>of intelligent dolphins who somehow never bothered to invent the radio
>telescope. SETI researchers simply will never find such beings.
Reminds me of the great Far Side cartoon, where the scientists were
trying to determine if dolphins could talk. From a web site from a
search:
"The other is two dolphins in a tank, being watched by
the white-coated mad scientists typical of Larson, with a
blackboard in the background on which they've been making
notes about the sounds the dolphins have been making, trying
to decipher dolphin language, and the caption reads something
like "There's some more of that 'Se Habla Espaniol' stuff". "
[snip]
Tracy P. Hamilton
Building Manager, Alco Hall
University of Ediacara
Ferrous Patella
news:slrnbbl6a6.v...@keck.vandewettering.net by Mark
VandeWettering <wett...@attbi.com>:
> Your examples are hand tailored to demonstrate things that are
> familiar to us as designed objects. Suppose I hand you a rock, and
> ask you whether it was designed or not. How could you tell? Suppose
> you'd observed similar rocks scattered all over the place, seemingly
> the result of erosion processes and weathering. How could you tell if
> _this particular_ rock was the result of these natural forces, or the
> result of somebody intelligently working to create a rock of this
> precise shape?
Hey! I claim priority on that analogy. See:
http://makeashorterlink.com/?M2A352F74
--
Ferrous Patella
"To announce that there must be no criticism of the President,
or that we are to stand by the President, right or wrong, is not
only unpatriotic and servile, but is morally treasonable to the
American public."
--Theodore Roosevelt
May 7, 1918
Von Smith
> On Thu, 8 May 2003 17:43:25 +0000 (UTC), We get signal. Main screen
> turn on. Mark VandeWettering <wett...@attbi.com> said:
>
> >In article <80d0c26f.03050...@posting.google.com>, Sean Pitman wrote:
>
> [snip]
>
> Reminds me of the great Far Side cartoon, where the scientists were
> trying to determine if dolphins could talk. From a web site from a
> search:
> "The other is two dolphins in a tank, being watched by
> the white-coated mad scientists typical of Larson, with a
> blackboard in the background on which they've been making
> notes about the sounds the dolphins have been making, trying
> to decipher dolphin language, and the caption reads something
> like "There's some more of that 'Se Habla Espaniol' stuff". "
> [snip]
>
Or, to rip off the old "Alien" slogan:
In space, no one can hear you speak Spanish.
Bigdakine
>From: seanpi...@naturalselection.0catch.com (Sean Pitman)
>Date: 5/8/03 6:49 AM Hawaiian Standard Time
>Message-id: <80d0c26f.03050...@posting.google.com>
>
>Frank J wrote in message
>news:<38c5d0dd.03050...@posting.google.com>...
>
>> But ID is not itself a mechanism, so it has nothing to offer but
>> incredulity. Perhaps if you were to offer a molecular organization,
>> molecular drive, or genomic potential mechanism, all of which have
>> been postulated (and mostly ignored by anti-evolutionists), then you
>> might have something worth pursuing.
>
>This is ridiculous. ID certainly is a mechanism. The use of ID can
>also be recognized by the scientific method without a need to know the
>identity of the designer ahead of time. For example, forensic science
>is all about the detection of design in the assessment of the evidence
>without knowing the identity of the designer ahead of time.
You're already wrong. Almost a record for you, but not quite.
Forensic science works under the postulate that it is investigating *human*
criminal activity, not alien criminal mischief.
FBI profilers for example, study human behavior and proclivities. Their whole
knowledge base is itself based on *known* designers, us.
Forensics attempts to figure out which particular human did the deed. But that
is not the same as the ID hypothesis, which assumes hypothetical designers
using hypothetical mechanisms..
In this case we know from whence the deisgner came, what his habits are etc..
Stuart
Dr. Stuart A. Weinstein
Ewa Beach Institute of Tectonics
"To err is human, but to really foul things up
requires a creationist"
Frank J
>
> > But ID is not itself a mechanism, so it has nothing to offer but
> > incredulity. Perhaps if you were to offer a molecular organization,
> > molecular drive, or genomic potential mechanism, all of which have
> > been postulated (and mostly ignored by anti-evolutionists), then you
> > might have something worth pursuing.
>
>
> So please, try and suggest something that actually makes rational
> sense instead of falling for that old weak dogma of modern scientific
> philosophy that "ID offers nothing but incredulity"
maybe when they start publishing some original research in the
biological literature. Heck, even Stuart Kauffman can do that.
> and that
> "Naturalism must explain everything concerning origins . . . no matter
> how counterintuitive." Such positions are really not logical or
> scientific, but are more akin to the dogmatism of religious doctrine
> and fervor.
I never said that "Naturalism must explain everything concerning
origins . . . no matter how counterintuitive." Methodological
naturalism can provide some answers. Interestingly, before Dembski
fine-tuned the art of evasion, some IDers, like Behe, actually
attempted to use some MN in their arguments. I'm still waiting for him
to publish more on his "complex origins" hypothesis.
>
> Sean
Jason Cortina
You are assuming that these two possibilities are exhaustive of the
universal set; that they are A and ~A. As this is demonstrably not the
case, the statement itself is invalid.
The set 'A' given is the set of purely naturalistic processes *that we
know at this time*. It wrongly excludes the possibility of future
discoveries.
Additionally, the set 'B' given and wrongfully presented as '~A' is the
set of non-naturalistic processes *involving outside intelligence*. This
wrongly excludes the possibility of non-intelligent non-natural
agencies, unless you know of some way to disprove the possibility of
such.
And finally, even if the above two points did not pertain, you must
acknowledge the consequences of your use of this logic: if the two sets
*are* exhaustive of the universal set, then it is just as valid to claim
that because no creative intervention by any outside intelligent agent can
be demonstrated, then naturalistic processes can be concluded (if X not in
A implies membership in B then X not in B implies membership in A).
The attempt to make design (and specifically 'intelligent' design)
the default position, to be considered as valid in any and all cases
where natural processes cannot *at this time* be clearly demonstrated,
is not warranted when Dembski does it with his "Explanatory Filter"
and it is not warranted here.
This does *not* assume that a naturalistic explanation will be found.
This is simply declaring the matter to be unknown because of
insufficient data. Investigations can and should proceed in the
direction any given researcher wishes to pursue so that we can
get sufficient data to resolve it. If we cannot show that X belongs
in one set or another it should be held as being incapable of being
placed *at this time*.
[snip]
--
Jason A Cortina
"I am not a vegetarian because I love animals. I am a
vegetarian because I hate plants."
-- A. Whitney Brown
Jason Cortina
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
> Frank J wrote in message news:<38c5d0dd.03050...@posting.google.com>...
>
> > But ID is not itself a mechanism, so it has nothing to offer but
> > incredulity. Perhaps if you were to offer a molecular organization,
> > molecular drive, or genomic potential mechanism, all of which have
> > been postulated (and mostly ignored by anti-evolutionists), then you
> > might have something worth pursuing.
>
> This is ridiculous. ID certainly is a mechanism. The use of ID can
> also be recognized by the scientific method without a need to know the
> identity of the designer ahead of time. For example, forensic science
> is all about the detection of design in the assessment of the evidence
> without knowing the identity of the designer ahead of time. For
> example, was a person deliberately killed or did they die of "natural"
> causes? If they were deliberately killed, then the investigators look
> for evidence of deliberate intelligent design that might give some
> backing for the charge of murder.
When the determination of 'deliberately killed' is made, an
identification most definitely *is* made: it was a another human
using know methods. It was not accumulation of cell aging or
pathogenic microbes or any number of traumas possible by interacting
with non-ling aspects of nature (falling off a cliff or being
crushed in a landslide) or that act of wild beasts.
Further this identification of a specifically human agent first
*requires* knowing the possible methods/mechanisms human agents are
capable of employing and recognizing the use of such methods in the
particular case.
Forensic investigators most definitely do not say "Person X (or even
'persons unknown') did it using methods not yet detected, let alone
identified; we just know it was done by someone somehow."
Further, imagine a case where no cause of death can be determined. The
most thorough examination rules out any *natural* cause of death (which
means it must be 'designed', right?) as well as any cause of death
attributable to human agency. As far as they can tell, the person just
ceased all life processes for no reason. I really doubt this would be
assumed to be murder. In fact, even if someone stepped forward and
claimed "I killed him, but I won't say how I did it", I would still
doubt this would be assumed to be murder (I'd like to hear it from the
D.A. who would try and the judge who would convict in this case).
You will, in fact, find that all such fields in which we detect design
or agency rely on prior knowledge of human design and/or agency. It does
*not* proceed by eliminating naturalistic explanations.
>
> Also, many scientists, such as those spending millions on the SETI
> projects, suggest the possibility of intelligent beings living
> elsewhere in the universe. These scientists think that they can
> detect the activity of intelligent design without having ever met
> these proposed intelligent alien life forms. Now, what do you propose
> that they are looking for? They are looking for evidence of phenomena
> that cannot be explained via any known mindless naturalistic process.
> In other words, they are looking for phenomena that require a
> thoughtful, purposeful, intelligent mind.
Wrong. They are looking for the use of an already known and recognized
method/mechanism of technology. They are not looking for some vague
"other than can be explained now" phenomenon. They are looking for the
exact thing that we are capable of, something already defined.
>
> The lame argument is often used that we can assume design in certain
> cases, such as in a case of murder or in the workings of a wristwatch,
> because we have seen intelligent human designers create such works
> before. However, since we have never seen any designer create living
> things, we cannot therefore present any evidence to support any theory
> that proposes such a designer of life. Now, this is just about the
> most mysterious and lame argument that I have every heard, but it is
> used all the time by many very intelligent people. Just because we
> have never seen a particular object created before does not mean that
> it will not give us conclusive evidence of its origin in intelligent
> design. If I were to go off traveling through the universe and end up
> in some far distant galaxy on the planet Zorg, would I not be able to
> assume deliberate intelligent design if I were to find a rock on that
> planet with strange hieroglyphic-like symbols on it, or a collection
> of large rocks shaped like a local starry constellation? . . .
> something on the order of Stonehenge which any alien visiting earth
> would instantly recognize as being intelligently designed? I mean,
> without a logical naturalistic explanation for a given phenomenon, ID
> is the only logical recourse to explain its existence even without
> having ever met the designer or ever seeing such a phenomenon created
> before.
>
> So, for you to claim then that ID is not a mechanism that explains any
> sort of phenomena is quite misinformed. ID obviously explains many
> phenomena quite well.
ID is not a mechanism. Period. It is at best a label for a manner of
applying mechanisms.
A watch has never been *made* by ID. If you don't believe me, go to the
nearest Timex or Casio assembly plant. Or the factories which
manufacture the parts to be assembled. Or those that refine/generate the
materials used in the parts. If ID was the mechanism by which watches
were *made*, those companies would be able to save a lot on material and
labor as they could have their draftsmen simply 'design' the watch into
being.
ID has to be *applied* in order to materially effect *anything*. We know
the mechanisms by which humans *apply* design and all design with which
we are familiar require mechanisms of application (if they are to have
any effect; whether or not you believe that designing something as in
imagining it has an underlying mechanism, applying those thoughts to
manufacture real-world objects requires mechanism(s)).
Additionally, without exception, all application of intelligent design
that we are sure of (i.e. human design) are for the benefit of or serve the
purpose of the designer(s). Whether said purpose is practical or esthetic
or experimental in nature, some such purpose is *always* present and is
*always* a purpose of the designer's.
To date, ID 'theory' is unable to provide methods/mechanisms, and it
posits no detectable purpose of the designer. Lacking these it is forced
to claim identification by elimination and proclaiming itself the
default position when no naturalistic explanation is currently
confirmed. I am baffled as to why proponents think designer-of-the-gaps
is any more rational or tenable than god-of-the-gaps.
But the fact is that ID does offer nothing but incredulity. It must try to
legitimize itself by claiming the default/neutral/unknown position in
analysis.
That does not say that naturalism must explain everything. It simply says
that, to date, ID explains nothing.
--
Jason A Cortina
"It's just a job. Grass grows, birds fly, waves pound the
sand. I just beat people up."
-- Muhammed Ali
H,R.Gruemm
>
> > But ID is not itself a mechanism, so it has nothing to offer but
> > incredulity. Perhaps if you were to offer a molecular organization,
> > molecular drive, or genomic potential mechanism, all of which have
> > been postulated (and mostly ignored by anti-evolutionists), then you
> > might have something worth pursuing.
>
> This is ridiculous. ID certainly is a mechanism.
No. ID is the preliminary stage to the *starting* of a mechanism. No
pot, car or computer was ever made by intelligent design per se; they
were made by known physical and chemical mechanisms.
It's exactly this implementation stage of design which is carefully
left unspecified by ID proponents.
The use of ID can
> also be recognized by the scientific method without a need to know the
> identity of the designer ahead of time. For example, forensic science
> is all about the detection of design in the assessment of the evidence
> without knowing the identity of the designer ahead of time.
Come on. They are looking specifically for human "designers", with
known abilities and motivations.
> For
> example, was a person deliberately killed or did they die of "natural"
> causes?
I hope you realize that the meaning of "natural" in forensic science
is different from what we are discussing here.
> If they were deliberately killed, then the investigators look
> for evidence of deliberate intelligent design that might give some
> backing for the charge of murder.
No, they are looking for the well-known patterns associated with human
actions. They couldn't care less whether a human-emulating robot or a
human caused those patterns.
IOW, they are not looking for human design, but for human actions.
<snip>
Regards,
HRG.
Sean Pitman
<jascortin...@comcast.net> wrote in message news:<md2mbvcs3c4sv41n0...@4ax.com>...
> > ID certainly is a mechanism. The use of ID can
> > also be recognized by the scientific method without a need to know the
> > identity of the designer ahead of time. For example, forensic science
> > is all about the detection of design in the assessment of the evidence
> > without knowing the identity of the designer ahead of time. For
> > example, was a person deliberately killed or did they die of "natural"
> > causes? If they were deliberately killed, then the investigators look
> > for evidence of deliberate intelligent design that might give some
> > backing for the charge of murder.
>
> When the determination of 'deliberately killed' is made, an
> identification most definitely *is* made: it was a another human
> using known methods. It was not accumulation of cell aging or
> pathogenic microbes or any number of traumas possible by interacting
> with non-ling aspects of nature (falling off a cliff or being
> crushed in a landslide) or that act of wild beasts.
Yes . . .
> Further this identification of a specifically human agent first
> *requires* knowing the possible methods/mechanisms human agents are
> capable of employing and recognizing the use of such methods in the
> particular case.
First off, no one need say for sure that the "agent" in question that
"caused" a specific event be "human". Design can be inferred without
saying for sure that a human being was the designer. Many methods or
mechanisms that have never been seen before by a particular
investigator can be determined to have been designed by some sort of
deliberate purposeful intelligence because of a knowledge of what
mindless naturalistic mechanisms are capable and incapable of doing.
A scientist in not limited to the use of knowledge concerning the
known abilities of human creativity alone, but a scientist can also
take into account the known limitations of naturalistic processes as
well. For example, if I went to the moon and found a series of
perfectly round 10kg rocks all arranged in a perfect geometric square
measuring a mile on each side, it would be very reasonable of me to
theorize that some sort of purposeful intelligence, above any sort of
mindless naturalistic process, was at work here.
Would this conclusion be so shocking to you? Would you propose a
different theory as an explanation for this phenomenon? Of course,
you might suggest that humans are perfectly capable of creating such
an unnatural setup as this, and so therefore we can assume design in
such a case based on this similarity to what humans can do. And, I
would have to agree. The problem is, the genetic information
contained in DNA is very much like the coded language systems that
humans have created and use, such as English, Greek, Spanish, computer
code, the Morse Code, sign language, etc. In fact, it is so similar
to such language systems that humans are quite capable and quite
comfortable playing with the genetic codes and language-like sequences
that code for living things. And, we are getting better at it all the
time. It seems to almost come naturally to us; like genetics is
written in a language that is so similar to what we understand that
playing with it is practically second nature. How then, given that
life and the basic codes of life are so similar to the languages
systems and codes of our own making, can we exclude the possibility
that such a coded language system that we find in living things was in
fact designed in much the same way that we have designed very similar
languages and codes? Of course, if we were to one day find some
naturalistic mechanism that could adequately explain the existence of
such an obviously creative phenomena, very similar to what humans
create all the time, then we might be able to overcome such ideas of
ID. However, without such a naturalistic mechanism, and without
anything else in nature that produces such design-like systems of
function as comparable to what humans produce, we are left for the
time being with the only other logical alternative that life was in
fact designed by a purposeful intelligence.
> Forensic investigators most definitely do not say "Person X (or even
> 'persons unknown') did it using methods not yet detected, let alone
> identified; we just know it was done by someone somehow."
Certainly true . . . This is my whole point. It was done by someone
somehow, but we can still detect that it was done with the use of
intelligent purposeful design.
> Further, imagine a case where no cause of death can be determined. The
> most thorough examination rules out any *natural* cause of death (which
> means it must be 'designed', right?) as well as any cause of death
> attributable to human agency. As far as they can tell, the person just
> ceased all life processes for no reason.
Actually, since I do autopsies regularly and occasionally work with
the coroner's office, if a cause of death cannot be found, the death
is assumed to be the result of natural causes. Even the most
"thorough" examination cannot rule out all "natural" causes of death.
The human body is an extremely complex machine and because of this
there are an almost endless list of ways that it can be "broken" and
die. However, if it were possible to know every single working of the
human body, and if it could be determined that absolutely none of
these systems failed via some "normal" mindless naturalistic process,
design still could not be inferred. Nothing could be inferred as a
cause for such a death. It would have to remain a mystery.
Evidence of deliberate design is not found in a complete lack of all
evidence. Evidence for design is found in positive evidence that is
beyond the known capabilities of mindless naturalistic processes and
yet within the realm of known powers of intelligent design (namely our
own). Now, if you were to find some defect in the body that would
have reasonably led to the person's death, then this is a positive
finding. This positive finding can be consistent with either a
natural event or cause, or a designed process beyond the powers of any
known mindless process. For example, if at autopsy it is found that a
person's heart has been cleanly cut in four equal parts without any
evidence of skin penetration by a knife or other such devise, it can
still be assumed, without knowing who did this or how they did it,
that this tetrasected heart was the result of intelligent, purposeful
design.
> I really doubt this would be
> assumed to be murder. In fact, even if someone stepped forward and
> claimed "I killed him, but I won't say how I did it", I would still
> doubt this would be assumed to be murder (I'd like to hear it from the
> D.A. who would try and the judge who would convict in this case).
Murder is a different issue altogether. Not only does murder require
that evidence of process be produced, but evidence to support motive
as well. As you point out, a confession without evidence is not
enough to convict anyone of murder. But, although interesting, I fail
to see your point here.
> You will, in fact, find that all such fields in which we detect design
> or agency rely on prior knowledge of human design and/or agency. It does
> *not* proceed by eliminating naturalistic explanations.
It seems to me that you are mistaken here. We do not need to assume
human involvement at all to assume or detect design. You admitted as
much above when you said, " . . .we just know it was done by someone
somehow." Well if you can determine that something was done by
someone somehow, who is to say that this "someone" had to have been
human? Could it have been an animal? Could it have been an
intelligent alien with human-like capabilities? Or, maybe an
extremely intelligent alien who still used human-like capabilities far
more effectively than most humans use their own abilities? You know,
there is a range of intelligence among humans. Some humans are not so
brilliant while others, by comparison, are extremely brilliant. Is
the less intelligent human incapable of recognizing the works of the
more intelligent human as being designed, just because these works are
beyond the less intelligent human's ability to know exactly how or
even who designed such a marvelous and mysterious work? Must the less
intelligent human first meet and become familiar in detail with the
work of the more brilliant creator of the work that sits before him in
order to appreciate design over some naturalistic or potential
naturalistic process? Are we humans really that limited in our
abilities to at least detect deliberate design? I don't think so.
> > Also, many scientists, such as those spending millions on the SETI
> > projects, suggest the possibility of intelligent beings living
> > elsewhere in the universe. These scientists think that they can
> > detect the activity of intelligent design without having ever met
> > these proposed intelligent alien life forms. Now, what do you propose
> > that they are looking for? They are looking for evidence of phenomena
> > that cannot be explained via any known mindless naturalistic process.
> > In other words, they are looking for phenomena that require a
> > thoughtful, purposeful, intelligent mind.
>
> Wrong. They are looking for the use of an already known and recognized
> method/mechanism of technology. They are not looking for some vague
> "other than can be explained now" phenomenon. They are looking for the
> exact thing that we are capable of, something already defined.
Yes . . . something already defined although not necessarily human.
What they are looking for is some pattern that is different from the
normal background of "noise" that is normally produced by known
mindless naturalistic processes. They are looking for something
comparable to what we humans are capable of producing with our
intelligent minds. Of course, these alien life forms may be very much
different from us. They may use very different means of creativity or
design. How then do we hope to understand or even detect such
activity? By judging if such activity is beyond what we know
naturalistic processes are capable of producing. These scientists are
looking for unnatural order or patterns of code or language.
You know, just because we are capable of producing a given phenomenon
does not mean that this phenomenon can be recognized as having been
deliberately designed. For example, a human can break a window, but
so can a strong gust of wind. A human can form an amorphous rock so
that it looks quite "natural." But, so can a mindless natural
processes of erosion. You see then, something else is needed to
theorize intelligent design besides the ability for a human to have
made it. The something else that is needed to theorize design is the
inability for any known naturalistic processes to have produced a
given phenomenon.
So yes, as you suggest we need to ask the question, "Is this something
that the human ability for creative design might be capable of
producing?" If the answer to this question is yes, then the second
question that needs to be asked is, "Can any known naturalistic
process produce anything even close to this?" If the answer to this
question is no, then intelligent design is a reasonable choice. Your
example of a dead body with absolutely no identifiable cause of death
fails the first question. So, there is no automatic default to
determine cause of death in such a case. The answers to the first
question must be "yes" and the answer to the second question must be
"no" before the theory of intelligent design can be adequately
supported. Of course, there is always the chance that sometime in the
future a discovery might be made detailing previously unknown
abilities for mindless naturalistic processes which would change the
answer to the second question to a "yes." However, until this time,
the predictive power of the scientific method supports the theory of
ID better than it supports the theory of a mindless naturalistic
process.
Again, it seems to me that you are mistaken. Let me ask you, by what
"mechanism" was the Mona Lisa painted? By what mechanism do you brush
your teeth, turn on your radio, kiss your wife, build a house, or eat
a sandwich? Intelligent design certainly is a mechanism or a force
behind activities and creations. It is a mechanism just as much as
random mutation and natural selection is the "mechanism" or the
"driving force" for evolution. ID was the mechanism or driving force
for the design and construction of Michelangelo's David. Without ID
as a driving force, this sculpture would never have been formed. I'm
curious now, what term would you apply to ID if not a "mechanism" for
creative activities that require the workings of human-like
intelligence? Or, are you like the many who think that all mechanisms
that give rise to various phenomena must be mindless naturalistic
ones?
> A watch has never been *made* by ID. If you don't believe me, go to the
> nearest Timex or Casio assembly plant. Or the factories which
> manufacture the parts to be assembled. Or those that refine/generate the
> materials used in the parts. If ID was the mechanism by which watches
> were *made*, those companies would be able to save a lot on material and
> labor as they could have their draftsmen simply 'design' the watch into
> being.
Come again? Timex and Casio watches are indeed made with the use of
ID. Nothing in the process of their assembly happened without the use
of ID. The assembly plant itself was made with the use of ID. ID is
a mechanism in that it is a process of higher reasoning or mindful
intelligence that can be expressed in a directed way to affect objects
or events outside of the mind (ie: a Timex factory). Therefore, the
Timex watch was indeed created via the mechanism of ID as this
mechanism expressed itself. In any case, this seems to be an argument
of semantics at this point. You certainly know what I mean even if
you disagree with my use of the term "mechanism".
> ID has to be *applied* in order to materially effect *anything*. We know
> the mechanisms by which humans *apply* design and all design with which
> we are familiar require mechanisms of application (if they are to have
> any effect; whether or not you believe that designing something as in
> imagining it has an underlying mechanism, applying those thoughts to
> manufacture real-world objects requires mechanism(s)).
Ok fine. What "mechanisms" does a mindless nature use to change
things? The exact same mechanisms that humans use to create. So,
what is the difference here between human creation and the creations
of a mindless nature? The difference is that humans employ the power
of intelligent design to the "mechanisms of application" (as you
define the term) while mindless naturalistic processes do not have
access to intelligence purposeful design. You do actually seem to
realize that ID is a mechanism of thought. This thought mechanism is
able to express itself through mindless cause and effect processes
that the thoughtful mind can give rise to. However, without the
underlying *mechanism* of thought, the attached naturalistic
"mechanisms" are incapable of producing anything much in comparison.
For example, ask Christopher Reeves how creative his arms and legs are
without the mechanism of thought from his brain to guide them. Do the
nerves, muscles and bones of his limbs do anything much without the
mechanism of his higher mind? They certainly have the potential, but
potential just isn't good enough is it? The atoms just don't work
together to make much of anything without the thought mechanism of the
mind.
Please, you are really reaching here for something. Do try and be
reasonable or who is going to take you seriously?
> Additionally, without exception, all application of intelligent design
> that we are sure of (i.e. human design) are for the benefit of or serve the
> purpose of the designer(s). Whether said purpose is practical or esthetic
> or experimental in nature, some such purpose is *always* present and is
> *always* a purpose of the designer's.
Ok . . . and your point here is?
> To date, ID 'theory' is unable to provide methods/mechanisms, and it
> posits no detectable purpose of the designer. Lacking these it is forced
> to claim identification by elimination and proclaiming itself the
> default position when no naturalistic explanation is currently
> confirmed. I am baffled as to why proponents think designer-of-the-gaps
> is any more rational or tenable than god-of-the-gaps.
You have got to be joking, right? Intelligent design is certainly
capable of providing "methods/mechanisms" for the production of many
phenomena. Again, what was the "method/mechanism" by which ID was
involved with the formation of a Timex watch? Obviously, the idea of
a Timex watch came to the intelligent mind of an intelligent designer.
That idea was sent out through the nerves of the of the brain and
body to activate the body to act on the idea. The body manipulated
various external objects and events until eventually, the internal
reality or idea was turned into an external reality.
The concept of intelligent design is very reasonably applied or
proposed as an explanation of phenomena associated with all kinds of
activities having to do with forensic science, physics, astronomy,
medicine, biology, chemistry, and just about anything else one can
imagine. It seems strange then that this concept of ID is not allowed
into popular scientific theories concerning the origin of life. The
mechanism for the creation of all parts of various life forms would
logically be very similar to human creations that use ID. The idea of
life occurred to the mind of the designer. That thought was then
translated from the internal world of the designer's mind to the
external world. Various objects and events were manipulated in much
the same what that human designers manipulate things to create their
ideas. Such manipulation was continued until the inner idea of life
was reproduced in the external world. There . . . that is a
mechanism that matches exactly the human idea and use of ID to create.
The same process could easily have been used by the designer of life.
Obviously then, the theory of ID as it applies to the origin of
living things is certain NOT "unable to provide methods/mechanisms" as
an explanation for living things. This can easily be done. In fact,
humans are getting to the point where we can just about write our own
genetic sequences to produce novel life forms ourselves. So, the
original creation of such sequences and structures by another
intelligent mind is certainly not out of the question. Perhaps a
brilliant alien mind created life on this planet? It is not
unrealistic to think so. After all, humans are in fact capable of
making complex machines, like computers, that function in a similar
fashion to many of the systems and codes used by living things.
Also, to say that there is no detectable purpose of the designer and
thus no evidence of design is ludicrous. I might have trouble
detecting the purpose of Picaso, but I certainly have no trouble
detecting deliberate intelligent design in his paintings. You
yourself indicated that some designer's create for their own pleasure
or esthetic sensibilities. Well, just look around you? Do you see or
recognize anything that you can appreciate as esthetically pleasing in
nature? Do you take pleasure in anything that you experience in life?
If you find aesthetically pleasing sights and if you find pleasure in
your life, why then wouldn't you be able to see that a designer of
such an amazing place might not just find a bit of pleasure in it as
well?
As far as you confusion about the difference between a "god" and a
"designer", there is none. All designers are basically "gods" of
their creations. The ability to create is basically a godlike
ability. In fact, the word "creator" is often used in books like the
Bible as being synonymous with the word, "god." Even humans are
described in the Bible with the term "gods" by Christ Himself. So,
the "god-of-the-gaps" argument is exactly the same as the
"designer-of-the-gaps" argument. There is no differences. Who ever
is the designer and creator of life is the God of life, just as you
are the god of whatever you create (ie: It is indebted to you for its
existence).
Now, it is my turn to be baffled. I am baffled by those who cling to
the notion that a naturalistic explanation must exist somewhere
somehow to explain life when there is every indication that it is far
more easily and reasonably explained by human-like forces of
intelligent design. There is nothing even close in the workings of a
mindless nature than can explain the workings of life forms. Without
such a naturalistic mechanism, the answer to the first question that I
asked earlier (Is this something that the human ability for creative
design might be capable of producing?) is yes, though maybe not on as
high a level. The answer to the second question (Can any known
naturalistic process produce anything even close to this?) is a clear
. . . No. Given these answers the only current reasonable conclusion
is that ID was/is most likely responsible for the origins of life on
this planet.
Not so as detailed above. You are really reaching and seem to have an
almost desperate need to hang onto the theory of naturalism as a cause
or explanations for the origins of life even though you clear
understand the role of ID in many other phenomena. Yet, you draw the
line at the origin of life without an understanding or ability to
detail any means by which a mindless nature could have produced such
wonders that only have their shadow of a comparison in the works of
the highest human intelligence and creativity. This simply boggles my
mind. How blind can one get?!
> That does not say that naturalism must explain everything. It simply says
> that, to date, ID explains nothing.
Not so. ID is the only force that comes even close to explaining the
origin of life. Human ID is the only parallel that even seems to
approach the complexity and obvious ingenuity that we see in living
things. In comparison, naturalism is pure nonsense. It explains a
few things, but in comparison to ID, naturalism is the theory that
explains "nothing" when it comes to the origins of living things.
Sean
Ron Okimoto
You don't remember your own calculations you claimed that with a
population of a trillion (trivial for bacteria) that in 2 years you
would span a gap of 20 amino acids changes. It got to be unwieldy at
30. That was an order of magnitude shift in your goal posts. This is
not barely budging. I know that your probable estimate of the age of
the earth is likely 5 orders of magnitude off, but most people think
that a two fold shift is big and an order of magnitude is huge.
Perceptions seem to be relative, but you only think the way you do
because your view of reality is so far off that an order of magnitude
seems small.
You still don't have an example where even 4 or 5 is necessary.
Dawkins is wrong, just by what variation we know there are only 5 or 7
(I can't recall exactly) invariant positions that have to be in the
hemoglobin molecule to keep it functioning. All the other positions
are known to have changed in one species or another. You have to also
figure out how many other possible ways besides those 5 or 7 invariant
positions that you could get similar function using some other oxygen
carrier other than heme. It looks like heme got used because it was
very similar in structure to existing porforin ring compounds being
used for other things in the cells. Do you have some proof that heme
had to be used as the oxygen carrier? The designer wouldn't have to
do these things, but lifeforms would be expected to cobble things
together from what was available.
>
> So, it is true that many if not most proteins have a degree of
> plasticity, but generally speaking, proteins are quite rigid or
> specific in their sequencing. If changed beyond a certain point, they
> loose ALL function. At this point, further changes to the sequence of
> a non-functional protein are, yes, functionally neutral. Your
> hypothetical plane of function becomes perfectly flat at this point.
> Random walk takes over and further mutations are lost on an almost
> endless sea of random drift.
Your problem is that this isn't true for anything that we seem to want
to get to. Can you come up with an example of this? Remember the
antibody examples and only 10^12 trials to get a novel function. If
you were right, what is the chance that they would get any new
enzymatic function in 10^12 trials let alone the one that they test
for. John may be pretty close to pegging it with his idea. How come
it is possible if you claim that it is impossible?
>
> You and Ron like to think that these depressions or islands of
> functional land that surround maximal protein function are almost
> infinite, but clearly they aren't even close. If they were just about
> "infinite" as Ron has suggested, then why did Hall's E.coli, who
> lacked the ebg and lacZ genes, have such a difficult time evolving the
> lactase function back again? Despite a high mutation rate, a large
> population size, and thousands upon thousands of generations, they
> never did evolve the lactase function back again. The same thing
> happens with many other types of bacteria. Our hospital logs have
> records on many types of bacteria going back over 40 years and many of
> these have never tested lactase positive over this entire time
> (representing over a million generations for many of them). If the
> depression around this function were truly close to infinite in scope,
> then just about any other gene or genetic sequence in the E. coli
> genome would be expected to have at least *some* beneficial lactase
> type function . . . wouldn't you think? And, given this "slope", one
> would expect a more rapid tendency to slide down toward the middle . .
> . right? So then, where did our hypothesis go wrong with Hall's mutant
> E. coli bacteria? Hmmmmmm?
Well if you have read my other posts you know that Hall didn't have
the proper selection scheme for finding these types of mutations. He
even gave his explanation for why he didn't expect to find these
mutations, but you blew it off and tried to claim that this meant it
was impossible. Hall requires fixation of the first two mutations
before he is likely to see the third mutation in his system. The
reason for this is that you have to see the third mutation within a
very few cell divisions after the bacteria is plated in order to see a
white or pink colony. It would be nearly imposible for Hall to span a
gap of two let alone 3 mutations using his selection scheme. Hall was
able to span your gap when all he was selecting for was better growth
instead of red or white. What does that tell you? Your own
calculations tell you why it is possible to do this. Normal evolution
does not require fixation of each mutation before you get the next one
does it?
How many individual bacteria have been tested for lactase activity in
40 years? Why would you expect them to have enough activity to show
up on some test? No one but you expect them to have full blown
activity. The thing is that when E coli was evolving lactase activity
no other bacteria had such activity and there was no competition in
that area. Now we have bacteria that can do it and any new bug that
evolves this activity has to compete with these bacteria for the food
source. Who is going to win? Why can Hall get other species to
evolve lactase activity? My search turned up two other species that
he was able to do his trick on. You lose on this one too.
>
> The problem is that, relatively speaking, these islands of function
> are quite small indeed. When compared to the total number of
> completely non-functional sequences out there in the ocean of
> non-function, those sequences that have any function whatsoever (from
> the perspective of a given life form in a given environment), make up
> only the tiniest of fractions, especially when you start talking about
> functions that require amino acid sequences that average more than one
> enzymatic-type protein in length. When functions require multiple
> proteins totaling several hundred, thousand, or even tens or hundreds
> of thousands of amino acids in length, then your little islands with
> their little impressions don't come near close enough to avoid the
> random drift problem.
They are likely small for any one sequence, but there are a lot of
sequences and a lot of possible functions, and when you change a
sequence you change its functional potential. You can't just look at
the potential functions of any single extant proteins, but you have to
look at the potential function of all the molecules that you can get
by changing just 1 to 3 amino acid positions. You know that this is
possible. If you make one or two changes you can significantly change
the landscape for any function, can't you?
You keep forgetting that according to science, evolution doesn't have
a plan and that lactase activity isn't some goal. If it happens,
fine, you get something that may be useful. If it doesn't happen,
fine, the bacteria keeps on going just like it always did.
Explain the antibody results if you are correct. Why is the
impossible, possible for antibodies? Why do you only have to score
10^12 events before you find the activity that you select for? By the
early 1990's they had already produced over 70 different enzymatic
activities using antibodies. I think that they have their own name,
now, and they are called abzymes. If you do a PubMed search you will
likely find references to a whole lot more enzymatic activities by
now.
>
> But, there is something hopeful about your hypothetical suggestion.
> The very fact that you proposed such a hypothetical solution to the
> problem means that you might actually recognize the problem, which is
> a significant step. In any case, I remain most interested in your
> thoughts and struggles with this issue.
>
> Sean
It is not an explanation for a problem, but for what we observe
occuring in nature. There is a difference that you seem to be
missing. We see this happening. You have to claim that what we
already observe to occur is impossible. That is what is wrong with
your argument. Our only problem seems to be trying to explain why it
seems to be so easy to get function from a protein sequence. A better
argument for you and one that the ID people use is that since we don't
have a good explanation for how we evolve these functions that some
designer must be responsible for guiding these mutations and making
the results happen. The problem with the ID argument is that it is
stupid. Just try and find some evidence to support it.
Ron Okimoto
Jason Cortina
Please show reference to documentation showing current regular use of
the methodology in which the determination of "deliberate purposeful
intelligence" is based *solely* on consideration of mindless
naturalistic mechanisms, without any consideration of mechanisms known
to be used by or thought reasonably possible to be used by known
intelligences.
> A scientist in not limited to the use of knowledge concerning the
> known abilities of human creativity alone, but a scientist can also
> take into account the known limitations of naturalistic processes as
> well. For example, if I went to the moon and found a series of
> perfectly round 10kg rocks all arranged in a perfect geometric square
> measuring a mile on each side, it would be very reasonable of me to
> theorize that some sort of purposeful intelligence, above any sort of
> mindless naturalistic process, was at work here.
Because you already have prior knowledge of humans using (and tending
to prefer) perfect shapes and geometries.
>
> Would this conclusion be so shocking to you? Would you propose a
> different theory as an explanation for this phenomenon? Of course,
> you might suggest that humans are perfectly capable of creating such
> an unnatural setup as this, and so therefore we can assume design in
> such a case based on this similarity to what humans can do. And, I
> would have to agree. The problem is, the genetic information
> contained in DNA is very much like the coded language systems that
> humans have created and use, such as English, Greek, Spanish, computer
> code, the Morse Code, sign language, etc. In fact, it is so similar
> to such language systems that humans are quite capable and quite
> comfortable playing with the genetic codes and language-like sequences
> that code for living things.
I have done some (not extensive) study on (human) languages. I have
worked professionally in computer languages and coding for nearly
three decades. While I appreciate the usefulness of the analogy,
I see no actual correspondence between DNA and language, coded or
not.
> And, we are getting better at it all the
> time. It seems to almost come naturally to us; like genetics is
> written in a language that is so similar to what we understand that
> playing with it is practically second nature. How then, given that
> life and the basic codes of life are so similar to the languages
> systems and codes of our own making, can we exclude the possibility
> that such a coded language system that we find in living things was in
> fact designed in much the same way that we have designed very similar
> languages and codes? Of course, if we were to one day find some
> naturalistic mechanism that could adequately explain the existence of
> such an obviously creative phenomena, very similar to what humans
> create all the time, then we might be able to overcome such ideas of
> ID. However, without such a naturalistic mechanism, and without
> anything else in nature that produces such design-like systems of
> function as comparable to what humans produce, we are left for the
> time being with the only other logical alternative that life was in
> fact designed by a purposeful intelligence.
I still see no more than the slightest correspondence between
language and DNA. I don't know any language in which messages
consist of a majority of gibberish which is itself communicated
in successive iterations of the message.
>
> > Forensic investigators most definitely do not say "Person X (or even
> > 'persons unknown') did it using methods not yet detected, let alone
> > identified; we just know it was done by someone somehow."
>
> Certainly true . . . This is my whole point. It was done by someone
> somehow, but we can still detect that it was done with the use of
> intelligent purposeful design.
Please read what I wrote. The sentence clearly states that no method of
any kind was detected, let alone identified. With no method, no mechanism
used, the conclusion of being done by somebody is not reached. Assigning
cause to an intelligent agent in such a case is not done. Of course, you
could give me reference to such.
Keep that thought, "yet within the realm of known powers of intelligent
design (namely our own)". What are the systems/phenomena which ID says,
regarding life's origin, are the result of design which are "within the
realm of known powers of intelligent design (namely our own)"?
>
> > I really doubt this would be
> > assumed to be murder. In fact, even if someone stepped forward and
> > claimed "I killed him, but I won't say how I did it", I would still
> > doubt this would be assumed to be murder (I'd like to hear it from the
> > D.A. who would try and the judge who would convict in this case).
>
> Murder is a different issue altogether. Not only does murder require
> that evidence of process be produced, but evidence to support motive
> as well. As you point out, a confession without evidence is not
> enough to convict anyone of murder. But, although interesting, I fail
> to see your point here.
>
> > You will, in fact, find that all such fields in which we detect design
> > or agency rely on prior knowledge of human design and/or agency. It does
> > *not* proceed by eliminating naturalistic explanations.
>
> It seems to me that you are mistaken here. We do not need to assume
> human involvement at all to assume or detect design. You admitted as
> much above when you said, " . . .we just know it was done by someone
> somehow."
And pointed out that this was a conclusion never validly reached. You
said nothing which contradicted my statement, only showed that you did
not read it as written. As I note below, my limitation to humans is
erroneous, yet detection still uses prior knowledge of purposeful
mechanisms to determine purposeful agency.
> Well if you can determine that something was done by
> someone somehow, who is to say that this "someone" had to have been
> human? Could it have been an animal? Could it have been an
> intelligent alien with human-like capabilities? Or, maybe an
> extremely intelligent alien who still used human-like capabilities far
> more effectively than most humans use their own abilities? You know,
> there is a range of intelligence among humans. Some humans are not so
> brilliant while others, by comparison, are extremely brilliant. Is
> the less intelligent human incapable of recognizing the works of the
> more intelligent human as being designed, just because these works are
> beyond the less intelligent human's ability to know exactly how or
> even who designed such a marvelous and mysterious work? Must the less
> intelligent human first meet and become familiar in detail with the
> work of the more brilliant creator of the work that sits before him in
> order to appreciate design over some naturalistic or potential
> naturalistic process? Are we humans really that limited in our
> abilities to at least detect deliberate design? I don't think so.
You are correct; I worded that erroneously. It should not be limited
to humans, rather it should read:
You will, in fact, find that all such fields in which we detect design
or agency rely on prior knowledge of purposeful directed design and/or
agency. It does *not* proceed by eliminating naturalistic explanations.
>
> > > Also, many scientists, such as those spending millions on the SETI
> > > projects, suggest the possibility of intelligent beings living
> > > elsewhere in the universe. These scientists think that they can
> > > detect the activity of intelligent design without having ever met
> > > these proposed intelligent alien life forms. Now, what do you propose
> > > that they are looking for? They are looking for evidence of phenomena
> > > that cannot be explained via any known mindless naturalistic process.
> > > In other words, they are looking for phenomena that require a
> > > thoughtful, purposeful, intelligent mind.
> >
> > Wrong. They are looking for the use of an already known and recognized
> > method/mechanism of technology. They are not looking for some vague
> > "other than can be explained now" phenomenon. They are looking for the
> > exact thing that we are capable of, something already defined.
>
> Yes . . . something already defined although not necessarily human.
> What they are looking for is some pattern that is different from the
> normal background of "noise" that is normally produced by known
> mindless naturalistic processes. They are looking for something
> comparable to what we humans are capable of producing with our
> intelligent minds. Of course, these alien life forms may be very much
> different from us. They may use very different means of creativity or
> design. How then do we hope to understand or even detect such
> activity? By judging if such activity is beyond what we know
> naturalistic processes are capable of producing. These scientists are
> looking for unnatural order or patterns of code or language.
I repeat. They are looking for a specific *effect*, that of a radio
signal, having the narrow range of characteristics already known to
have purposefully directed action as a cause.
By the application of paints to, well, wood I believe in the specific case
of that work. The mechanism was directed by the design specification of
a human agent.
> By what mechanism do you brush
> your teeth, turn on your radio, kiss your wife, build a house, or eat
> a sandwich? Intelligent design certainly is a mechanism or a force
> behind activities and creations. It is a mechanism just as much as
> random mutation and natural selection is the "mechanism" or the
> "driving force" for evolution. ID was the mechanism or driving force
> for the design and construction of Michelangelo's David.
I disagree. For this to be so, it must be restated as 'ID was the driving
force for the design of Michelangelo's David directing the mechanism of
applying chisel to marble(?) for its construction'.
> Without ID
> as a driving force, this sculpture would never have been formed. I'm
> curious now, what term would you apply to ID if not a "mechanism" for
> creative activities that require the workings of human-like
> intelligence? Or, are you like the many who think that all mechanisms
> that give rise to various phenomena must be mindless naturalistic
> ones?
Design may be necessary for these things. But it is not sufficient.
>
> > A watch has never been *made* by ID. If you don't believe me, go to the
> > nearest Timex or Casio assembly plant. Or the factories which
> > manufacture the parts to be assembled. Or those that refine/generate the
> > materials used in the parts. If ID was the mechanism by which watches
> > were *made*, those companies would be able to save a lot on material and
> > labor as they could have their draftsmen simply 'design' the watch into
> > being.
>
> Come again? Timex and Casio watches are indeed made with the use of
> ID.
Necessary but not sufficient.
> Nothing in the process of their assembly happened without the use
> of ID.
Necessary but not sufficient.
> The assembly plant itself was made with the use of ID.
Necessary but not sufficient.
> ID is
> a mechanism in that it is a process of higher reasoning or mindful
> intelligence that can be expressed in a directed way to affect objects
> or events outside of the mind (ie: a Timex factory).
No. Mindful intelligence cannot, as far as has been unambiguously
demonstrated, "affect objects or events outside of the mind". It can
only, by known/demonstrable naturalistic neural/chemical/electrical
processes, direct a physical system to do so (or direct a physical
system, the body, to take such actions as direct another physical
system, e.g. a machine, to do so). The work of those systems is the
mechanism by which the design is applied/implemented/realized.
> Therefore, the
> Timex watch was indeed created via the mechanism of ID as this
> mechanism expressed itself. In any case, this seems to be an argument
> of semantics at this point. You certainly know what I mean even if
> you disagree with my use of the term "mechanism".
I know what you have said. Design is indeed a necessary component
in manufacturing these things. It is not sufficient. The mechanism
lies in the application of design.
>
> > ID has to be *applied* in order to materially effect *anything*. We know
> > the mechanisms by which humans *apply* design and all design with which
> > we are familiar require mechanisms of application (if they are to have
> > any effect; whether or not you believe that designing something as in
> > imagining it has an underlying mechanism, applying those thoughts to
> > manufacture real-world objects requires mechanism(s)).
>
> Ok fine. What "mechanisms" does a mindless nature use to change
> things? The exact same mechanisms that humans use to create. So,
> what is the difference here between human creation and the creations
> of a mindless nature? The difference is that humans employ the power
> of intelligent design to the "mechanisms of application" (as you
> define the term) while mindless naturalistic processes do not have
> access to intelligence purposeful design.
And, most often, humans use combinations (usually series, actually) of
otherwise mindless naturalistic processes that are thought unlikely (at
least have not been observed) to occur without guidance. The manufacture
of a stainless steel place setting requires a number of steps, each one
of which can occur naturally, resulting in something nature is highly
unlikely to produce. On the other hand, nature seems to employ
combinations (often simultaneous) of processes which we do not (if/when
we attain fusion, I doubt it will take the formation of an entire star
to implement it).
> You do actually seem to
> realize that ID is a mechanism of thought. This thought mechanism is
> able to express itself through mindless cause and effect processes
> that the thoughtful mind can give rise to. However, without the
> underlying *mechanism* of thought, the attached naturalistic
> "mechanisms" are incapable of producing anything much in comparison.
> For example, ask Christopher Reeves how creative his arms and legs are
> without the mechanism of thought from his brain to guide them.
Please show a single documented unambiguous case where thought
expressed itself externally without attached naturalistic
mechanisms. Just one.
But I do thank you for bringing up an excellent illustration. You see,
no matter what purpose or plan or intent Mr. Reeves' mind may envision,
there will be no affect on material reality as those things have no way
of being applied. No matter how hard he wills himself, no matter how
perfectly his visualizes it, no matter how closely his brain matches the
signaling he once used (at least hypothetically) to implement the act
of brushing his teeth, he lacks the means, the mechanism to do so.
The design is not the mechanism.
> Do the
> nerves, muscles and bones of his limbs do anything much without the
> mechanism of his higher mind? They certainly have the potential, but
> potential just isn't good enough is it? The atoms just don't work
> together to make much of anything without the thought mechanism of the
> mind.
>
> Please, you are really reaching here for something. Do try and be
> reasonable or who is going to take you seriously?
I consider this quite reasonable. Design has no effect on material
reality until it is applied. That application requires mechanism,
and the design itself is not it.
>
> > Additionally, without exception, all application of intelligent design
> > that we are sure of (i.e. human design) are for the benefit of or serve
the
> > purpose of the designer(s). Whether said purpose is practical or esthetic
> > or experimental in nature, some such purpose is *always* present and is
> > *always* a purpose of the designer's.
>
> Ok . . . and your point here is?
>
> > To date, ID 'theory' is unable to provide methods/mechanisms, and it
> > posits no detectable purpose of the designer. Lacking these it is forced
> > to claim identification by elimination and proclaiming itself the
> > default position when no naturalistic explanation is currently
> > confirmed. I am baffled as to why proponents think designer-of-the-gaps
> > is any more rational or tenable than god-of-the-gaps.
>
> You have got to be joking, right? Intelligent design is certainly
> capable of providing "methods/mechanisms" for the production of many
> phenomena. Again, what was the "method/mechanism" by which ID was
> involved with the formation of a Timex watch?
Already-known human-used methods/mechanisms. You have failed to show any
case where the detection methods proposed by ID 'theory' are actually
used. This smoke screen they (and you) promote that such detection is no
different whether detecting human work or some unknown intelligence is
just that, a smoke screen.
> Obviously, the idea of
> a Timex watch came to the intelligent mind of an intelligent designer.
> That idea was sent out through the nerves of the of the brain and
> body to activate the body to act on the idea. The body manipulated
> various external objects and events until eventually, the internal
> reality or idea was turned into an external reality.
And that manipulation of external reality is mechanism. For any design
to impact external reality, it must be applied via some mechanism.
The design is *not* the mechanism.
>
> The concept of intelligent design is very reasonably applied or
> proposed as an explanation of phenomena associated with all kinds of
> activities having to do with forensic science, physics, astronomy,
> medicine, biology, chemistry, and just about anything else one can
> imagine.
No, the general concept of *human* design is used. The detection of
such does not use the principles put forth by ID 'theory'.
> It seems strange then that this concept of ID is not allowed
> into popular scientific theories concerning the origin of life. The
> mechanism for the creation of all parts of various life forms would
> logically be very similar to human creations that use ID. The idea of
> life occurred to the mind of the designer. That thought was then
> translated from the internal world of the designer's mind to the
> external world. Various objects and events were manipulated in much
> the same what that human designers manipulate things to create their
> ideas.
And these manipulations *are* the mechanisms. As these are, by your own
description, interacting with material reality they should be subject,
at least in principle, to investigation. So what are these mechanisms.
At the moment, you propose a Christopher Reeves designer, one with no
means of implementing design. If there are no ideas now, what research
is proposed in order to discover this?
> Such manipulation was continued until the inner idea of life
> was reproduced in the external world. There . . . that is a
> mechanism that matches exactly the human idea and use of ID to create.
> The same process could easily have been used by the designer of life.
> Obviously then, the theory of ID as it applies to the origin of
> living things is certain NOT "unable to provide methods/mechanisms" as
> an explanation for living things.
Again, design is not mechanism. Design can direct mechanism; mechanism
can apply design. For purposeful direction to be implemented in
material reality, both design and mechanism are necessary.
> This can easily be done. In fact,
> humans are getting to the point where we can just about write our own
> genetic sequences to produce novel life forms ourselves. So, the
> original creation of such sequences and structures by another
> intelligent mind is certainly not out of the question. Perhaps a
> brilliant alien mind created life on this planet? It is not
> unrealistic to think so. After all, humans are in fact capable of
> making complex machines, like computers, that function in a similar
> fashion to many of the systems and codes used by living things.
>
> Also, to say that there is no detectable purpose of the designer and
> thus no evidence of design is ludicrous. I might have trouble
> detecting the purpose of Picaso, but I certainly have no trouble
> detecting deliberate intelligent design in his paintings.
And I tried to make clear that either a clear mechanism or clear purpose
must be detectable. Design is not mechanism and no mechanism by which
purported design has been applied in order to affect material reality
has been proposed. Neither has any purpose behind such design. In
absence of knowledge (or any idea whatsoever) of 'how' something
happened (applied mechanism indicative of implementing design), one
could still logically and provisionally allow the possibility of design
if there is a rather clear purpose for the thing being examined.
If one finds an object which appears to be quite well suited to be an
axe head despite any clear tools on it, one might still consider it for
further investigation. If it matches no human work previously found and
no sign of shaping it can be detected, I do not think it can be
considered as a designed thing. Even if a geologist or other mineral
specialist finds that the particular material the thing is composed of
has never been known to naturally fracture into such shapes.
> You
> yourself indicated that some designer's create for their own pleasure
> or esthetic sensibilities. Well, just look around you? Do you see or
> recognize anything that you can appreciate as esthetically pleasing in
> nature? Do you take pleasure in anything that you experience in life?
> If you find aesthetically pleasing sights and if you find pleasure in
> your life, why then wouldn't you be able to see that a designer of
> such an amazing place might not just find a bit of pleasure in it as
> well?
So, as with the "axe" above, given a posited purpose, one would still
need to show a possible method/mechanism by which the thing might have
come to be.
>
> As far as you confusion about the difference between a "god" and a
> "designer", there is none. All designers are basically "gods" of
> their creations. The ability to create is basically a godlike
> ability. In fact, the word "creator" is often used in books like the
> Bible as being synonymous with the word, "god." Even humans are
> described in the Bible with the term "gods" by Christ Himself. So,
> the "god-of-the-gaps" argument is exactly the same as the
> "designer-of-the-gaps" argument. There is no differences. Who ever
> is the designer and creator of life is the God of life, just as you
> are the god of whatever you create (ie: It is indebted to you for its
> existence).
At least someone is willing to state this outright. But then, I don't
consider human designers to be gods to their implemented designs.
>
> Now, it is my turn to be baffled. I am baffled by those who cling to
> the notion that a naturalistic explanation must exist somewhere
> somehow to explain life when there is every indication that it is far
> more easily and reasonably explained by human-like forces of
> intelligent design. There is nothing even close in the workings of a
> mindless nature than can explain the workings of life forms. Without
> such a naturalistic mechanism, the answer to the first question that I
> asked earlier (Is this something that the human ability for creative
> design might be capable of producing?) is yes, though maybe not on as
> high a level. The answer to the second question (Can any known
> naturalistic process produce anything even close to this?) is a clear
> .. . . No. Given these answers the only current reasonable conclusion
Not so blind that I think it should be scientifically accepted that mind
can directly manipulate external reality. That's what would be necessary
for design to be considered a mechanism.
I draw no lines. I do not hold nature *must* explain the origin of life
and recognize naturalistic explanations have not done so.
Any supreme being I envision could alter reality by act of will. This is
a metaphysical stance and not subject to any known or postulated method
of verification or testing. It has no place in science.
And I do not see how anything in the current postulates of ID comes any
closer to demonstrating this. It most definitely gives no explanation of
it (in any truly useful sense of the word 'explanation'). It posits the
tiniest fraction of a prologue to 'how': the guidance of intelligence
doing...who knows what (no mechanism(s); as they must interact with
material reality they are, at least in principle, subject to
investigation). And current known design detection relies on detection of
mechanism.
So the current situation is either:
Life originated from unguided natural forces doing...we don't know
or
Life originated from intelligent guidance doing...we don't know
Odd that you could call anyone blind if you think the latter
actually explains anything in any scientifically useful sense
of the word.
>
> > That does not say that naturalism must explain everything. It simply says
> > that, to date, ID explains nothing.
>
> Not so. ID is the only force that comes even close to explaining the
> origin of life. Human ID is the only parallel that even seems to
> approach the complexity and obvious ingenuity that we see in living
> things. In comparison, naturalism is pure nonsense. It explains a
> few things, but in comparison to ID, naturalism is the theory that
> explains "nothing" when it comes to the origins of living things.
>
--
Jason A Cortina
Marge, please. Old people don't need companionship. They
need to be isolated and studied so that it can be determined
what nutrients they have that might be extracted for our
personal use.
-- Homer Simpson
John Harshman
Ron Okimoto wrote:
Just a couple of thoughts: another problem with Hall's selection
experiments on bacteria is that he's relying on existing genes to pick
up the function of a deleted gene. But they aren't entirely free to
evolve, even neutrally. Each of those proteins has a function which it
must maintain. A mutation that helps to replace the lost function must
also preserve the protein's current function, so there is the
possibility of selection rejecting mutations because, even if they help
regain the lost function, they may degrade the protein's current
function enough to make net selection negative. I don't know how
important that factor would be in practice, but it's something to
consider. A lot of evolution can get around this problem by beginning
with a gene duplication, allowing different copies to experience
selection in different directions.
Second, there really should be a FAQ on all the selection experiments
like this, especially the ones that involve functions evolved from
random sequences. How much of that literature do you know?
John Harshman
Jason Cortina wrote:
[snip]
> I still see no more than the slightest correspondence between
> language and DNA. I don't know any language in which messages
> consist of a majority of gibberish which is itself communicated
> in successive iterations of the message.
That's easy: English, as embodied in talk.origins posts. See
particularly posts by J. McCoy, G. Sheldon, and that weird "lichens are
plants" person whose name I mercifully forget.
Jason Cortina
Wasn't that Sh/B*boo
(who may be posting now as, or has some connection to, Andromeda for the
Skeptical Christian site)?
--
Jason A Cortina
So far as I can remember, there is not one word in the Gospels in praise
of intelligence.
-- Bertrand Russell
catshark
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>For example, if I went to the moon and found a series of
>perfectly round 10kg rocks all arranged in a perfect geometric square
>measuring a mile on each side, it would be very reasonable of me to
>theorize that some sort of purposeful intelligence, above any sort of
>mindless naturalistic process, was at work here.
Before or after I went to a beehive and saw "perfectly" hexagonal
honeycombs? Or are bees Intelligent Designers?
And what would I do after I then went to Devil's Tower and saw the
hexagonal basalts? Volcanos are "purposeful"?
---------------
J. Pieret
---------------
The devil is in the details.
Science explains them.
Intelligent design explains them away.
- Mark VandeWettering -
Ron Okimoto
> Ron Okimoto wrote:
>
Snip:
> >
> > It is not an explanation for a problem, but for what we observe
> > occuring in nature. There is a difference that you seem to be
> > missing. We see this happening. You have to claim that what we
> > already observe to occur is impossible. That is what is wrong with
> > your argument. Our only problem seems to be trying to explain why it
> > seems to be so easy to get function from a protein sequence. A better
> > argument for you and one that the ID people use is that since we don't
> > have a good explanation for how we evolve these functions that some
> > designer must be responsible for guiding these mutations and making
> > the results happen. The problem with the ID argument is that it is
> > stupid. Just try and find some evidence to support it.
>
>
> Just a couple of thoughts: another problem with Hall's selection
> experiments on bacteria is that he's relying on existing genes to pick
> up the function of a deleted gene. But they aren't entirely free to
> evolve, even neutrally. Each of those proteins has a function which it
> must maintain. A mutation that helps to replace the lost function must
> also preserve the protein's current function, so there is the
> possibility of selection rejecting mutations because, even if they help
> regain the lost function, they may degrade the protein's current
> function enough to make net selection negative. I don't know how
> important that factor would be in practice, but it's something to
> consider. A lot of evolution can get around this problem by beginning
> with a gene duplication, allowing different copies to experience
> selection in different directions.
Just like antibodies have structural constraints that do not seem to
matter other protein structures would have their contraints too. Even
with these constraints new activity is observed to evolve in
antibodies. It is just another indication that proteins are probably
very plastic and that only a small fraction of the sequence space
needs to be explored before your divots are found that facilitate
evolution to function.
>
> Second, there really should be a FAQ on all the selection experiments
> like this, especially the ones that involve functions evolved from
> random sequences. How much of that literature do you know?
I haven't kept up with this research since I was a graduate student.
I used to have some references the latest one was probably 1992 or 93.
There is likely to be a lot more on the subject by now. I saw a
paper within the last couple of years that may support your idea, but
other factors could be involved. This was a mouse abzyme paper where
they evolved the same enzymatic activity from the same clonal start
several times. Since they knew the starting sequence, they found that
all the replicates had one mutation in common. They indicated that
this could be a key mutation that had to occur in order for either
other mutations to be selected for or to push the molecule in enough
of the right direction to enable initial selection. I can't remember
the authors. I don't keep track of this literature.
Ron Okimoto
Sean Pitman
> Just a couple of thoughts: another problem with Hall's selection
> experiments on bacteria is that he's relying on existing genes to pick
> up the function of a deleted gene. But they aren't entirely free to
> evolve, even neutrally. Each of those proteins has a function which it
> must maintain. A mutation that helps to replace the lost function must
> also preserve the protein's current function, so there is the
> possibility of selection rejecting mutations because, even if they help
> regain the lost function, they may degrade the protein's current
> function enough to make net selection negative. I don't know how
> important that factor would be in practice, but it's something to
> consider. A lot of evolution can get around this problem by beginning
> with a gene duplication, allowing different copies to experience
> selection in different directions.
Yes, this is quite a problem indeed. Gene duplication is supposed to
get around this problem by creating sequences that can undergo neutral
drift while maintaining previous functional sequences. However,
Hall's E. coli didn't do this either. They simply didn't evolve the
lactase function by any means, not even by gene duplication. Neither
have many other types of bacteria despite huge numbers of observed
generations (over a million).
In any case, even given gene duplication, the problem remains. The
gaps between what there is and new beneficial sequences are smaller
with more simple functions, but they quickly expand beyond any
reachable distance with increasing complexity, especially when one
starts considering functions that require multiple proteins with total
sequence lengths in the thousands, tens of thousands, or even hundreds
of thousands of amino acids. Very quickly neutral gaps (between such
functions and the current genomic real estate of a given gene pool)
develop that are simply enormous. . . too enormous for neutral drift
to ever cross in any sort of reasonable amount of time.
Ron Okimoto likes to argue that experiments done with antibodies
(where other enzymatic type functions are also detected in such
antibody collections) are good evidence of the power of selection to
produce new functions from a random collection of amino acid
sequences. This is a deceptive argument in that it glosses over
several problems. One problem is that a given gene pool is limited in
its ability to produce such varieties of random sequences, as you
noted above. E. coli bacteria, for example, are limited in the amount
of genetic real estate that they can devote to the production of
random amino acid sequences. In fact, they are very limited indeed
since most of the genome of a given bacterium is actually
"functional". Another problem is that even when "new" functions are
isolated in these experiments with antibodies, these new functions are
always relatively simple (almost always enzymatic type functions) that
require a single, relatively short, amino acid sequence. As
previously noted, simple functions, like three-letter-words in the
English language, will be found closer together in the sea of
non-function. However, more complex functions, requiring longer and
still longer sequences, are far more rare when one starts looking for
them in a random pile of sequences. For example, if I were to throw a
bunch of Scrabble letters out on a table, just by random chance alone,
I would most likely be able to see many 3-letter words lined up in the
pile of blocks. However, I would see fewer 4-letter words and
probably only one or two 5-letter words and maybe, after a several
tries, a 6-letter word. You get the point. Antibody experiments work
the same way.
Perhaps though, the most important problem with these antibody
experiments having much of anything to do with evolution in real life
is that just because a cell comes up with a sequence that does a
particular function does not mean that this cell will be set up in
such a way that it can use this sequence to its own advantage or for
the advantage of the larger organism or community of organisms that it
is a part of. For example, just because a human plasma cell (antibody
producing cell) makes an antibody that also has a lactase function
does not mean that this lactase function will be of any benefit.
Almost certainly, the lactase function of the antibody will be
completely worthless because this protein is not produced in the right
place at the right time (ie: The intestines for example). Also, the
memory of this plasma cell or clonal B-cell population cannot be
passed on to the next generation of humans even if it were to have
some beneficial function beyond its normal antibody function. In
reality, all this antibody would be good for is to work like an
antibody, not as a lactase enzyme. You see, just because a functional
sequence comes along by random chance or drift does not mean that it
can be used to some benefit or contribute to genetic evolution over
time.
So, although these antibody experiments are intriguing indeed, they
obviously say very little about the evolution of much of anything.
The gap problem remains a mystery for those who continue to hold to
purely naturalistic explanations of the origin of life on this planet.
It has not been explained and it seems as though it never will be
adequately explained except by employing the concept of intelligent
design.
> Second, there really should be a FAQ on all the selection experiments
> like this, especially the ones that involve functions evolved from
> random sequences. How much of that literature do you know?
All the literature that I have ever read on the subject only deals
with the evolution of relatively simple functions that rely on single,
relatively short, amino acid sequences, such as those that produce
various enzymatic activities (ie: lactase, nylonase, lipase etc.).
This is why Behe argues that there are no experiments or papers in
scientific literature that detail the evolution of any functional
biological system of the level of complexity of such multipart systems
as a bacterial flagellum or any other multipart system of similar
complexity. He proposes a reason for this, which is basically a
god-of-the-gaps argument. He argues that many complex functions, such
as bacterial motility, require a level of complexity that is beyond
the ability of random mutation and natural selection to achieve. He
goes on to explain that the reason for this is that there are far more
non-functional arrangements of parts, of a given length for such
complex systems of function, than there are functional arrangements.
This problem creates a "gap" between what is and any one of a number
of potentially beneficial functions of a given level of complexity.
Of course, Behe calls this problem, "irreducible complexity." What
this term really means is that it is actually possible to destroy a
given function without the gain of any other function from the
perspective of a given system of function. Yes, it is true. It is
actually possible to destroy and not create anything new or
beneficial. In fact, the problem for evolution is that it is sooooo
much easier to destroy current function than it is to create new
function. The reason that it is so much easier to destroy than it is
to create is found in the fact that there are a whole lot more
non-functional sequences of a given length than there are functional
sequences of that same length or level of complexity. If it were just
as easy to create new function as to loose old function, as you and
Ron seem to suggest, then there wouldn't really be a problem. But you
know, at least intuitively, that it really is very much easier to
destroy than it is to create and that this problem increases
exponentially with increasing complexity. You said so yourself
initially. In fact, before you "changed your mind" you said that this
concept was, "obviously true." What is it then that makes the
intuitively obvious suddenly difficult to comprehend?
Sean
Pokemoto
>lobby!ngtf-m01.news.aol.com!ngpeer.news.aol.com!newsfeed1!bredband!uio.no
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no.cabal
>From: seanpi...@naturalselection.0catch.com (Sean Pitman)
>Newsgroups: talk.origins
>Date: Mon, 19 May 2003 23:27:37 +0000 (UTC)
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>
>
>John Harshman <jharshman....@pacbell.net> wrote in message
>news:<3EBC2072...@pacbell.net>...
>
>> Just a couple of thoughts: another problem with Hall's selection
>> experiments on bacteria is that he's relying on existing genes to pick
>> up the function of a deleted gene. But they aren't entirely free to
>> evolve, even neutrally. Each of those proteins has a function which it
>> must maintain. A mutation that helps to replace the lost function must
>> also preserve the protein's current function, so there is the
>> possibility of selection rejecting mutations because, even if they help
>> regain the lost function, they may degrade the protein's current
>> function enough to make net selection negative. I don't know how
>> important that factor would be in practice, but it's something to
>> consider. A lot of evolution can get around this problem by beginning
>> with a gene duplication, allowing different copies to experience
>> selection in different directions.
>
>Yes, this is quite a problem indeed. Gene duplication is supposed to
>get around this problem by creating sequences that can undergo neutral
>drift while maintaining previous functional sequences. However,
>Hall's E. coli didn't do this either. They simply didn't evolve the
>lactase function by any means, not even by gene duplication. Neither
>have many other types of bacteria despite huge numbers of observed
>generations (over a million).
Hall didn't use the proper system to identify the mutants that you would need
did he? Why don't you answer my posts on this subject?
Just tell us one thing, if you are right about how difficult it is to evolve
function in a protein would antibodies be able to evolve the novel enzyme
functions in less than 10^12 trials? Yes or no.
You can claim anything else about these results that you want, but the plain
fact is that these results demonstrate that your reservations are bogus. Let's
see you admit that simple fact. How many trials would it take to create new
function if you were right? Why does it only take less than 10^12?
You also can't seem to get it through your misperceptions that there is no
goal. For some reason you are stuck with your bogus analogy of fixing broken
windows. Lactase function was just a quirk that the bug found gave it some
advantage. Without lactase function the bacteria was dividing happily in some
mammal's guts. It didn't have to evolve lactase function to survive.
Gene duplication has been documented. There are so many cases of likely gene
duplication in all lifeforms that it would be pretty stupid of you to deny that
it happens on a regular basis. What is one of the ways mosquitos evolve
resistance to DDT? Isn't it gene duplication? Isn't this a favorite
creationist misdirection ploy about evolved resistance? "It is only gene
duplication." Apparently lifeforms can survive happily with these duplications
and if we look at genomes many of these gene duplications have evolved novel
functions. We have evidence that this evolution is possible. What do you have
to claim that it isn't possible?
Your arguments are so much of a crock that you know that you should be ashamed
to still be trying to defend them. Your own calculations should tell you that
crossing 3 mutations to get function is well within the bounds of possibility,
but Hall didn't see any for what reason? He told you why he didn't expect it
to happen in his system. He requires fixation of the first two before he has a
chance of seeing the third. Your own calculations tell you that in nature
fixation is not necessary. How did Hall cross your boundry of 3 mutations when
all he selected for was better growth on lactose? Why didn't his argument
about fixation not apply to that situation? Did it have anything to do with
the fact that he wasn't relying on a one step selection?
Ron Okimoto
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
On Mon, 19 May 2003 23:27:37 +0000 (UTC),
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>John Harshman <jharshman....@pacbell.net> wrote in message news:<3EBC2072...@pacbell.net>...
>
>> Just a couple of thoughts: another problem with Hall's selection
>> experiments on bacteria is that he's relying on existing genes to pick
>> up the function of a deleted gene. But they aren't entirely free to
>> evolve, even neutrally. Each of those proteins has a function which it
>> must maintain. A mutation that helps to replace the lost function must
>> also preserve the protein's current function, so there is the
>> possibility of selection rejecting mutations because, even if they help
>> regain the lost function, they may degrade the protein's current
>> function enough to make net selection negative. I don't know how
>> important that factor would be in practice, but it's something to
>> consider. A lot of evolution can get around this problem by beginning
>> with a gene duplication, allowing different copies to experience
>> selection in different directions.
>
>Yes, this is quite a problem indeed. Gene duplication is supposed to
>get around this problem by creating sequences that can undergo neutral
>drift while maintaining previous functional sequences. However,
>Hall's E. coli didn't do this either. They simply didn't evolve the
>lactase function by any means, not even by gene duplication. Neither
>have many other types of bacteria despite huge numbers of observed
>generations (over a million).
See 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)
where they have evolved a beta galactosidase that acts on lactose from
an enzyme other than the "spare tyre". I believe I have directed you
to this paper before.
[snip]
>Ron Okimoto likes to argue that experiments done with antibodies
>(where other enzymatic type functions are also detected in such
>antibody collections) are good evidence of the power of selection to
>produce new functions from a random collection of amino acid
>sequences. This is a deceptive argument in that it glosses over
>several problems.
No, it is a powerful counter argument to claim that there is a limited
number of ways to make a given enzymic activity. You can get lactose
metabolizing enzymes in a variety of ways, all with simple random
mutations, crossing the "gaps" that you claim are there.
>One problem is that a given gene pool is limited in
>its ability to produce such varieties of random sequences, as you
>noted above.
They don't need to do this, the antibody example shows that you can
get functional enzymes when you start from the extreme case of a
random peptide. Duplicating of existing genes makes the job easier, as
you have pre-existing functional territory to build on.
>E. coli bacteria, for example, are limited in the amount
>of genetic real estate that they can devote to the production of
>random amino acid sequences. In fact, they are very limited indeed
>since most of the genome of a given bacterium is actually
>"functional".
Nonetheless, there is enough spare space that some bacteria can evolve
lactose utilizing enzymes without the apparent trouble that Hall had.
>Another problem is that even when "new" functions are
>isolated in these experiments with antibodies, these new functions are
>always relatively simple (almost always enzymatic type functions) that
>require a single, relatively short, amino acid sequence.
So? this is the very enzymic reaction you said couldn't occur in a
reasonable time, yet they did.
>As
>previously noted, simple functions, like three-letter-words in the
>English language, will be found closer together in the sea of
>non-function. However, more complex functions, requiring longer and
>still longer sequences, are far more rare when one starts looking for
>them in a random pile of sequences.
Except, more complex functions are just a bunch of simple functions
strung together, typically by forming a complex of small proteins with
simple functions. Once you have "cat" "mat" "sat", its not so hard to
string them together into "cat sat mat" (biology, like Indonesian,
doesn't do definite articles). The coagulation system for example is
just a bunch of duplicated protease strung together.
>For example, if I were to throw a
>bunch of Scrabble letters out on a table, just by random chance alone,
>I would most likely be able to see many 3-letter words lined up in the
>pile of blocks. However, I would see fewer 4-letter words and
>probably only one or two 5-letter words and maybe, after a several
>tries, a 6-letter word. You get the point.
Except biology isn't like scrabble (there is a lot of redundancy built
in, and don't forget many amino acids are interchangeable, as if cat,
cot and cut were equivalent), and complex functions aren't like 6
letter scrabble words, but bunches of three letter scabble words. You
can build up a word like "antidisestablishmentarianisim" quite rapidly
by agglomeration of smaller subunits (mostly 4 letter subunits in this
example).
>Antibody experiments work the same way.
No, they show that you can start out from a random peptide and get to
a functional enzyme without getting hung up on these "neutral gaps"
that you allege occur.
[snip Dr. Pitman missing the point, that you can get from random to
functional without getting stopped by his neutral gaps]
>> Second, there really should be a FAQ on all the selection experiments
>> like this, especially the ones that involve functions evolved from
>> random sequences. How much of that literature do you know?
>
>All the literature that I have ever read on the subject only deals
>with the evolution of relatively simple functions that rely on single,
>relatively short, amino acid sequences, such as those that produce
>various enzymatic activities (ie: lactase, nylonase, lipase etc.).
Nylonase is simple? You can support that contention can't you.
However, all the complex functions are built up of simple functions
such as these. And of course there is the irreducibly complex
multistep poly chlorophenol degradation pathway, which has only
recently evolved. I believe I have pointed you to that pathway before
as well.
>This is why Behe argues that there are no experiments or papers in
>scientific literature that detail the evolution of any functional
>biological system of the level of complexity of such multipart systems
>as a bacterial flagellum or any other multipart system of similar
>complexity.
Except he is wrong, there is a lot of literature and experiments that
detail the evolution of the clotting system (just a bunch of proteases
strung together), the complement system (another bunch of proteases
strung together), the innate immune system (which builds on the
complement system) and the adaptive immune system. There is less
literature on the evolution of the eubacterial and archebacterial
flagella as we have only just begun to work out how they are put
together, much less work out how they evolve, even so we have a large
number of clues about how the flagella are put together (basically a
group of transporters strung together).See
http://www.health.adelaide.edu.au/Pharm/Musgrave/essays/flagella.htm
for one example of step by step assembly of functional motile flagella
from functional non-motile precursors and see www.talkdesign.org for
detailed examples of the complement system evolution.
Why do you take so much heed of someone who cannot even read the basic
literature in their own field.
[snip]
Cheers! Ian
=====================================================
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
Sean Pitman
The reason why this "shift" is relatively small is because when you
start talking about gaps in function, the orders of magnitude involved
are in the hundreds, thousands and even millions. So, compared to the
problem at hand, a shift of just one order of magnitude is nothing.
You see Ron, all you did was to point out that increasing a
population's size or mutation rate or the total number of base pair
sequences will in fact reduce the time needed to cross a given gap.
Well, this is in fact true. A steady state population of just one
individual would take trillions of years to cross a gap of 3 point
mutations, but a steady state population of a trillion individuals
would take only a few days. Of course, you suggest, when we are
talking about bacteria, that a trillion individuals in a population is
nothing. This is also true. However, the problem remains because
each doubling in gap size increases the number of potential options by
a *power* of 2. So, if it would take a trillion individuals to cross
a given gap in one year, it would take a trillion trillion individuals
to cross a gap that was just 2-times wider in the same amount of time.
The gaps quickly outpace the ability of population size to keep up.
Pretty soon, the total number of bacteria living on this entire planet
cannot keep up with even relatively small gaps of just 20 or 30 base
pairs (coding for a protein of just a dozen amino acids or so) . . .
even if the entire world were made up of a solid ball of bacteria.
You do understand this problem . . . don't you? You do see why a
single order of magnitude is not the issue here? You do understand
that with doubling in gap size that must be taken that the order of
magnitude doubles? For example, if the order of magnitude is 10 for a
given gap, making the gap just one step wider will increase the order
of magnitude for the gap to 20 (ie: a 1 with 20 zeros after it).
> You still don't have an example where even 4 or 5 is necessary.
Sure I do. When a sizable colony of bacteria cannot evolve a given
function in the time needed to cross a gap of 4 or 5 neutral
mutations, then the only logical reason for this lack of evolution is
that there is a neutral gap in function that is actually wider than 4
or 5 mutations. Again, Hall's experiment clearly illustrates this
point. Such gaps do exist and even Hall admits that such gaps do in
fact "limit" the "evolutionary potential" of these non-evolving
bacteria.
There are several potential problems here. First off, you must give
some sort of reference for this estimate of yours since you and
Dawkins seem to be reading different material. Also, you must give
your estimates from the perspective of a given type of life form . . .
like a human for example. There is also another problem. Many of the
amino acids in a given protein can be changed individually without a
complete loss of protein function as long as none of the other amino
acids in that sequence are changed. However, these same changes,
taken with a few other changes, can also destroy protein function. It
really doesn't take much alteration to destroy the function of a 3-D
protein structure. In reality, such statements that claim that
proteins can change practically "all" of their amino acids without a
loss of function are misleading in that "all" of the amino acids in
such experiments are not changed at the same time. One amino acid is
changed, and then corrected and another is changed . . . and so on.
However, the reality of the situation is that proteins are quite rigid
as far as their functional 3-D shapes and structure. They cannot be
changed to any significant degree without a *complete* loss of protein
function. There are in fact many many more "non-functional" amino
acid sequences than there are "functional" amino acid sequences when
considered from the perspective of any one given life form/gene pool.
> You have to also
> figure out how many other possible ways besides those 5 or 7 invariant
> positions that you could get similar function using some other oxygen
> carrier other than heme.
This is true. However, there are far fewer amino acid sequences that
can function as oxygen carrier molecules than there are sequences than
cannot. There may be millions or even billions of sequences of the
length of hemoglobin or smaller that could function as a fairly
effective oxygen carrier, but by no means are there anywhere near the
1e700 or so possible sequences out there.
> It looks like heme got used because it was
> very similar in structure to existing porforin ring compounds being
> used for other things in the cells. Do you have some proof that heme
> had to be used as the oxygen carrier? The designer wouldn't have to
> do these things, but lifeforms would be expected to cobble things
> together from what was available.
Actually, a designer would be expected to use similar designs in
various creations. It is called, "conservation of design." Also, I
never said nor do I suggest that the heme molecule is the *only*
molecule that can be used as an effective oxygen carrier. However, it
certainly does its job extremely well. Also, I would also suggest
that given the total number of potential sequences out there that
there is only a very tiny fraction of them than can in fact perform
the function that hemoglobin does.
> > So, it is true that many if not most proteins have a degree of
> > plasticity, but generally speaking, proteins are quite rigid or
> > specific in their sequencing. If changed beyond a certain point, they
> > loose ALL function. At this point, further changes to the sequence of
> > a non-functional protein are, yes, functionally neutral. Your
> > hypothetical plane of function becomes perfectly flat at this point.
> > Random walk takes over and further mutations are lost on an almost
> > endless sea of random drift.
>
> Your problem is that this isn't true for anything that we seem to want
> to get to. Can you come up with an example of this?
Are you dense or something? Everybody knows that proteins are quite
rigid in structure and function and that their functions can very
easily be destroyed via mutation or various denaturing methods. To
suggest otherwise is simply insane.
> Remember the
> antibody examples and only 10^12 trials to get a novel function. If
> you were right, what is the chance that they would get any new
> enzymatic function in 10^12 trials let alone the one that they test
> for. John may be pretty close to pegging it with his idea. How come
> it is possible if you claim that it is impossible?
Again, it seems to me that you just aren't understanding the problem
here. Simple enzymatic type functions are relatively easy to evolve,
given enough genetic real estate that can undergo neutral drift.
Actually 10e12 trials are quite a few trials to come up with a given
enzymatic type functions. I would expect that far fewer trials would
be needed to come up with a great many enzymatic type functions in
antibody sequences, given a relatively large number of antibody
sequences that were mutating in each trial. This is not a problem at
all. The problem is really more complicated than this. There are
several factors involved. One problem is that from the perspective of
a given life form, the evolution of a particular enzymatic "function"
might not be beneficial to it in its current environment. Evolution
must be considered from the perspective of a particular life form in a
particular environment. Evolution is limited in this way. Also, one
must consider that functions that require relatively short amino acid
sequences, such as single enzymatic type proteins, are not all that
complex. Odds are that there are a higher percentage of functional
proteins of such short lengths or shorter as compared to the total
number of potential sequences available. However, when functions of
higher complexity are considered, functions that require longer amino
acid lengths, or even multiple lengths (multiple proteins), there are
far fewer functional sequences available when compared to the total
number of potential sequences of such lengths. This means that the
gaps between such functions of higher complexity are that much wider
than the gaps that exist between functions of lower complexity (such
as many single protein enzymes).
You do really need to read Hall's paper for yourself instead of only
reading abstracts all the time. You still do not seem to understand
the way Hall's experiments work. The colonies that evolve the ability
to utilize lactose not only produce a red color, they also grow better
at the same time. So, there is no need for a time limit on this
experiment. This works very much as it would work in real life. In
fact, Hall did cross a neutral gap that was two mutations wide. He
didn't understand how this was possible, but the gap was in fact
crossed very rapidly, in just a few days. By his own calculations,
such a gap should have taken over 100,000 years to cross. Of course,
Hall was wrong, but this makes me think that Hall does not fully
understand the binomial statistical problem here. He was calculating
the odds based on my previous misconception. He does not seem to
understand that an average colony can in fact cross gaps of 2 or 3 or
even 12 or 13 mutations in short order with simple random walk. The
reason why such gaps do not seem to be readily crossed in his own
experiments may have several explanations. One possibility is that
the gaps in Hall's experiments are actually wider than one or
two-dozen steps. Another possibility is one that John suggested, and
that is that E. coli are already using almost all of their genetic
real estate for beneficial functions and have little left over for
random walk or the evolution of new functions. In any case, Hall's
experiments are very good for detecting any mutations that achieve the
lactase function even over the course of hundreds or thousands of
generations.
> How many individual bacteria have been tested for lactase activity in
> 40 years?
Probably trillions upon trillions upon trillions of them.
> Why would you expect them to have enough activity to show
> up on some test?
Because, if they have evolved this very beneficial ability/function
over the course of a million generations or so, it would easily be
detected by a positive lactase test.
> No one but you expect them to have full blown
> activity.
Not so. If they were to evolve such a lactase function, it would in
fact be a benefit to them in their current environments. Given this
benefit, the activity would be enhanced once evolved and it would be
"full blown" and testable. There is no doubt about it. The same
happened in Hall's experiments. Those bacteria that evolved the
lactase function started outgrowing their peers in the petri dish.
They were more "fit" and they clearly showed it. Natural selection
gave them the advantage in that lactase rich environment. The same
thing would happen with other types of bacteria in real life. This is
not unexpected as you suggest.
> The thing is that when E coli was evolving lactase activity
> no other bacteria had such activity and there was no competition in
> that area. Now we have bacteria that can do it and any new bug that
> evolves this activity has to compete with these bacteria for the food
> source. Who is going to win?
When a colony of bacteria is living in a given environment, each
individual bacterium is also competing against other members of that
same colony of bacteria. If any one of those bacteria suddenly
developed the lactase ability in a lactose rich environment, it
wouldn't matter how many other types bacteria in that environment also
had the lactase ability, the bacterium in the colony without this
ability would quickly outgrow its peers in the lactase negative
colony. It might not outgrow the other types of bacteria with better
lactase enzymes, but it would certainly outgrow the other members of
its own colony.
> Why can Hall get other species to
> evolve lactase activity? My search turned up two other species that
> he was able to do his trick on. You lose on this one too.
Amazing! Are you actually this slow in your thinking? In the same
way that E. coli evolved lactase ability once it was deleted, so other
bacterial species and even other life forms would be expected to do
the same thing if they had some sequence as close to a potential
lactase enzyme as the ebg sequence that E. coli had. Why do you even
propose this as an issue? How exactly do I "loose" here? Where did I
ever propose that such a thing would not be likely. I would in fact
propose that such experiments would not only be likely, but extremely
common place.
> > The problem is that, relatively speaking, these islands of function
> > are quite small indeed. When compared to the total number of
> > completely non-functional sequences out there in the ocean of
> > non-function, those sequences that have any function whatsoever (from
> > the perspective of a given life form in a given environment), make up
> > only the tiniest of fractions, especially when you start talking about
> > functions that require amino acid sequences that average more than one
> > enzymatic-type protein in length. When functions require multiple
> > proteins totaling several hundred, thousand, or even tens or hundreds
> > of thousands of amino acids in length, then your little islands with
> > their little impressions don't come near close enough to avoid the
> > random drift problem.
>
> They are likely small for any one sequence, but there are a lot of
> sequences and a lot of possible functions, and when you change a
> sequence you change its functional potential. You can't just look at
> the potential functions of any single extant proteins, but you have to
> look at the potential function of all the molecules that you can get
> by changing just 1 to 3 amino acid positions. You know that this is
> possible. If you make one or two changes you can significantly change
> the landscape for any function, can't you?
Yes, but you do not seem to understand the problem. You are thinking
that there are so many potential beneficial functions out there that
just about any change in bound to evolve at least one of them. The
problem is that even though there are a lot of potential functions out
there as far as an absolute number goes, this number is very tiny
indeed when compared to the total number of potential sequences out
there. For example, there may be a billion potential lactase enzymes
out there of 4,000aa or less (The approximate length of the lacZ and
ebg lactase enzymes). Is a billion a large number? Well, yes it is
until one compares it with a 1 with 5,200 zeros after it (the total
number of potential proteins of this length). So you see, the "large"
number of potential functional sequences is really an illusion of
bigness. Such "big" numbers are really small in comparison to the
bigness of the total number of possibilities. In other words, no
matter which direction that a sequence "drifts" in its random walk, it
is unlikely that it will come across any other beneficial function,
from the perspective of a given organism, in short order. And, this
problem becomes more and more significant with increasing functional
complexity . . . especially when we start talking functions that
require multiple proteins all working together at the same time . . .
like in bacterial motility etc.
> You keep forgetting that according to science, evolution doesn't have
> a plan and that lactase activity isn't some goal. If it happens,
> fine, you get something that may be useful. If it doesn't happen,
> fine, the bacteria keeps on going just like it always did.
And you keep forgetting that no matter which direction that random
walk takes toward ANY new function, all new functions are a good ways
away from any potential starting point. Therefore, the evolution of
ANY new function requires a certain amount of time and this time
increases exponentially as the complexity of functions increase. The
bacteria may keep going just fine with what they currently have, but
the odds that they will just happen to come across something as
complex as bacterial motility or any other function of such
complexity, simply requires too much time. Again, the illustration of
the English language system comes into play. It is relatively easy to
come across a series of 3-letter words with random walk, but it is
another thing entirely to come across a series of 6-letter words, not
to mention sentences or paragraphs with random walk. Start with any
average length sentence. Change one letter at a time with each change
making some sense in English, and see how many different meaningful,
functionally beneficial, sentences that you can come up with. It is a
LOT harder than you might initially imagine. This same problem holds
true for genetic evolution of life forms.
Dawkins tried to do it, somewhat, with his "Methinks it is like a
weasel" computer evolution experiment. However, where Dawkins went
wrong is that each of his generations of phrase evolution were
meaningless. He selected phrases of gibberish that were closer in
*spelling* but not in *meaning* to "Methinks it is like a weasel."
You do see the problem here don't you? There are a lot more
meaningless sequences of 28 characters in length than there are
meaningful sequences of this length. This poses a problem, as it did
for Dawkin's experiment, in that there simply is no path of function
from one sentence of this length to very many other meaningful
sentences, although there may in fact be millions of them, of similar
lengths. This same problem exists in genetic evolution experiments.
Natural selection is simply powerless without a change in function
with each change in genetic spelling.
> Explain the antibody results if you are correct. Why is the
> impossible, possible for antibodies? Why do you only have to score
> 10^12 events before you find the activity that you select for?
Because, as I have explained multiple times already, the activity that
was "selected for" was a relatively simple enzymatic type activity.
It is like throwing all the possible 3-letter sequences for English
words into a bag and asking me to pick out one of them that has a
particular function. It might take a while, but not very long
comparatively speaking because I am basically looking for a short
sequences with a simple function that has relatively high odds of
success.
> By the
> early 1990's they had already produced over 70 different enzymatic
> activities using antibodies. I think that they have their own name,
> now, and they are called abzymes. If you do a PubMed search you will
> likely find references to a whole lot more enzymatic activities by
> now.
Certainly true, and not suprising in the least. This is only to be
expected as many enzymatic activities are relatively simple protein
functions.
> > But, there is something hopeful about your hypothetical suggestion.
> > The very fact that you proposed such a hypothetical solution to the
> > problem means that you might actually recognize the problem, which is
> > a significant step. In any case, I remain most interested in your
> > thoughts and struggles with this issue.
> >
> > Sean
>
> It is not an explanation for a problem, but for what we observe
> occuring in nature.
You only observe this in nature as it relates to relatively simple
functions that are only very short neutral distances from what is
already there. The problem, as detailed over and over again above, is
far greater than this.
> There is a difference that you seem to be
> missing. We see this happening. You have to claim that what we
> already observe to occur is impossible.
Not so. I do not claim that what we observe happening is impossible
at all, only that it is very limited and easily explainable with the
use of random drift alone.
> That is what is wrong with
> your argument. Our only problem seems to be trying to explain why it
> seems to be so easy to get function from a protein sequence.
No . . . the problem is that with the increasing complexity of protein
function comes a vast increase in the average neutral gap that must be
crossed. Simple functions have smaller gaps. More complex functions
have larger gaps. That is the problem. How does a given life form
evolve such functions of higher complexity?
> A better
> argument for you and one that the ID people use is that since we don't
> have a good explanation for how we evolve these functions that some
> designer must be responsible for guiding these mutations and making
> the results happen.
Uh . . . that is my argument.
> The problem with the ID argument is that it is
> stupid. Just try and find some evidence to support it.
LOL - Ok . . . it is very easy to say that something is "stupid"
without giving any reasonable explanation as to why it is "stupid."
You are just spouting off without any basis for support of your
position whatsoever. I have been giving you the "evidence" to support
this ID argument all along. You seem to vaguely understand the
arguments, but you are so stuck in your rut of "naturalism explains
everything" that you are too blind to admit that there just might be
something to ID.
poke...@aol.com (Pokemoto) wrote in message news:<20030519212651...@mb-m25.aol.com>...
> >Subject: Re: Kenneth Miller's and Barry Hall's challenge of Michael Behe
> >> Just a couple of thoughts: another problem with Hall's selection
> >> experiments on bacteria is that he's relying on existing genes to pick
> >> up the function of a deleted gene. But they aren't entirely free to
> >> evolve, even neutrally. Each of those proteins has a function which it
> >> must maintain. A mutation that helps to replace the lost function must
> >> also preserve the protein's current function, so there is the
> >> possibility of selection rejecting mutations because, even if they help
> >> regain the lost function, they may degrade the protein's current
> >> function enough to make net selection negative. I don't know how
> >> important that factor would be in practice, but it's something to
> >> consider. A lot of evolution can get around this problem by beginning
> >> with a gene duplication, allowing different copies to experience
> >> selection in different directions.
> >
> >Yes, this is quite a problem indeed. Gene duplication is supposed to
> >get around this problem by creating sequences that can undergo neutral
> >drift while maintaining previous functional sequences. However,
> >Hall's E. coli didn't do this either. They simply didn't evolve the
> >lactase function by any means, not even by gene duplication. Neither
> >have many other types of bacteria despite huge numbers of observed
> >generations (over a million).
>
> Hall didn't use the proper system to identify the mutants that you would need
> did he? Why don't you answer my posts on this subject?
Yes, Hall did sue the proper system to identify the mutants. You
simply do not seem to understand the experiment . . . probably because
you haven't read anything more than the abstracts. (As discussed
above)
> Just tell us one thing, if you are right about how difficult it is to evolve
> function in a protein would antibodies be able to evolve the novel enzyme
> functions in less than 10^12 trials? Yes or no.
Again, it depends on the complexity of the function in question.
Simple functions would be easier to evolve since the gaps between
simple functions would obviously be smaller than gaps between more
complex functions. Abzymes are in fact relatively simple functions
that generally require one protein sequences of a relatively small
length. So yes, such functions would not be surprising to see
evolving in various life forms (also discussed above).
> You can claim anything else about these results that you want, but the plain
> fact is that these results demonstrate that your reservations are bogus.
LOL - Actually, the results of these experiments only support my
position. They in no way counteract my reservations in the least.
> Let's
> see you admit that simple fact. How many trials would it take to create new
> function if you were right? Why does it only take less than 10^12?
It depends on the level of complexity involved with the function? How
many amino acids, at minimum, would be required? How many sequences
of a given length would have this particular function? What is the
ratio of potentially functional sequences as compared to the total
number of potential sequences? You see, the evolution of some simple
enzymatic type function really isn't the issue here. Such
demonstratable evolution is not the salvation of the theory of common
descent of all life forms. Hopefully you can begin to recognize this
problem, but I am beginning to have my doubts. Your logical abilities
seem to be quite blinded by your naturalistic philosophy.
> You also can't seem to get it through your misperceptions that there is no
> goal.
Yes, there is a "goal" for evolution. You are clearly mistaken here.
The goal of genetic evolution is the goal of new beneficial functions,
whatever they may be. That is the goal. The goal is NOT the
evolution of just any random set of genetic sequences. Evolution must
evolve functional sequences that are actually beneficial at the same
time. This means that there is some specificity to evolution. And,
this creates a problem for evolution which gets larger and larger to
the point of impossibility as the level of functions increases.
> For some reason you are stuck with your bogus analogy of fixing broken
> windows. Lactase function was just a quirk that the bug found gave it some
> advantage. Without lactase function the bacteria was dividing happily in some
> mammal's guts. It didn't have to evolve lactase function to survive.
Actually, it did have to evolve the lactase function if it wished to
use the potential energy source of the surrounding lactose for some
advantage. The window analogy is not "bogus" at all. It shows that
some "functions" simply have no naturalistic explanation while others
do have such explanations. A broken window has a naturalistic
explanation while a fixed window has no naturalistic explanation
outside of deliberate design. The same situation aplies to genetic
functions. If no naturalistic explanation exists to explain the
variety or level of certain genetic functions that exist in various
life forms, the only logical explanation available to explain their
obvious existence is ID.
> Gene duplication has been documented. There are so many cases of likely gene
> duplication in all lifeforms that it would be pretty stupid of you to deny that
> it happens on a regular basis.
Certainly gene duplication does happen, but it does not happen on a
"regular" basis. And, even if it did, it wouldn't really help the
theory of evolution out of the neutral gap problem. The only thing
that gene duplication would do is to increase the available genetic
real estate that can undergo neutral drift. Increasing the genetic
real estate does help, but only to a point. Increasing gap size
quickly outpaces the ability of increasing genetic real estate to keep
up with the statistical time needed for random walk to succeed.
> What is one of the ways mosquitos evolve
> resistance to DDT? Isn't it gene duplication?
No. It is not gene duplication in the vast majority of cases. Such
resistance-type evolution is almost always the result of single point
mutations in target proteins or the like. It works much like the
evolution of many types of antibiotic resistance. For further
discussion of this, I have written a paper on various types of
antibiotic resistance at:
http://naturalselection.0catch.com/Files2/antibioticresistance.html
> Isn't this a favorite
> creationist misdirection ploy about evolved resistance? "It is only gene
> duplication."
Not at all. If it is, it is not a very good argument as it really
explains very little. I certainly don't use such an argument.
> Apparently lifeforms can survive happily with these duplications
> and if we look at genomes many of these gene duplications have evolved novel
> functions. We have evidence that this evolution is possible. What do you have
> to claim that it isn't possible?
Most of the literature that suggests certain functions arose via gene
duplication are not based on any direct experimental evidence or
observation, but only on a "just-so-story of what must have happened.
Very few if any of these "examples" are based on any sort of real time
experiments. Such suggestions are based on certain similarities that
exist between various genes with different functions, but such
similarities could just as easily have been designed, again, with the
use of the principle of "conservation of design." You see,
similarities do not automatically support the theory of common
evolutionary origin over the concept of ID. The support of the theory
must be found in an explanation of the differences, not the
similarities. The similarities can equally be explained by both
theories, but the differences cannot. So, it is in the differences
where one must find evidence for or against naturalistic evolution vs.
intelligent design.
> Your arguments are so much of a crock that you know that you should be ashamed
> to still be trying to defend them.
Funny thing, I was thinking pretty much the same thing about your
arguments.
> Your own calculations should tell you that
> crossing 3 mutations to get function is well within the bounds of possibility,
> but Hall didn't see any for what reason?
As detailed above, either the gaps may have been wider than this or
the E. coli didn't have enough free genetic real estate to undergo
random walk.
> He told you why he didn't expect it
> to happen in his system. He requires fixation of the first two before he has a
> chance of seeing the third. Your own calculations tell you that in nature
> fixation is not necessary.
Yes, evidently Hall does not understand that fixation is not necessary
to cross such gaps. However, Hall's experiments are still very good.
You just do not like them because they do in fact support my theories
much better than they support your theories.
> How did Hall cross your boundry of 3 mutations when
> all he selected for was better growth on lactose?
He didn't cross a gap of 3 mutations. There was no gap in this
experiment at all. Each and every step in this "3-step evolution" was
beneficially advantageous. You see then, there was no gap here. When
each step is functionally different, in a beneficial way, from the
previous sequence, there is no gap. A neutral gap means that a step
will have no functional change over what came before. You really must
understand this concept before you will have any hope of understanding
the problem.
> Why didn't his argument
> about fixation not apply to that situation?
Because, each step here was fixed or at least would be fixed in short
order in the population. Each step was beneficially advantageous and
did in fact cause those with each mutation to outgrow their peers.
But, in any case, Hall is clearly wrong in his ideas about fixation
being required for the crossing of such gaps. So, this really isn't a
problem.
> Did it have anything to do with
> the fact that he wasn't relying on a one step selection?
But, he was in this case. Read the paper again. Each step was in
fact selectable. Again, you really do need to read more than the
abstracts of these papers. It seems to me that John Harshman is
actually more reasonable in his thinking and discussions than you seem
to be.
> Ron Okimoto
Sean
Sean Pitman
Sean Pitman
> >For example, if I went to the moon and found a series of
> >perfectly round 10kg rocks all arranged in a perfect geometric square
> >measuring a mile on each side, it would be very reasonable of me to
> >theorize that some sort of purposeful intelligence, above any sort of
> >mindless naturalistic process, was at work here.
>
> Before or after I went to a beehive and saw "perfectly" hexagonal
> honeycombs? Or are bees Intelligent Designers?
A robot can be programmed to produce a beautiful work of art or to put
together an intricate wristwatch. However, this ability was
originally designed via some intelligent mind. The same could be said
of the honeybee's ability to make hexagonal compartments out of wax
and put honey in them.
> And what would I do after I then went to Devil's Tower and saw the
> hexagonal basalts? Volcanos are "purposeful"?
Not all geometric shapes imply intelligent design. The hexagonal
basalts at Devil's Tower are crystalline structures. Crystals self
assemble on the basis of their underlying molecular structure. No
higher informational input or intelligence is needed since all the
information for assembly is self-contained by the molecules
themselves.
However, this self-contained information for assembly is not contained
by many other systems of function, such as the parts to watch, or the
code for a bacterial flagellum, or the letters and word sequences in a
book or in this paragraph. Many such phenomena give clear evidence of
higher intelligent input in their formation that is beyond the
mindless processes naturalistic mechanisms. The origin of this
intelligence does not need to be identified in order for it to be
recognized. The inability for any known naturalistic process to
produce a given phenomenon is itself evidence of intelligent design.
> J. Pieret
>
> The devil is in the details.
> Science explains them.
> Intelligent design explains them away.
>
> - Mark VandeWettering -
Science or the scientific method certainly is a very powerful tool for
the searching out of truth concerning the external world. In fact,
there is no other method that I know of that can do as good a job as
the scientific method. However, the scientific method does not
pre-suppose only naturalistic causes as explanations for phenomena
that occur in the external world. The a priori assumption of
naturalistic causes is not in fact a scientific assumption. In fact,
by using the scientific method, it is very reasonable to conclude that
intelligent design was involved with the existence of many phenomena.
The theory of ID can in fact be scientifically supported in many many
undisputable cases and situations. Forensic science, for example, is
based on this fact. So, to suggest that the origin of life must, by
"a priori" definition, have a naturalistic cause . . . is really
scientific heresy. Mark VandeWettering is obviously clueless, a
devoted disciple of the religion of naturalism. If I were to propose
ID as an explanation of the origin of the wristwatch on my arm, would
that be "explain it away"? or would it be a scientific explanation of
the evidence?
Please, you don't seem to have a clue what you are talking about. You
repeat these meaningless catch phrases because you have seen them work
before in similar arguments. But really, they are only helping to
delude you into thinking that you are being rational when you are
actually contradicting yourself. The devil really is in the details
and science does search them out, but science does NOT always come up
with a naturalistic explanation as the most reasonable explanation.
To say that this must be the case is to be either misinformed or
deliberately insane.
Sean
Jason Cortina
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
> catshark <cats...@yahoo.com> wrote in message news:<4s0pbv8u2irsu8kd4...@4ax.com>...
>
> > >For example, if I went to the moon and found a series of
> > >perfectly round 10kg rocks all arranged in a perfect geometric square
> > >measuring a mile on each side, it would be very reasonable of me to
> > >theorize that some sort of purposeful intelligence, above any sort of
> > >mindless naturalistic process, was at work here.
> >
> > Before or after I went to a beehive and saw "perfectly" hexagonal
> > honeycombs? Or are bees Intelligent Designers?
>
> A robot can be programmed to produce a beautiful work of art or to put
> together an intricate wristwatch. However, this ability was
> originally designed via some intelligent mind. The same could be said
> of the honeybee's ability to make hexagonal compartments out of wax
> and put honey in them.
And just where is the evidence that points to instincts being the result of
intelligent agency?
>
> > And what would I do after I then went to Devil's Tower and saw the
> > hexagonal basalts? Volcanos are "purposeful"?
>
> Not all geometric shapes imply intelligent design. The hexagonal
> basalts at Devil's Tower are crystalline structures. Crystals self
> assemble on the basis of their underlying molecular structure. No
> higher informational input or intelligence is needed since all the
> information for assembly is self-contained by the molecules
> themselves.
>
> However, this self-contained information for assembly is not contained
> by many other systems of function, such as the parts to watch, or the
> code for a bacterial flagellum, or the letters and word sequences in a
> book or in this paragraph. Many such phenomena give clear evidence of
> higher intelligent input in their formation that is beyond the
> mindless processes naturalistic mechanisms.
If it is so clear evidence *for* design, then name it.
> The origin of this
> intelligence does not need to be identified in order for it to be
> recognized.
Please give a method of unambiguously identifying design since you seem to
think this is possible.
> The inability for any known naturalistic process to
> produce a given phenomenon is itself evidence of intelligent design.
That is completely inadequate. It is the epitome of argument from
ignorance: we don't know how nature could do it so it must have been
design. This would have quite erroneously identified the orbit of Mercury
as dictated by intelligence prior to the development of relativity. It
depends completely on our current state of (lack of) knowledge (without
adding anything to our knowledge).
And then, if your assertion is valid, it *must* be just as valid to say
that the inability for any known intelligences to initiate a given
phenomenon must therefore be evidence for naturalistic processes (if you
can't show X to be a member of set A it must be in set B works both ways
for sets A and B which exhaust the universal set).
This is, of course, absurd. The default position is neither. The default
position is 'unknown'. If we can't identify set membership, then we can't
identify set membership.
Then the work starts on how to end that position. The reason ID as it
exists now (and has existed for two centuries) is seen as such a complete
joke and worthless for any scientific endeavor is that it gives no hint as
to how to proceed from there, what type of investigations can be undertaken
in order to expand and solidify the knowledge.
>
> > J. Pieret
> >
> > The devil is in the details.
> > Science explains them.
> > Intelligent design explains them away.
> >
> > - Mark VandeWettering -
>
> Science or the scientific method certainly is a very powerful tool for
> the searching out of truth concerning the external world. In fact,
> there is no other method that I know of that can do as good a job as
> the scientific method. However, the scientific method does not
> pre-suppose only naturalistic causes as explanations for phenomena
> that occur in the external world. The a priori assumption of
> naturalistic causes is not in fact a scientific assumption. In fact,
> by using the scientific method, it is very reasonable to conclude that
> intelligent design was involved with the existence of many phenomena.
> The theory of ID can in fact be scientifically supported in many many
> undisputable cases and situations. Forensic science, for example, is
> based on this fact.
No, it is not! Your repetition of this falsehood does not change it.
Such science looks for known mechanisms used by known entities which in no
way resembles the 'we don't know how nature did it, somebody must have'
which you seem to think makes sense.
> So, to suggest that the origin of life must, by
> "a priori" definition, have a naturalistic cause . . . is really
> scientific heresy. Mark VandeWettering is obviously clueless, a
> devoted disciple of the religion of naturalism. If I were to propose
> ID as an explanation of the origin of the wristwatch on my arm, would
> that be "explain it away"? or would it be a scientific explanation of
> the evidence?
Once again, your confusion (or attempted obfuscation) comes through. A
watch is a *known* type of object composed of materials already *known* to
be fabricated by *known* entities. It is quite telling that even after two
hundred years the argument from design is still at this level.
>
> Please, you don't seem to have a clue what you are talking about. You
> repeat these meaningless catch phrases because you have seen them work
> before in similar arguments. But really, they are only helping to
> delude you into thinking that you are being rational when you are
> actually contradicting yourself. The devil really is in the details
> and science does search them out, but science does NOT always come up
> with a naturalistic explanation as the most reasonable explanation.
> To say that this must be the case is to be either misinformed or
> deliberately insane.
Please name a verified conclusion ("most reasonable explanation") by
science (using the definition of the word as currently used; ie. within the
last century of two) which involved other than a naturalistic explanation.
Your declaration above indicates you know of such. Or is this just more of
your denial?
--
Jason A Cortina
"If it turns out that there is a God, I don't think that he's evil. But
the worst that you can say about him is that basically he's an
underachiever."
-- Woody Allen
Ron Okimoto
> roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.0305...@posting.google.com>...
>
I don't know if it is worth responding to this post or not. The
arguments are so schisophrenic that they defeat themselves. I had to
check the header to see if someone wasn't forging Sean's post.
All you are saying is that I'm right and that an order of magnitude
shift in your goal posts was a huge difference. You only made that
shift because you found out that your original goalposts were shown to
be within the realm of what we can easily obtain in nature. An order
of magnitude shift is huge. As you indicate it has very significant
implications. You have to justify that shift when you do not have a
single example of a gap of double your original goalposts (6). If you
have one just point it out. You keep claiming that the flagellum is
such a case, but as you concede you can't demonstrate that there is
such a gap. I know very well that an order of magnitude shift makes a
huge difference. You have to justify such a shift.
>
> > You still don't have an example where even 4 or 5 is necessary.
>
> Sure I do. When a sizable colony of bacteria cannot evolve a given
> function in the time needed to cross a gap of 4 or 5 neutral
> mutations, then the only logical reason for this lack of evolution is
> that there is a neutral gap in function that is actually wider than 4
> or 5 mutations. Again, Hall's experiment clearly illustrates this
> point. Such gaps do exist and even Hall admits that such gaps do in
> fact "limit" the "evolutionary potential" of these non-evolving
> bacteria.
Schizoid argument beginning. Demonstrate that the Hall experiment
demonstrated a need for 4 or 5 neutral mutations to cross the gap when
Hall himself claimed that it would have been impossible for him to see
a gap of three crossed. You presented that quote yourself. Hall's
selection was a one step selection. This is worse than do or die
Cairn's type of experiment. Hall grows up bacteria and plates them on
a plate with a color indicator. If he is lucky he will see single
mutations in a reasonable number of plates (up to a few thousand
plates depending on how many bacteria he can screen per plate). He
would be plating until doomsday to see three mutations in a single
bacteria, unless all the bacteria he was plating were fixed for two of
the three mutations. Fixation would take years for each mutation.
Later on you claim that he would have seen 3 or more mutations crossed
by how well the colony grew. I'm assuming even if it were red instead
of white. The colonies would be scored after only around 30
generations, the chance of three mutations occurring in a colony soon
enough to help you out and make the colony grow faster is laughable.
Remember how you are using Hall's experiment when we get to the point
later on where you claim that evolving enzyme function is trivial.
You can't have it both ways.
I believe I saw it in Stryer's Biochemistry text around 20 years ago
in the section about hemoglobin. The number of invariant positions
was stated.
You are correct that the number of combinations out of the 140 amino
acids that do not make a functional hemoglobin is probably greater
than the combinations that do, but so what. This is still a very
large number constrained by the evolutionary boundaries of the
sequence. How many dimers would have worked? How many 130 amino acid
combinations? How many 150 amino acid combinations? How many 200
amino acid combinations?
If I recall correctly two hemoglobin molecules from different species
can go down to less than 30% similarity. That means that more than
70% of the positions can be different between the two functional
molecules. Does that give you a better idea of how plastic proteins
are? This is where Dawkins might be getting his incorrect notion.
The fact is that it is a different 30% for any two divergent species.
Humans and some simple metazoan might have 30% of the same amino acid
sequences, but a modern fish and this same simple metazoan would have
a different 30% similarity etc. This number revolves around a small
number of invariant positions found in all hemoglobin molecules.
>
> > You have to also
> > figure out how many other possible ways besides those 5 or 7 invariant
> > positions that you could get similar function using some other oxygen
> > carrier other than heme.
>
> This is true. However, there are far fewer amino acid sequences that
> can function as oxygen carrier molecules than there are sequences than
> cannot. There may be millions or even billions of sequences of the
> length of hemoglobin or smaller that could function as a fairly
> effective oxygen carrier, but by no means are there anywhere near the
> 1e700 or so possible sequences out there.
>
> > It looks like heme got used because it was
> > very similar in structure to existing porforin ring compounds being
> > used for other things in the cells. Do you have some proof that heme
> > had to be used as the oxygen carrier? The designer wouldn't have to
> > do these things, but lifeforms would be expected to cobble things
> > together from what was available.
>
> Actually, a designer would be expected to use similar designs in
> various creations. It is called, "conservation of design." Also, I
> never said nor do I suggest that the heme molecule is the *only*
> molecule that can be used as an effective oxygen carrier. However, it
> certainly does its job extremely well. Also, I would also suggest
> that given the total number of potential sequences out there that
> there is only a very tiny fraction of them than can in fact perform
> the function that hemoglobin does.
This is really stupid. You should just leave it at the fact that you
can't tell what the designer would do. You are trying to tell us that
the designer is as stupid as humans. Your designer is a tinkerer and
not a creator that you'd expect for an omnipotent being. Why would a
designer use something that he used in the electron transport chain in
some bacteria to make an oxygen carrying molecule in a multicellular
animal? Why wouldn't this designer create the perfect oxygen carrier
for multicellular animals instead of kludging something together from
spare parts? Why did it use other oxygen carriers in other animals
that were kludged together using different spare parts? Look up the
animals with blue blood that use copper.
>
> > > So, it is true that many if not most proteins have a degree of
> > > plasticity, but generally speaking, proteins are quite rigid or
> > > specific in their sequencing. If changed beyond a certain point, they
> > > loose ALL function. At this point, further changes to the sequence of
> > > a non-functional protein are, yes, functionally neutral. Your
> > > hypothetical plane of function becomes perfectly flat at this point.
> > > Random walk takes over and further mutations are lost on an almost
> > > endless sea of random drift.
> >
> > Your problem is that this isn't true for anything that we seem to want
> > to get to. Can you come up with an example of this?
>
> Are you dense or something? Everybody knows that proteins are quite
> rigid in structure and function and that their functions can very
> easily be destroyed via mutation or various denaturing methods. To
> suggest otherwise is simply insane.
Your density seems infinte. There may be a black hole in your future
if you keep this up. Everybody doens't know this. If you do you
should publish. The work coming out of proteomics seems to be telling
us something quite different. For some reason proteins seem to be
quite resistant to large structural shifts. There are certain
mutations that do cause major changes, but they are finding that most
mutations don't change very much. Reality is going to fall somewhere
in the middle for this one.
This is also an argument that is schizoid. You can't have it both
ways. You admit that it is easy to evolve simple enzymatic functions,
so it doesn't matter how much the structure changes. If it changes a
lot fine for us, if it changes a little, fine for us because what we
observe is that no matter which way it falls we get function fairly
easily and we just don't care. You are arguing that small changes can
cause major shifts in protein structure and at the same time claim
that it is impossible to develop the activities that you think are
impossible to develop. It is all moot because no matter what the
answer is we win because we see activity evolve easily even though a
small fraction of the total number of sequences have been searched.
I think that it is pretty clear who doesn't understand the argument.
10^12 is the total number of sequences that could possibly have been
tested, no matter how many starting sequences there were. The total
number is limited to the number of immune cells that are produced
during the selection process. 10^12 is such a small fraction of the
total possible number of sequences that could have been generated that
it is practically zero. You give a number of 1 with over 5000 zeros
after it later on. 10^12 can be considered approximately zero
compared to the number of possible sequences. You calculate what
fraction of the sequence space that is. Is it even worth noting? Is
1 X 10^-5000 a significant fraction above zero for everyday
approximations?
Demonstrate that your gaps exist. You keep trying, but you never
present an example that you can backup. Can you find an example that
anyone has been able to put forward to back up your claims? If you
claim Behe or Dembski, present the method that they used to verify
their claims, and the results of the verification experiments.
Remember the Hall experiment and what you are trying to claim about
it. So why tell us that your Hall argument is bogus by saying that
evolving simple single protein enzymatic functions is so trivial?
This just means that you should dump the Hall experiment, just like
I've been telling you all along. It doesn't tell you what you think
it does because of how the experiment is designed and you are giving
away the store by admitting that it is trivial to evolve these
enzymatic functions.
I think that you've pretty much admitted that Hall is a dead issue. A
colony cannot cross these gaps for the simple reason that there isn't
enough time to do it inside a single colony growing from a single
bacteria. What generation would all three mutations have to occur by
to see a difference in growth for the colony? If it didn't happen
within the first 6 generations (64 bacteria) would you expect to see a
growth difference in the colony due to 1/64 of the population? What
is the chance of three mutations occuring in the first 64 bacteria?
You have less than 64 chances to see a 1 in 10^24 event. At this
population level thinking about equilibrium mutations is moot because
the 64 bacteria would be pretty far from equilibrium drift.
>
> > How many individual bacteria have been tested for lactase activity in
> > 40 years?
>
> Probably trillions upon trillions upon trillions of them.
As a pathologist what fraction of these would be tested to see if they
were a new mutation in a species that did not have lactase activity or
would they simply be scored as lactase plus? How many individual
bacteria have been scored so that you could detect such a mutation?
To identify species is a pretty laborious activity and the number
would not be even a trillion. I doubt that there have been enough
technician to score a bacteria for species identification to have
scored that many.
>
> > Why would you expect them to have enough activity to show
> > up on some test?
>
> Because, if they have evolved this very beneficial ability/function
> over the course of a million generations or so, it would easily be
> detected by a positive lactase test.
Again, why would you expect enough activity to show up on the tests?
Why would it be beneficial to them if they have to compete with
bacteria that are much better at it than they are. You've made the
point yourself that genomes are only so large in bacteria and that if
you are going to muck about with something that there is no such thing
as a free lunch. The price of lunch is a lot higher if someone has
already eaten most of it.
>
> > No one but you expect them to have full blown
> > activity.
>
> Not so. If they were to evolve such a lactase function, it would in
> fact be a benefit to them in their current environments. Given this
> benefit, the activity would be enhanced once evolved and it would be
> "full blown" and testable. There is no doubt about it. The same
> happened in Hall's experiments. Those bacteria that evolved the
> lactase function started outgrowing their peers in the petri dish.
> They were more "fit" and they clearly showed it. Natural selection
> gave them the advantage in that lactase rich environment. The same
> thing would happen with other types of bacteria in real life. This is
> not unexpected as you suggest.
Demonstrate that this is true. You know that lactase function can
evolve in other species other than E. coli, why haven't we seen this
in nature. Why do we have to take these bacteria out of their normal
environment to see it. If it is possible and as beneficial as you
claim, demonstrate it. Just think for 5 minutes. We observe these
mutations happening in the lab. There is no reason to believe that
they do not happen in the bacteria in your guts, so why don't all the
bacterial species in your guts evolve lactase activity as redily as we
observe in the lab.
>
> > The thing is that when E coli was evolving lactase activity
> > no other bacteria had such activity and there was no competition in
> > that area. Now we have bacteria that can do it and any new bug that
> > evolves this activity has to compete with these bacteria for the food
> > source. Who is going to win?
>
> When a colony of bacteria is living in a given environment, each
> individual bacterium is also competing against other members of that
> same colony of bacteria. If any one of those bacteria suddenly
> developed the lactase ability in a lactose rich environment, it
> wouldn't matter how many other types bacteria in that environment also
> had the lactase ability, the bacterium in the colony without this
> ability would quickly outgrow its peers in the lactase negative
> colony. It might not outgrow the other types of bacteria with better
> lactase enzymes, but it would certainly outgrow the other members of
> its own colony.
Sounds simple enough, why doesn't it work? The first thing that you
have to demonstrate is that it would outgrow the other members of its
species in the same gut over the lifespan of the mammal. These
bacteria have adapted to an environment in which they are at a
disadvantage to bacteria that can metablolize lactose. They have
evolved to compensate and survive in such an environment competing
with all the other bacteria. What are you doing to them and is it
really an advantage when after the animal is weened you do not have
access to lactose anymore? For the larger fraction of its life a
mammal doesn't have lactose in its guts. The bacteria have to compete
there as well.
>
> > Why can Hall get other species to
> > evolve lactase activity? My search turned up two other species that
> > he was able to do his trick on. You lose on this one too.
>
> Amazing! Are you actually this slow in your thinking? In the same
> way that E. coli evolved lactase ability once it was deleted, so other
> bacterial species and even other life forms would be expected to do
> the same thing if they had some sequence as close to a potential
> lactase enzyme as the ebg sequence that E. coli had. Why do you even
> propose this as an issue? How exactly do I "loose" here? Where did I
> ever propose that such a thing would not be likely. I would in fact
> propose that such experiments would not only be likely, but extremely
> common place.
Your claim about the Hall experiment is that if you took away ebg that
it was difficult (you claimed impossible) to evolve lactase function
again. You lose because at least one of these species didn't use ebg
to evolve the new lactase function. Now you have given up on claiming
that it is difficult to evolve enzyme function and are calling it
trivial, so you should just drop the Hall argument. You lose.
I've had enough of this. It isn't worth continuing. Counter the
above arguments if you think that you can.
Ron Okimoto
snip:
John Harshman
Ian Musgrave & Peta O'Donohue wrote:
> G'Day All
> Address altered to avoid spam, delete RemoveInsert
[snip it all]
Can we get together a bibliography of selection experiments on getting
new function from random sequences, or from sequences that happen to be
available in knockout organisms, and such like? I don't know very much
of the literature, but it seems to be pretty big, and should be in a FAQ
somewhere.
catshark
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>catshark <cats...@yahoo.com> wrote in message news:<4s0pbv8u2irsu8kd4...@4ax.com>...
>
>> >For example, if I went to the moon and found a series of
>> >perfectly round 10kg rocks all arranged in a perfect geometric square
>> >measuring a mile on each side, it would be very reasonable of me to
>> >theorize that some sort of purposeful intelligence, above any sort of
>> >mindless naturalistic process, was at work here.
>>
>> Before or after I went to a beehive and saw "perfectly" hexagonal
>> honeycombs? Or are bees Intelligent Designers?
>
>A robot can be programmed to produce a beautiful work of art or to put
>together an intricate wristwatch.
Ah, so sunsets are designed? God arranges the atmospheric conditions for
each beautiful sunset we see? Hurricanes are "intricate". Are those
designed?
>However, this ability was
>originally designed via some intelligent mind.
I'm having trouble understanding your point. Because *some* things are
designed, all things are?
>The same could be said
>of the honeybee's ability to make hexagonal compartments out of wax
>and put honey in them.
You *could* say "the moon is made of green cheese". It would help if you
had evidence.
>
>> And what would I do after I then went to Devil's Tower and saw the
>> hexagonal basalts? Volcanos are "purposeful"?
>
>Not all geometric shapes imply intelligent design.
But bees do? Why?
>The hexagonal
>basalts at Devil's Tower are crystalline structures. Crystals self
>assemble on the basis of their underlying molecular structure. No
>higher informational input or intelligence is needed since all the
>information for assembly is self-contained by the molecules
>themselves.
And DNA is what?
>
>However, this self-contained information for assembly is not contained
>by many other systems of function, such as the parts to watch,
Watches do not contain self-replicating molecules, that's true.
>or the
>code for a bacterial flagellum,
Which "code" are you talking about?
>or the letters and word sequences in a
>book or in this paragraph.
Oh? Are you just a robot designed to write paragraphs? That would seem to
follow from your example about robots and art.
>Many such phenomena give clear evidence of
>higher intelligent input in their formation that is beyond the
>mindless processes naturalistic mechanisms.
Nice assertion. Why should I accept it?
>The origin of this
>intelligence does not need to be identified in order for it to be
>recognized.
Yes it does. Hey, this assertion without proof thing is kinda easy, isn't
it?
>The inability for any known naturalistic process to
>produce a given phenomenon is itself evidence of intelligent design.
You've found out how to prove a negative? Have you alerted the
philosophers and logitians yet? Do they give a Nobel for philosophy?
>
>> J. Pieret
>>
>> The devil is in the details.
>> Science explains them.
>> Intelligent design explains them away.
>>
>> - Mark VandeWettering -
>
>Science or the scientific method certainly is a very powerful tool for
>the searching out of truth concerning the external world. In fact,
>there is no other method that I know of that can do as good a job as
>the scientific method. However, the scientific method does not
>pre-suppose only naturalistic causes as explanations for phenomena
>that occur in the external world. The a priori assumption of
>naturalistic causes is not in fact a scientific assumption. In fact,
>by using the scientific method, it is very reasonable to conclude that
>intelligent design was involved with the existence of many phenomena.
>The theory of ID can in fact be scientifically supported in many many
>undisputable cases and situations. Forensic science, for example, is
>based on this fact.
So humans murderers aren't "naturalistic"?
>So, to suggest that the origin of life must, by
>"a priori" definition, have a naturalistic cause . . . is really
>scientific heresy. Mark VandeWettering is obviously clueless, a
>devoted disciple of the religion of naturalism. If I were to propose
>ID as an explanation of the origin of the wristwatch on my arm, would
>that be "explain it away"? or would it be a scientific explanation of
>the evidence?
No, the proposal of an *unknown* and *undescribable* manufacturer whose
methods and means of building watches is *unknown* and (apparently)
*unknowable* (since no one has proposed any way of investigating the ID
"designer") is *not* a scientific explanation, anymore than proposing to an
ME that a ghost killed someone is. And yes, saying god created your watch
*would* be explaining it away.
>
>Please, you don't seem to have a clue what you are talking about.
Ad hominin. That's a shame. I had heard you were better than that. I
guess creationists can't help reverting to type.
>You
>repeat these meaningless catch phrases because you have seen them work
>before in similar arguments.
And because it's funny . . .
Please, you don't seem to have a clue about that "sense of humor" thing.
>But really, they are only helping to
>delude you into thinking that you are being rational when you are
>actually contradicting yourself. The devil really is in the details
>and science does search them out, but science does NOT always come up
>with a naturalistic explanation as the most reasonable explanation.
Ah, "reasonable" . . . as in the one you *prefer*, even if you don't have
evidence for it.
>To say that this must be the case is to be either misinformed or
>deliberately insane.
Damn, funny how many insane people keep getting those research grants,
Nobel prizes in science and all the rest, isn't it? . . .
>
>Sean
And if you like that last sig, you'll *love* this one!
---------------
J. Pieret
---------------
SETI is based on the simple assumption that nature
operates elsewhere the same way it does here.
ID is based on the assumption
that nature doesn't even work here.
- Bobby Bryant -
Bigdakine
>Date: 5/20/03 12:28 PM Hawaiian Standard Time
>Message-id: <80d0c26f.03052...@posting.google.com>
>
>catshark <cats...@yahoo.com> wrote in message
>news:<4s0pbv8u2irsu8kd4...@4ax.com>...
>
>> >For example, if I went to the moon and found a series of
>> >perfectly round 10kg rocks all arranged in a perfect geometric square
>> >measuring a mile on each side, it would be very reasonable of me to
>> >theorize that some sort of purposeful intelligence, above any sort of
>> >mindless naturalistic process, was at work here.
>>
>> Before or after I went to a beehive and saw "perfectly" hexagonal
>> honeycombs? Or are bees Intelligent Designers?
>
>A robot can be programmed to produce a beautiful work of art or to put
>together an intricate wristwatch. However, this ability was
>originally designed via some intelligent mind. The same could be said
>of the honeybee's ability to make hexagonal compartments out of wax
>and put honey in them.
>
>> And what would I do after I then went to Devil's Tower and saw the
>> hexagonal basalts? Volcanos are "purposeful"?
>
>Not all geometric shapes imply intelligent design. The hexagonal
>basalts at Devil's Tower are crystalline structures. Crystals self
>assemble on the basis of their underlying molecular structure.
Hexagonal basalts have nothing to do with crystal symmetry. Nice attempt at
bullshit.
In fact the xls symmetries of the minerals comprising basalt are quite
non-hexagonal. The hexagonal shapes are a case of tensional cracking during
cooling.
No
>higher informational input or intelligence is needed since all the
>information for assembly is self-contained by the molecules
>themselves.
In fact, the molecueles in question contain no such information. In fact the
information they contain is decidedly non-hexagonal. Perhaps you'd like my
remedial mineralogy class?
Basalt is comprised mainly of plagioclase feldspar.. triclinic xls system
(lowest symmetry of the xls groups), pyroxene which is orthorhombic, and
varying amounts of olivine, also othorhombic.
<rest of gibberish based on erroneous premises snipped>
What cock and bull story will you come up with next?
Stuart
Stuart
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
Sure, it might take a while, but it should be a valuable resource.
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
On Tue, 20 May 2003 17:18:17 +0000 (UTC),
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.0305...@posting.google.com>...
[snip]
>> You don't remember your own calculations you claimed that with a
>> population of a trillion (trivial for bacteria) that in 2 years you
>> would span a gap of 20 amino acids changes. It got to be unwieldy at
>> 30. That was an order of magnitude shift in your goal posts. This is
>> not barely budging. I know that your probable estimate of the age of
>> the earth is likely 5 orders of magnitude off, but most people think
>> that a two fold shift is big and an order of magnitude is huge.
>> Perceptions seem to be relative, but you only think the way you do
>> because your view of reality is so far off that an order of magnitude
>> seems small.
>
>The reason why this "shift" is relatively small is because when you
>start talking about gaps in function, the orders of magnitude involved
>are in the hundreds, thousands and even millions.
No they are on the order of a handful of amino acid changes generally,
often no more than one or two.
Substitution at position 216 converts a D-Ala D-Ala ligase into a
D-Ala-D-Ser ligase[1]. A single mutation, Leu91Arg converts
Trichomonas vaginalis lactate dehydrogenase to Malate dehydrogenase.
Ketosteroid 5-beta reductase is converted to 3-alpha hydroxysteroid
dehydrogenase by a His117Glu mutation[2]. A Gly17His mutation in human
butyrylcholinesterase makes it a phosphotriesterase [2]. Mutation of
epimerase His94 to Asp makes it an aldolase [2]. Not that you can get
both mechanistically similar, and mechanistically quite different
functions.
Other examples that I don't have references close to hand for include
generation of amidase activity and changing substrate specificity in
several sugar hydrolysing enzymes.
[1] Park IS, Lin CH, and Walsh CT. (1996 Aug 13). Gain of
D-alanyl-D-lactate or D-lactyl-D-alanine synthetase activities in
three active-site mutants of the Escherichia coli D-alanyl-D-alanine
ligase B. Biochemistry, 35, 10464-71.
[2] O'Brien PJ, Herschlag D. Catalytic promiscuity and the evolution
of new enzymatic activities. Chem Biol. 1999 Apr;6(4):R91-R105.
See also Gerlt JA, and Babbitt PC. (1998 Oct). Mechanistically diverse
enzyme superfamilies: the importance of chemistry in the evolution of
catalysis. Curr Opin Chem Biol, 2, 607-12.
Babbitt PC, Gerlt JA. New functions from old scaffolds: how nature
reengineers enzymes for new functions. Adv Protein Chem. 2000;55:1-28.
Seffernick JL, Wackett LP.Rapid evolution of bacterial catabolic
enzymes: a case study with atrazine chlorohydrolase. Biochemistry.
2001 Oct 30;40(43):12747-53.
Gerlt JA, Babbitt PC. Can sequence determine function? Genome Biol.
2000;1(5):REVIEWS0005.
http://genomebiology.com/content/pdf/gb-2000-1-5-reviews0005.pdf
Galperin MY, Walker DR, Koonin EV. Analogous enzymes: independent
inventions in enzyme evolution. Genome Res. 1998 Aug;8(8):779-90.
http://www.genome.org/cgi/reprint/8/8/779.pdf
>So, compared to the
>problem at hand, a shift of just one order of magnitude is nothing.
On the contrary, an order of magnitude is quite large compared to the
kinds of substitutions that make enormous differences to the chemistry
of enzymic action and the generation of new functions. (normally only
one or two see references above).
Even in a case where it looks like 9 substitutions are required to
convert melamine deaminase to the functionally quite different
atrazine dehalogenase (a synthetic halogenated triazine herbicide not
found in nature), this occured in the wild in under 40 years (however,
all these gene substitutions look selective rather than neutral).
Seffernick JL, de Souza ML, Sadowsky MJ, Wackett LP. Melamine
deaminase and atrazine chlorohydrolase: 98 percent identical but
functionally different. J Bacteriol. 2001 Apr;183(8):2405-10.
[snip]
>> Dawkins is wrong, just by what variation we know there are only 5 or 7
>> (I can't recall exactly) invariant positions that have to be in the
>> hemoglobin molecule to keep it functioning. All the other positions
>> are known to have changed in one species or another.
Orotidine 5' phosphate decarboxylase is another which seems to have
only 5 invariant positions.
>There are several potential problems here. First off, you must give
>some sort of reference for this estimate of yours since you and
>Dawkins seem to be reading different material. Also, you must give
>your estimates from the perspective of a given type of life form . . .
>like a human for example. There is also another problem. Many of the
>amino acids in a given protein can be changed individually without a
>complete loss of protein function as long as none of the other amino
>acids in that sequence are changed. However, these same changes,
>taken with a few other changes, can also destroy protein function.
Or make the protein function better. Or create a completely new
function (see references above and also Jurgens C, Strom A, Wegener D,
Hettwer S, Wilmanns M, Sterner R. Directed evolution of a (beta
alpha)8-barrel enzyme to catalyze related reactions in two different
metabolic pathways. Proc Natl Acad Sci U S A. 2000 Aug
29;97(18):9925-30. http://www.pnas.org/cgi/reprint/97/18/9925.pdf and
Stehlin C, Dahm A, Kirschner K.Deletion mutagenesis as a test of
evolutionary relatedness of indoleglycerol phosphate synthase with
other TIM barrel enzymes FEBS Lett. 1997 Feb 24;403(3):268-72..).
>It
>really doesn't take much alteration to destroy the function of a 3-D
>protein structure. In reality, such statements that claim that
>proteins can change practically "all" of their amino acids without a
>loss of function are misleading in that "all" of the amino acids in
>such experiments are not changed at the same time.
Well, in evolution they rarely are all changed at the same time
either, they are usually changed step wise with <gasp> selection
taking place to cull unfit variants. However, in many experiments many
amino acids are achanged at the same time (for example Barnase, below,
and the TrpC enzyme also below)
>One amino acid is
>changed, and then corrected and another is changed . . . and so on.
>However, the reality of the situation is that proteins are quite rigid
>as far as their functional 3-D shapes and structure. They cannot be
>changed to any significant degree without a *complete* loss of protein
>function.
This is just not true, many, if not most, protiens are quite flexible.
Take for example the RNase Barnase. You can replace the entire core of
the protein (that's a fair whack of the protein) with random amino
acids and still have function (Axe DD, Foster NW, Fersht AR. Active
barnase variants with completely random hydrophobic cores. Proc Natl
Acad Sci U S A. 1996 May 28;93(11):5590-4.).
Analysis of the TrpC enzyme which helps syntesize tryptophan showed
that you could randomize whole loops and still have a functioning
protein (and then undergo selection to produce a different enzyme
function). You can convert HisA to TrpF with one mutation that _also_
flips the enzyme into a different fold strucure (ie 3D shape).
[snip]
>> Your problem is that this isn't true for anything that we seem to want
>> to get to. Can you come up with an example of this?
>
>Are you dense or something? Everybody knows that proteins are quite
>rigid in structure and function and that their functions can very
>easily be destroyed via mutation or various denaturing methods. To
>suggest otherwise is simply insane.
You should tell protein chemists that, they have been messing with
protein structures via mutation without destroying their function for
ages.
In fact, protein engineers generate new functional proteins to do
weird or extreme chemistry by, wait for it, random mutation and
selection.
Skandalis A, Encell LP, Loeb LA. Creating novel enzymes by applied
molecular evolution. Chem Biol. 1997 Dec;4(12):889-98.
Soumillion P, Fastrez J. Novel concepts for selection of catalytic
activity. Curr Opin Biotechnol. 2001 Aug;12(4):387-94.
see also
Todd AE, Orengo CA, Thornton JM. Plasticity of enzyme active sites.
Trends Biochem Sci. 2002 Aug;27(8):419-26.
>> Remember the
>> antibody examples and only 10^12 trials to get a novel function. If
>> you were right, what is the chance that they would get any new
>> enzymatic function in 10^12 trials let alone the one that they test
>> for. John may be pretty close to pegging it with his idea. How come
>> it is possible if you claim that it is impossible?
Note also that there are several examples where unrelated protein have
evolved the same function (see Galperin above) which further confirms
that functions are not isolated peaks in a plain of functionless
sequences.
>Again, it seems to me that you just aren't understanding the problem
>here. Simple enzymatic type functions are relatively easy to evolve,
Like lactase
>given enough genetic real estate that can undergo neutral drift.
Doesn't even need neutral drift, most intermediate sequences are
functional (eg atarazine dehalogenases).
>Actually 10e12 trials are quite a few trials to come up with a given
>enzymatic type functions. I would expect that far fewer trials would
>be needed to come up with a great many enzymatic type functions in
>antibody sequences, given a relatively large number of antibody
>sequences that were mutating in each trial. This is not a problem at
>all. The problem is really more complicated than this. There are
>several factors involved. One problem is that from the perspective of
>a given life form, the evolution of a particular enzymatic "function"
>might not be beneficial to it in its current environment. Evolution
>must be considered from the perspective of a particular life form in a
>particular environment. Evolution is limited in this way. Also, one
>must consider that functions that require relatively short amino acid
>sequences, such as single enzymatic type proteins, are not all that
>complex.
And complex functions are usually carried out by bunches of simple
enzymes, or a large protein that is a fusion of a bunch of small
enzymes (like the AABB casette ATPases, which are basically a fusion
of a number of small duplicated proteins, and the sdic, which is a
fusion bewteen dynenin and anexin). The origin of these functions is
unproblematic as most of the hard work is done on smaller proteins.
see Davidson JN, Peterson ML. Origin of genes encoding
multi-enzymatic proteins in eukaryotes. Trends Genet. 1997
Jul;13(7):281-5.
Another example is the evolution of the tryptophan and histidine
synthesis pathways (see Gerlt and Babbitt 2000 above) where simple
mutations and duplications give rise to more complex biochemical
pathways.
[snip]
>> Explain the antibody results if you are correct. Why is the
>> impossible, possible for antibodies? Why do you only have to score
>> 10^12 events before you find the activity that you select for?
>
>Because, as I have explained multiple times already, the activity that
>was "selected for" was a relatively simple enzymatic type activity.
And lactase is just such a relatively simple enzymic acitvity.
[big snip]
>I have written a paper on various types of
>antibiotic resistance at:
>
>http://naturalselection.0catch.com/Files2/antibioticresistance.html
>
It is nice to see that you have fixed some of the errors I pointed
out, but it still has a number of errors (and is very hard to read),
you still have the loop information mixed up for example.
Cheers! Ian
Other useful references on the plasticity of enzymes and evolution of
complex systems from simple precurssors
Henn-Sax M, Hocker B, Wilmanns M, Sterner R. Divergent evolution of
(betaalpha)8-barrel enzymes. Biol Chem. 2001 Sep;382(9):1315-20.
Review.
Lang D, Thoma R, Henn-Sax M, Sterner R, Wilmanns M. Structural
evidence for evolution of the beta/alpha barrel scaffold by gene
duplication and fusion. Science. 2000 Sep 1;289(5484):1546-50.
Sean Pitman
> Hexagonal basalts have nothing to do with crystal symmetry. Nice attempt at
> bullshit.
The same principle applies to both crystal formation as well as the
formation of these hexagonal basalts at Devils Tower (Also, not all of
them are "hexagonal" in shape. Some of them have 4, 5, or 7 sides
etc). The information for their shapes was self contained in the
molecules themselves. No outside informational input was need in
their formation.
> In fact the xls symmetries of the minerals comprising basalt are quite
> non-hexagonal. The hexagonal shapes are a case of tensional cracking during
> cooling.
True, but the point remains. The information needed for their
formation was self-contained. No need for outside input for their
formation. Their formation was a type of self-assembly just as it is
for crystal formation.
> > No
> >higher informational input or intelligence is needed since all the
> >information for assembly is self-contained by the molecules
> >themselves.
>
> In fact, the molecueles in question contain no such information. In fact the
> information they contain is decidedly non-hexagonal. Perhaps you'd like my
> remedial mineralogy class?
Yes, the information is in fact there, self-contained. The molecules
are not forming an actual crystaline hexagonal structure here, but the
molecules do in fact play a role in how they react to external
stressors.
> Basalt is comprised mainly of plagioclase feldspar.. triclinic xls system
> (lowest symmetry of the xls groups), pyroxene which is orthorhombic, and
> varying amounts of olivine, also othorhombic.
Yes... but this does not change the point of my argument in the least.
> What cock and bull story will you come up with next?
You evidently do not seem to get the point of my argument. There is a
naturalistic cause that easily and clearly explains both the formation
of the crystaline structures as well as the formations at Devils
Tower. No external intelligence or informational input was needed as
the required information was self contained by the molecules and
environment of the system itself. These are basically examples of
self assembly, no thoughtful mind required. This is not the case for
honey comb formation. Bees are required. This is not he case for the
formation of my wristwatch, ID is required. So you see, when there is
no known naturalistic method of formation, a naturalistic cause cannot
be an automatic default assumption. In fact, in such a situation, ID
is a very reasonable hypothesis.
> Stuart
>
> Stuart
> Dr. Stuart A. Weinstein
> Ewa Beach Institute of Tectonics
> "To err is human, but to really foul things up
> requires a creationist"
Sean
Evolutionists are just as prone to error and to "fouling things up" as
anyone else. It has happened throughout history and it will continue
to happen. Evolutionists are also just as religiously fundamental and
dogmatic in their devotion and bias for the non-scientific philosophy
of naturalism as any Christian Bible-thumping church-going
creationist.
Rodjk
>
> > Hexagonal basalts have nothing to do with crystal symmetry. Nice attempt at
> > bullshit.
>
> The same principle applies to both crystal formation as well as the
> formation of these hexagonal basalts at Devils Tower (Also, not all of
> them are "hexagonal" in shape. Some of them have 4, 5, or 7 sides
> etc). The information for their shapes was self contained in the
> molecules themselves. No outside informational input was need in
> their formation.
And how is this different than for living things?
>
> > In fact the xls symmetries of the minerals comprising basalt are quite
> > non-hexagonal. The hexagonal shapes are a case of tensional cracking during
> > cooling.
>
> True, but the point remains. The information needed for their
> formation was self-contained. No need for outside input for their
> formation. Their formation was a type of self-assembly just as it is
> for crystal formation.
And you still miss the point.
Where is the need for outside input with living things?
What chemical laws are different for living vs non-living things?
>
> > > No
> > >higher informational input or intelligence is needed since all the
> > >information for assembly is self-contained by the molecules
> > >themselves.
> >
> > In fact, the molecueles in question contain no such information. In fact the
> > information they contain is decidedly non-hexagonal. Perhaps you'd like my
> > remedial mineralogy class?
>
> Yes, the information is in fact there, self-contained. The molecules
> are not forming an actual crystaline hexagonal structure here, but the
> molecules do in fact play a role in how they react to external
> stressors.
Way to miss the point. A typical lying piece of shit creationist.
>
> > Basalt is comprised mainly of plagioclase feldspar.. triclinic xls system
> > (lowest symmetry of the xls groups), pyroxene which is orthorhombic, and
> > varying amounts of olivine, also othorhombic.
>
> Yes... but this does not change the point of my argument in the least.
>
> > What cock and bull story will you come up with next?
>
> You evidently do not seem to get the point of my argument.
Which is to lie and squirm untill you change the subject.
>There is a
> naturalistic cause that easily and clearly explains both the formation
> of the crystaline structures as well as the formations at Devils
> Tower.
How is it different than the naturalistic causes for living things?
>No external intelligence or informational input was needed as
> the required information was self contained by the molecules and
> environment of the system itself.
Why are external intelligences required for living things.
>These are basically examples of
> self assembly, no thoughtful mind required.
How is this different than living things?
>This is not the case for
> honey comb formation. Bees are required.
Nice misdirection. Bees are the issue.
>This is not he case for the
> formation of my wristwatch, ID is required.
We see the designer of watches.
>So you see, when there is
> no known naturalistic method of formation, a naturalistic cause cannot
> be an automatic default assumption. In fact, in such a situation, ID
> is a very reasonable hypothesis.
I think you are full of crap.
Rodjk #613
Sean Pitman
> >> >For example, if I went to the moon and found a series of
> >> >perfectly round 10kg rocks all arranged in a perfect geometric square
> >> >measuring a mile on each side, it would be very reasonable of me to
> >> >theorize that some sort of purposeful intelligence, above any sort of
> >> >mindless naturalistic process, was at work here.
> >>
> >> Before or after I went to a beehive and saw "perfectly" hexagonal
> >> honeycombs? Or are bees Intelligent Designers?
> >
> >A robot can be programmed to produce a beautiful work of art or to put
> >together an intricate wristwatch.
>
> Ah, so sunsets are designed? God arranges the atmospheric conditions for
> each beautiful sunset we see? Hurricanes are "intricate". Are those
> designed?
You seem not to be following my point very well. The point is that
just because a robot is not itself "intelligent" does not mean that
the actions of the robot cannot be detected as being the result of a
mindful intelligence. A robot can be programmed to put together a
wristwatch. Does the fact that the robot is not intelligent mean that
the wristwatch was formed without intelligent design? No. Certainly
not.
Your suggestion that sunsets are the same level of complexity as the
formation of honeycombs is misguided. The information needed to
produce sunsets is self-contained within the cause and effect actions
of the molecules and mindless forces of this solar system and planet.
This is different from the formation of honeycombs in that bee's wax
does not self-assemble to form honeycombs whereas sunsets do
self-assemble. Honeycomb formation is actually on a higher level of
complexity than is sunset formation in that outside information is
needed for honeycomb formation.
> >However, this ability was
> >originally designed via some intelligent mind.
>
> I'm having trouble understanding your point. Because *some* things are
> designed, all things are?
No, not at all. Many phenomena have a purely naturalistic
explanation. Mindless naturalistic processes can and do create or
form some amazing things, such as sunsets, rainbows, rivers, water
falls, tornados, super novas, volcanic explosions, snow flakes and
etc. None of these phenomena require the input of information from an
intelligent mind.
> >The same could be said
> >of the honeybee's ability to make hexagonal compartments out of wax
> >and put honey in them.
>
> You *could* say "the moon is made of green cheese". It would help if you
> had evidence.
Pardon me? The evidence is that no known mindless naturalistic
process, outside of the workings of living things, like humans and
honey bees, can form honeycombs, wristwatches, language systems, or,
as I am arguing here, the language-like coded information written in
the DNA of all living things.
Many argue that just because no one has seen anyone design life or
living systems that no intelligent designer can be reasonably
hypothesized. However, if there is no naturalistic explanation or
mechanism to explain the existence of life, then it is in fact quite
reasonable to hypothesize an intelligent designer of life on this
planet... especially when one considers that modern scientists are
already manipulating the very codes of life and are creating "designer
genes". Add to this the fact that, without an adequate naturalistic
mechanism in place, no one has ever seen a mindless natural process
create life either. So, since no one has seen any mindless process
create life or change life forms to the degree that scientists, with
the aid of intelligent minds, are able to change the codes of life, it
is ridiculous to argue that science is incapable of hypothesizing
design. It is especially ridiculous to suggest this since the
argument is based on a lack of observation of origin, which also holds
true for any naturalistic explanation to date. Naturalistic mechanism
have clearly failed to explain the existence of neutral genetic gaps
that do in fact exist between various functional systems in living
things.
> >> And what would I do after I then went to Devil's Tower and saw the
> >> hexagonal basalts? Volcanos are "purposeful"?
> >
> >Not all geometric shapes imply intelligent design.
>
> But bees do? Why?
Again, no mindless naturalistic process can explain the creation of
bees or even the honeycombs that bees make. The only process than can
explain either one has its best explanatory power in the concept of
intelligent design.
> And DNA is what?
DNA is nothing outside of the coded information that it contains. The
ability to decode this information to create the phenotypic forms of
various living things imbues DNA with power that is above and beyond
its inherent molecular structure and natural ability.
> >However, this self-contained information for assembly is not contained
> >by many other systems of function, such as the parts to watch,
>
> Watches do not contain self-replicating molecules, that's true.
Exactly. This is a major point.
> >or the
> >code for a bacterial flagellum,
>
> Which "code" are you talking about?
The coded information contained in the DNA of the bacterium that makes
a flagellum. The information to make this flagellum is in fact coded
information that is decoded from the strand of DNA contained by that
bacterium. DNA works very much like a blueprint. Something must be
written on the blueprint and then something else must be able to read
or decode what has been written before the house that was coded by the
blueprint can be built. The same thing happens with the decoding of
information from DNA. Something sensible must first be written in the
DNA sequences and then something else must be able to read and
"understand" or "decode" the message contained in the DNA before the
flagellum can be built.
> >or the letters and word sequences in a
> >book or in this paragraph.
>
> Oh? Are you just a robot designed to write paragraphs? That would seem to
> follow from your example about robots and art.
No, I am the designer of these paragraphs. However, I could program a
computer to write out these same paragraphs over and over again.
However, just because a mindless computer is now printing these
paragraphs does not mean that these paragraphs could arise via the
mindless processes of this computer. Obviously, these paragraphs, no
matter the source of their subsequent production, where obviously
purposefully designed. This quality of purposeful design can also be
detected by the scientific method.
> >Many such phenomena give clear evidence of
> >higher intelligent input in their formation that is beyond the
> >mindless processes naturalistic mechanisms.
>
> Nice assertion. Why should I accept it?
Why shouldn't you? You accept it every day when you read a book, when
you look at the clock to see the time, when you see a sky scraper, or
when you hear a foreign language being spoken or when you see Egyptian
hieroglyphic writing that you cannot read or understand. How do you
recognize design in these cases? You assume design in such cases
because you know that humans are capable of such creations, but you
also know that naturalistic process are not capable of such creations.
For example, when you see an amorphous rock, you do not automatically
assume intelligent design even though a human could in fact have
formed that very rock or natural landscape. So, since humans are
capable of creating amorphous rocks, why not assume human design?
Because, naturalistic processes are also capable of producing
amorphous rocks. You see then, you assume intelligent design as the
most likely cause when no known naturalistic process could have
produced a given phenomenon; especially when this phenomenon resembles
other designed creations while, at the same time, not resembling any
known creations produced by purely mindless naturalistic processes.
> >The origin of this
> >intelligence does not need to be identified in order for it to be
> >recognized.
>
> Yes it does. Hey, this assertion without proof thing is kinda easy, isn't
> it?
It seems to me that you are mistaken. There are only two known
explanations for any given phenomenon. Either its origin or cause was
designed with the use of a mindful intelligence or it was not designed
and arose via a mindless naturalistic process. There is no other
option. If there is no known naturalistic mechanism, then a
naturalistic cause is NOT an automatic assumption. Without a known
naturalistic cause or mechanism, the possibility of design clearly
comes into play. In fact, if the phenomenon at hand does in fact
resemble other designed phenomena, then design is not only a possible
explanation, but it is a likely explanation.
> >The inability for any known naturalistic process to
> >produce a given phenomenon is itself evidence of intelligent design.
>
> You've found out how to prove a negative? Have you alerted the
> philosophers and logitians yet? Do they give a Nobel for philosophy?
No one every fully proves a negative. However, a negative can still
be believed in and scientifically supported based on the preponderance
of the evidence. Statistical negatives can be quite significant and
reasonable indeed although never fully provable.
> >> J. Pieret
> >>
> >> The devil is in the details.
> >> Science explains them.
> >> Intelligent design explains them away.
> >>
> >> - Mark VandeWettering -
> >
> >Science or the scientific method certainly is a very powerful tool for
> >the searching out of truth concerning the external world. In fact,
> >there is no other method that I know of that can do as good a job as
> >the scientific method. However, the scientific method does not
> >pre-suppose only naturalistic causes as explanations for phenomena
> >that occur in the external world. The a priori assumption of
> >naturalistic causes is not in fact a scientific assumption. In fact,
> >by using the scientific method, it is very reasonable to conclude that
> >intelligent design was involved with the existence of many phenomena.
> >The theory of ID can in fact be scientifically supported in many many
> >undisputable cases and situations. Forensic science, for example, is
> >based on this fact.
>
> So humans murderers aren't "naturalistic"?
No. Humans are not "naturalistic" in that humans have minds that are
intelligent. The processes of a mindless nature have no purpose or
deliberate intelligence. Such mindless purposeless processes are
supposed to have given rise to life as well as all the various life
forms that we see around us. The current theory of evolution does not
allow any intelligent processes to be involved. Any time human
tampering is involved in the "change" of genes, this is not
"evolution" because it is not "naturalistic" change. You do
understand this point I hope because it is vital to my argument.
> >So, to suggest that the origin of life must, by
> >"a priori" definition, have a naturalistic cause . . . is really
> >scientific heresy. Mark VandeWettering is obviously clueless, a
> >devoted disciple of the religion of naturalism. If I were to propose
> >ID as an explanation of the origin of the wristwatch on my arm, would
> >that be "explain it away"? or would it be a scientific explanation of
> >the evidence?
>
> No, the proposal of an *unknown* and *undescribable* manufacturer whose
> methods and means of building watches is *unknown* and (apparently)
> *unknowable* (since no one has proposed any way of investigating the ID
> "designer") is *not* a scientific explanation, anymore than proposing to an
> ME that a ghost killed someone is. And yes, saying god created your watch
> *would* be explaining it away.
No, it wouldn't. You need not know the identity of a designer at all
to reasonable know that intelligent design was involved in its
formation. No one need propose that the Christian God created life,
or my wristwatch to know that SOMEONE with an intelligent mind did
create both life and my wristwatch. I need not know who, exactly, did
it to know that some mindful intelligence was in fact involved in its
formation. To require direct knowledge of the actual identity of the
designer before one might be able to propose design is a ridiculous
argument. I have no idea why it is such a common argument. How on
earth can the SETI scientists be looking for signs of intelligent life
in outer space if they don't know the identity of the origin of these
signs of intelligence when they find them?
> >But really, they are only helping to
> >delude you into thinking that you are being rational when you are
> >actually contradicting yourself. The devil really is in the details
> >and science does search them out, but science does NOT always come up
> >with a naturalistic explanation as the most reasonable explanation.
>
> Ah, "reasonable" . . . as in the one you *prefer*, even if you don't have
> evidence for it.
The evidence is clear. It seems that your own preferences might be
blinding you to the correct meaning of the evidence, but bias is a
problem for everyone to one degree or another.
> >To say that this must be the case is to be either misinformed or
> >deliberately insane.
>
> Damn, funny how many insane people keep getting those research grants,
> Nobel prizes in science and all the rest, isn't it? . . .
Isn't it though ; ) But, this is an argument based on the authority
and supposed understanding of others, not on your own ability to know,
understand or explain the evidence. You are basically saying, "How
can so many brilliant scientists be wrong and you, an ignorant nobody,
even hope to have any concept of what might be going on?" This is a
lame authority-based argument that really has no explanatory value.
> >Sean
>
> And if you like that last sig, you'll *love* this one!
>
> ---------------
> J. Pieret
> ---------------
>
> SETI is based on the simple assumption that nature
> operates elsewhere the same way it does here.
> ID is based on the assumption
> that nature doesn't even work here.
>
> - Bobby Bryant -
SETI is based on the ability for scientists to detect ID. SETI is all
about ID. There is no separation of the terms. Both SETI and ID are
based on the assumption that purposeful mindful intelligence works
elsewhere as it works here and that mindless natural processes also
work elsewhere as they work here. Bobby Bryant seems not to
understand either ID or SETI. The fact is, nature does not work here
in the way that modern science is proposing that it does work.
Evolutionary scientists say that a mindless nature works on this earth
in a way in which they have no evidence to show how this work actually
happens. ID works on this earth in a way that can at least approach
an explanation for life while no known naturalistic process even comes
close.
Sean
Don Cates
>The information needed for their
>formation was self-contained. No need for outside input for their
>formation.
[next response paragraph]
>The molecules
>are not forming an actual crystaline hexagonal structure here, but the
>molecules do in fact play a role in how they react to external
>stressors.
--
Don Cates
ca...@cc.umanitoba.ca
Sean Pitman
> <snipping excellent but lengthy material, because my brief post would
> be lost in it.>
>
> Thanks, Sean, for another impressive post that reveals your erudition
> and wisdom. I understood your points, and can learn a lot from you.
>
> Thanks, too, John, for being the kind of mature and reasoned poster
> that Dr. Pitman can have a reasonable discussion with. It was a
> pleasure watching two minds sharpen off of each other.
>
> ----
> zoe
Thanks for the note. However, I'm not really here to convince anyone
of anything. . . although I don't mind if I end up sparking some
question of doubt concerning current evolutionary dogma. Basically
though, I'm really here for my own interest and benefit to see what
the best arguments are from those who ardently believe in evolution
and the doctrine of naturalism. So far, I'm less than impressed.
Sean
John Harshman
Ian Musgrave & Peta O'Donohue wrote:
> G'Day All
> Address altered to avoid spam, delete RemoveInsert
>
> On Wed, 21 May 2003 00:47:13 +0000 (UTC), John Harshman
> <jharshman....@pacbell.net> wrote:
>
>
>>
>>Ian Musgrave & Peta O'Donohue wrote:
>>
>>
>>>G'Day All
>>>Address altered to avoid spam, delete RemoveInsert
>>>
>>
>>[snip it all]
>>
>>Can we get together a bibliography of selection experiments on getting
>>new function from random sequences, or from sequences that happen to be
>>available in knockout organisms, and such like? I don't know very much
>>of the literature, but it seems to be pretty big, and should be in a FAQ
>>somewhere.
>>
>
> Sure, it might take a while, but it should be a valuable resource.
This is my sole contribution, at least for the moment (which is why I'm
asking you):
Hayashi, Y., H. Sakata, Y. Makino, I. Urabe, and T. Yomo. 2003. Can an
arbitrary sequence evolve towards acquiring a biological function. J.
Mol. Evol. 56:162-168.
John Harshman
Didn't you see it? Or do you have no interest?
John Harshman wrote:
>
> Sean Pitman wrote:
>
>
>>John Harshman pontificated:
>>
>
>
> [snip the whole thing]
>
> This post is becoming way too unwieldy. I printed it out so as to make
> an attempt at seeing the whole thing, and it came to 26 pages of small
> type. I will attempt to respond more at some later point, but here I'm
> trying to deal with two small goals: 1) to convince you that common
> descent and intelligent design are not mutually exclusive propositions
> and 2) to acquaint you with the gist of Hayashi et al.
>
> First, common descent and intelligent design. I take the first to mean
> that all species alive today are descended from one (or at any rate a
> very few) ancestral species by a continuous (and in sexual organisms,
> reticulating) series of invidual parents and offspring. I take the
> second to mean that the origins of major features of living species were
> guided by some intelligent being(s).
>
> As evidence that they are not mutually exclusive, I offer you examples
> of people who believe in both: 1) Alfred Russell Wallace, though he
> believed that natural selection could account for most features of
> organisms, believed that divine intervention was necessary to explain
> the origin of human intelligence; that is, he believed that we are
> related to apes by descent, but that our transition to intelligence must
> have been guided. 2) Charlie Wagner, fairly frequent poster to TO,
> believes in common descent, but also believes like you that natural
> selection is impotent; he thinks that all the subsequent diversity of
> life was pre-programmed into the first unicellular organisms. 3) Michael
> Behe, whom you cite so often, believes in common descent. It's not
> entirely clear what view he has of how the intelligent design was
> accomplished; at times, like Charlie, he seems to suggest
> pre-programming. The other obvious alternative would be the occasional
> directed mutation(s) of whatever size was necessary.
>
> Further, many creationists believe in common descent within limits. That
> is, they believe that a single kind, created as a single original
> species, can develop over time into multiple species. So a single
> "horse" kind can include not only horses (Equus caballus) but donkeys,
> zebras, quaggas, and the various extinct horses. If you go with that,
> our argument is not about common descent, which we both agree on, but on
> the original number of kinds. I go with one, and you with many. (How
> many would you estimate, by the way?)
>
>
> Add to that the millions of Christians who are, according to polls,
> theistic evolutionists, which means they accept common descent but
> believe that God guided the course of evolution in some fashion. Some of
> these believe he just set up the initial conditions so that evolution,
> proceeding naturally, would end up where he wanted; that would be
> contrary to your views. But others believe, as did Wallace, in direct
> intervention at various stages.
>
> If you reject the possibility of common descent combined with
> intelligent design (let's call it CD/ID), I would be interested to know
> why. What evidence can you present that argues against the CD/ID theory?
>
> And now, on to Hayashi, Y., H. Sakata, Y. Makino, I. Urabe, and T. Yomo.
> 2003. Can an arbitrary sequence evolve towards acquiring a biological
> function. J. Mol. Evol. 56:162-168.
>
> Here, typed in at great personal cost, is the abstract:
>
> To explore the possibility that an arbitrary sequence can evolve towards
> acquiring functional role when fused with other pre-existing protein
> modules, we replaced the D2 domain of the fd-tet phage genome with the
> soluble random polypeptide RP3-42. The replacement yielded an fr-RP
> defective phage that is six-order magnitude lower infectivity than the
> wild-type ft-tet phage. The evolvability of RP3-42 was investigated
> through iterative mutation and selection. Each generation consists of a
> maximum of ten arbitrarily chosen clones, whereby the clone with highest
> infectivity was selected to be the parent clone of the generation that
> followed. The eperimental evolution attested that, from an initial
> single random sequence, there will be selectable variation in a property
> of interest and that the property in question was able to improve over
> several generations. fd-7, the clone with highest infectivity at the end
> of the experimental evolution, showed a 240-fold increase in infectivity
> as compared to its origin, fd-RP. Analysis by phage ELISA using anti-M13
> antibody and anti-T7 antibody revealed that about 37-fold increase in
> the infectivity of fd-7 was attributed to changes in the molecular
> property of the single polypeptide that replaced the D2 domain of the
> g3p protein. This study therefore exemplifies the process of a random
> polypeptide generating a functional role in rejuvenating the infectivity
> of a defective baceteriophage when fused to some preexisting protein
> modules, indicating that an arbitrary sequence can evolve toward
> acquiring a functional role. Overall, this study could herald the
> conception of new perspective regarding primordial polypeptides in the
> field of molecular evolution.
>
> A few more facts: RP3-42 (the replacement domain) is an ORF that
> produces a polypeptide 139 residues long that has no secondary
> structure. g3p is the "minor coat protein" with, obviously, an essential
> role in getting the phage genome into bacterial cells. The replaced
> domain is the middle one of three, and when it's working, it "functions
> for the adsorption of g3p to the tip of the host F-pilus at the initial
> stage of the infection process". fd-tet is a phage containing a
> tetracycline-resistance gene, and thus only infected bacteria would grow
> colonies in a tetracycline-containing medium. Infectivity was assayed by
> counting colonies. The 250-fold increase in activity was achieved in 7
> "generations". I use the quotes becase mutation was not done in the
> phage itself, but by "error-prone PCR", in vitro, and the mutated
> sequences inserted into fresh phage. In this way they insured that all
> evolution that occurred was occurring in the random sequence. The
> sequence was then snipped out of chosen phage clones after each
> infectivity assay, subjected to more error-prone PCR, and stuck back
> into fresh phage. By the 7th generation, the most infective phage had
> experienced 26 replacement substitutions (as well as 11 silent
> substitutions).
>
> Would you agree that infectivity is a complex function?
>
>
Ron Okimoto
>
It looks like I quit too soon. I do screw up later on so I have to
continue.
The Hemoglobin citation is on page 63 of the 1981 version of Stryer
second edition Biochemistry. I too Biochem in 78-79 and I don't
remember the phrase "nine positions are nearly invariant." There is a
table with the nine amino acid residues, so I don't know why I
remember it as a lower number of invariant amino acids. It could be a
change between the first edition and the second, or I could just be
misremembering.
> > > The problem is that, relatively speaking, these islands of function
> > > are quite small indeed. When compared to the total number of
> > > completely non-functional sequences out there in the ocean of
> > > non-function, those sequences that have any function whatsoever (from
> > > the perspective of a given life form in a given environment), make up
> > > only the tiniest of fractions, especially when you start talking about
> > > functions that require amino acid sequences that average more than one
> > > enzymatic-type protein in length. When functions require multiple
> > > proteins totaling several hundred, thousand, or even tens or hundreds
> > > of thousands of amino acids in length, then your little islands with
> > > their little impressions don't come near close enough to avoid the
> > > random drift problem.
> >
> > They are likely small for any one sequence, but there are a lot of
> > sequences and a lot of possible functions, and when you change a
> > sequence you change its functional potential. You can't just look at
> > the potential functions of any single extant proteins, but you have to
> > look at the potential function of all the molecules that you can get
> > by changing just 1 to 3 amino acid positions. You know that this is
> > possible. If you make one or two changes you can significantly change
> > the landscape for any function, can't you?
>
> Yes, but you do not seem to understand the problem. You are thinking
> that there are so many potential beneficial functions out there that
> just about any change in bound to evolve at least one of them.
No, what we see is that for anything that we can think up a selection
for we can get that activity randomly changing the sequence of the
variable region of the antibody.
The
> problem is that even though there are a lot of potential functions out
> there as far as an absolute number goes, this number is very tiny
> indeed when compared to the total number of potential sequences out
> there. For example, there may be a billion potential lactase enzymes
> out there of 4,000aa or less (The approximate length of the lacZ and
> ebg lactase enzymes). Is a billion a large number? Well, yes it is
> until one compares it with a 1 with 5,200 zeros after it (the total
> number of potential proteins of this length). So you see, the "large"
> number of potential functional sequences is really an illusion of
> bigness. Such "big" numbers are really small in comparison to the
> bigness of the total number of possibilities. In other words, no
> matter which direction that a sequence "drifts" in its random walk, it
> is unlikely that it will come across any other beneficial function,
> from the perspective of a given organism, in short order. And, this
> problem becomes more and more significant with increasing functional
> complexity . . . especially when we start talking functions that
> require multiple proteins all working together at the same time . . .
> like in bacterial motility etc.
Like I said before 10^12 is such a minute fraction of the possible
sequences that there is something wrong with your evaluation of the
system.
Explain how function is obtained in so few trials if you are even
close to being correct in your inferences. This isn't some fluke, but
is done routinely. Do a PubMed search on Abzymes.
>
> > You keep forgetting that according to science, evolution doesn't have
> > a plan and that lactase activity isn't some goal. If it happens,
> > fine, you get something that may be useful. If it doesn't happen,
> > fine, the bacteria keeps on going just like it always did.
>
> And you keep forgetting that no matter which direction that random
> walk takes toward ANY new function, all new functions are a good ways
> away from any potential starting point. Therefore, the evolution of
> ANY new function requires a certain amount of time and this time
> increases exponentially as the complexity of functions increase. The
> bacteria may keep going just fine with what they currently have, but
> the odds that they will just happen to come across something as
> complex as bacterial motility or any other function of such
> complexity, simply requires too much time. Again, the illustration of
> the English language system comes into play. It is relatively easy to
> come across a series of 3-letter words with random walk, but it is
> another thing entirely to come across a series of 6-letter words, not
> to mention sentences or paragraphs with random walk. Start with any
> average length sentence. Change one letter at a time with each change
> making some sense in English, and see how many different meaningful,
> functionally beneficial, sentences that you can come up with. It is a
> LOT harder than you might initially imagine. This same problem holds
> true for genetic evolution of life forms.
Demonstrate that this means anything. DNA is not the English
language. Do something with your English in 10^12 trials of random
changes from something that was gibberish before.
>
> Dawkins tried to do it, somewhat, with his "Methinks it is like a
> weasel" computer evolution experiment. However, where Dawkins went
> wrong is that each of his generations of phrase evolution were
> meaningless. He selected phrases of gibberish that were closer in
> *spelling* but not in *meaning* to "Methinks it is like a weasel."
> You do see the problem here don't you? There are a lot more
> meaningless sequences of 28 characters in length than there are
> meaningful sequences of this length. This poses a problem, as it did
> for Dawkin's experiment, in that there simply is no path of function
> from one sentence of this length to very many other meaningful
> sentences, although there may in fact be millions of them, of similar
> lengths. This same problem exists in genetic evolution experiments.
> Natural selection is simply powerless without a change in function
> with each change in genetic spelling.
Um, it was an analogy and it is only used as something to get you to
understand the power of selection. You do understand that don't you?
It has limited biological relevance.
>
> > Explain the antibody results if you are correct. Why is the
> > impossible, possible for antibodies? Why do you only have to score
> > 10^12 events before you find the activity that you select for?
>
> Because, as I have explained multiple times already, the activity that
> was "selected for" was a relatively simple enzymatic type activity.
> It is like throwing all the possible 3-letter sequences for English
> words into a bag and asking me to pick out one of them that has a
> particular function. It might take a while, but not very long
> comparatively speaking because I am basically looking for a short
> sequences with a simple function that has relatively high odds of
> success.
Lactase is pretty simple. So you have given up on the bogus use of
the Halls work.
>
> > By the
> > early 1990's they had already produced over 70 different enzymatic
> > activities using antibodies. I think that they have their own name,
> > now, and they are called abzymes. If you do a PubMed search you will
> > likely find references to a whole lot more enzymatic activities by
> > now.
>
> Certainly true, and not suprising in the least. This is only to be
> expected as many enzymatic activities are relatively simple protein
> functions.
This is pretty tragic. What have you spent months arguing?
>
> > > But, there is something hopeful about your hypothetical suggestion.
> > > The very fact that you proposed such a hypothetical solution to the
> > > problem means that you might actually recognize the problem, which is
> > > a significant step. In any case, I remain most interested in your
> > > thoughts and struggles with this issue.
> > >
> > > Sean
> >
> > It is not an explanation for a problem, but for what we observe
> > occuring in nature.
>
> You only observe this in nature as it relates to relatively simple
> functions that are only very short neutral distances from what is
> already there. The problem, as detailed over and over again above, is
> far greater than this.
That is what we were talking about for lactase function, weren't we?
>
> > There is a difference that you seem to be
> > missing. We see this happening. You have to claim that what we
> > already observe to occur is impossible.
>
> Not so. I do not claim that what we observe happening is impossible
> at all, only that it is very limited and easily explainable with the
> use of random drift alone.
>
> > That is what is wrong with
> > your argument. Our only problem seems to be trying to explain why it
> > seems to be so easy to get function from a protein sequence.
>
> No . . . the problem is that with the increasing complexity of protein
> function comes a vast increase in the average neutral gap that must be
> crossed. Simple functions have smaller gaps. More complex functions
> have larger gaps. That is the problem. How does a given life form
> evolve such functions of higher complexity?
Demonstrate that this is true. You have to first demonstrate that the
gaps exist. This is just assertion without evidence. Take a complex
system and show us where the gaps are and how you determined that
these gaps exist.
>
> > A better
> > argument for you and one that the ID people use is that since we don't
> > have a good explanation for how we evolve these functions that some
> > designer must be responsible for guiding these mutations and making
> > the results happen.
>
> Uh . . . that is my argument.
No, because we see it happening in nature. If you want to claim
divine intervention, demonstrate that it is happening in the systems
that these researchers are studying. Your argument is that it
happened in the past because we obviously do not have any evidence
that it is happening now.
>
> > The problem with the ID argument is that it is
> > stupid. Just try and find some evidence to support it.
>
> LOL - Ok . . . it is very easy to say that something is "stupid"
> without giving any reasonable explanation as to why it is "stupid."
> You are just spouting off without any basis for support of your
> position whatsoever. I have been giving you the "evidence" to support
> this ID argument all along. You seem to vaguely understand the
> arguments, but you are so stuck in your rut of "naturalism explains
> everything" that you are too blind to admit that there just might be
> something to ID.
You are just laughing at ID and yourself. Where is this evidence? It
is the same stupid bull that the ID people are spouting, but if it
were real evidence they would have published by now and they would
have had something to teach in Ohio. What was the reason that they
could not present a single thing about ID that they could support
teaching if they had real evidence backing up their assertions? They
were asked what they could teach about ID and the answer was nothing.
Verify this evidence. What good is it if you can't verify that it
means anything? The ID people know this or they would have presented
some of it as teachable. Isn't it stupid to claim that you have a
viable argument when you know that it isn't viable, and you can't put
it forward as being presentable without looking like a fool or being
shown to be a liar?
What is your explanation for ID's failure to present anything
teachable in Ohio? Where was all this great evidence? The Discovery
Institute Reps were there and there were supposedly University Profs
on the side of teaching ID, so why didn't a single one of them come
forward with something to teach when it was requested of them? The ID
proponents know their limits or one of them would have been stupid
enough to put something forward. This tells you something about ID
proponents, but it isn't something good.
As I have discussed above Hall's system is not the system you can
select for multiple mutations in because it is a single step
selection. Can you get three mutations in 5 or 6 generations starting
from a single bacterium? If you are lucky you might see one mutation
if you plate enough bacteria.
>
> > Just tell us one thing, if you are right about how difficult it is to evolve
> > function in a protein would antibodies be able to evolve the novel enzyme
> > functions in less than 10^12 trials? Yes or no.
>
> Again, it depends on the complexity of the function in question.
> Simple functions would be easier to evolve since the gaps between
> simple functions would obviously be smaller than gaps between more
> complex functions. Abzymes are in fact relatively simple functions
> that generally require one protein sequences of a relatively small
> length. So yes, such functions would not be surprising to see
> evolving in various life forms (also discussed above).
If you look at the sequences of Abzymes you see that they are spread
quite a distance around the molecule and not just in a short sequence.
You still do not get how this makes your Hall argument irrelevant.
Lactase is a simple enzymatic function.
>
> > You can claim anything else about these results that you want, but the plain
> > fact is that these results demonstrate that your reservations are bogus.
>
> LOL - Actually, the results of these experiments only support my
> position. They in no way counteract my reservations in the least.
Demonstrate that this is true. You admit that it is trivial to evolve
new functions, but for some reason your Hall argument is still
relevant. Explain the relevance.
>
> > Let's
> > see you admit that simple fact. How many trials would it take to create new
> > function if you were right? Why does it only take less than 10^12?
>
> It depends on the level of complexity involved with the function? How
> many amino acids, at minimum, would be required? How many sequences
> of a given length would have this particular function? What is the
> ratio of potentially functional sequences as compared to the total
> number of potential sequences? You see, the evolution of some simple
> enzymatic type function really isn't the issue here. Such
> demonstratable evolution is not the salvation of the theory of common
> descent of all life forms. Hopefully you can begin to recognize this
> problem, but I am beginning to have my doubts. Your logical abilities
> seem to be quite blinded by your naturalistic philosophy.
We don't care, all we care about is that it is possible. You have
been claiming that it is highly improbable or impossible, but now it
is trivial and you can still claim that your argument still stands.
How can a 180 degree reversal support your original argument?
>
> > You also can't seem to get it through your misperceptions that there is no
> > goal.
>
> Yes, there is a "goal" for evolution. You are clearly mistaken here.
> The goal of genetic evolution is the goal of new beneficial functions,
> whatever they may be. That is the goal. The goal is NOT the
> evolution of just any random set of genetic sequences. Evolution must
> evolve functional sequences that are actually beneficial at the same
> time. This means that there is some specificity to evolution. And,
> this creates a problem for evolution which gets larger and larger to
> the point of impossibility as the level of functions increases.
There is no goal that we can observe. Things just happen. If you can
see some goal for the random mutations that create abzymes you could
become famous.
>
> > For some reason you are stuck with your bogus analogy of fixing broken
> > windows. Lactase function was just a quirk that the bug found gave it some
> > advantage. Without lactase function the bacteria was dividing happily in some
> > mammal's guts. It didn't have to evolve lactase function to survive.
>
> Actually, it did have to evolve the lactase function if it wished to
> use the potential energy source of the surrounding lactose for some
> advantage.
But it didn't have to and many bacteria didn't.
The window analogy is not "bogus" at all. It shows that
> some "functions" simply have no naturalistic explanation while others
> do have such explanations. A broken window has a naturalistic
> explanation while a fixed window has no naturalistic explanation
> outside of deliberate design.
Demonstrate this in nature.
What is a broken window? What is a fixed window? Give examples. How
does this demonstrate design?
The same situation aplies to genetic
> functions. If no naturalistic explanation exists to explain the
> variety or level of certain genetic functions that exist in various
> life forms, the only logical explanation available to explain their
> obvious existence is ID.
Only in ID fantasy. If this were true, why can't they demonstrate it
and support it with enough evidence to teach it to children? The fact
is that it is only good enough evidence to fool people like you into
thinking that there is a valid argument in there somewhere. Where is
this valid argument? Does the fact that the ID proponents admit that
it isn't valid by their own inaction count for anything?
>
> > Gene duplication has been documented. There are so many cases of likely gene
> > duplication in all lifeforms that it would be pretty stupid of you to deny that
> > it happens on a regular basis.
>
> Certainly gene duplication does happen, but it does not happen on a
> "regular" basis. And, even if it did, it wouldn't really help the
> theory of evolution out of the neutral gap problem. The only thing
> that gene duplication would do is to increase the available genetic
> real estate that can undergo neutral drift. Increasing the genetic
> real estate does help, but only to a point. Increasing gap size
> quickly outpaces the ability of increasing genetic real estate to keep
> up with the statistical time needed for random walk to succeed.
>
> > What is one of the ways mosquitos evolve
> > resistance to DDT? Isn't it gene duplication?
>
> No. It is not gene duplication in the vast majority of cases. Such
> resistance-type evolution is almost always the result of single point
> mutations in target proteins or the like. It works much like the
> evolution of many types of antibiotic resistance. For further
> discussion of this, I have written a paper on various types of
> antibiotic resistance at:
We're not talking about antibiotics, but of the case of DDT and
multiple copies of genes and their influence on resistance to that
pesticide.
>
> http://naturalselection.0catch.com/Files2/antibioticresistance.html
>
> > Isn't this a favorite
> > creationist misdirection ploy about evolved resistance? "It is only gene
> > duplication."
>
> Not at all. If it is, it is not a very good argument as it really
> explains very little. I certainly don't use such an argument.
You are right it wasn't a very good argument. If you want evidence
for gene duplication in the history of life look up the DDT papers and
look at the glutothione related genes.
>
> > Apparently lifeforms can survive happily with these duplications
> > and if we look at genomes many of these gene duplications have evolved novel
> > functions. We have evidence that this evolution is possible. What do you have
> > to claim that it isn't possible?
>
> Most of the literature that suggests certain functions arose via gene
> duplication are not based on any direct experimental evidence or
> observation, but only on a "just-so-story of what must have happened.
> Very few if any of these "examples" are based on any sort of real time
> experiments. Such suggestions are based on certain similarities that
> exist between various genes with different functions, but such
> similarities could just as easily have been designed, again, with the
> use of the principle of "conservation of design." You see,
> similarities do not automatically support the theory of common
> evolutionary origin over the concept of ID. The support of the theory
> must be found in an explanation of the differences, not the
> similarities. The similarities can equally be explained by both
> theories, but the differences cannot. So, it is in the differences
> where one must find evidence for or against naturalistic evolution vs.
> intelligent design.
Demonstrat that you can account for the data equally well with your
model. Remember the nested pattern of changes. When a gene
duplicates it starts changing relatively independently. We see
nesting within nesting in the successive duplication events of these
large families of genes. Explain the nesting in your model and why it
mimics biological evolution. I'd like to see you do this.
>
> > Your arguments are so much of a crock that you know that you should be ashamed
> > to still be trying to defend them.
>
> Funny thing, I was thinking pretty much the same thing about your
> arguments.
>
> > Your own calculations should tell you that
> > crossing 3 mutations to get function is well within the bounds of possibility,
> > but Hall didn't see any for what reason?
>
> As detailed above, either the gaps may have been wider than this or
> the E. coli didn't have enough free genetic real estate to undergo
> random walk.
This is where I screwed up and the first two changes were only
believed to be neutral until they were studied in more depth.
So selection may have played a roll in getting the three mutations.
We are stuck with no examples of 3 mutations needing to be bridged to
get function. In those terms your argument is now even worse. Nature
found a way to use selection to get the three changes. You claim that
neutral changes are needed, but we can't find them.
Demonstrate that even three neutral changes would be needed for any
system that you chose. You can't just claim that it is obvious. This
example demonstrates that it takes a lot of hard work to determine
these things and what was thought to be neutral really had some
selective advantage even if they missed it initially.
Snip:
Ron Okimoto
Bigdakine
>Date: 5/21/03 4:41 AM Hawaiian Standard Time
>Message-id: <80d0c26f.03052...@posting.google.com>
>
Funny, didn't you say their information was just *self-contained*?
Do endeavor to keep your baloney straight. I can't keep fixing your arguments
for you.
Basalts obey the laws of physics, just like DNA. Of course there are rules on
some level, but that doesn't qualify as intelligence or design.
Nothing new here.
>
>> Basalt is comprised mainly of plagioclase feldspar.. triclinic xls system
>> (lowest symmetry of the xls groups), pyroxene which is orthorhombic, and
>> varying amounts of olivine, also othorhombic.
>
>Yes... but this does not change the point of my argument in the least.
The point is, you have no argument.
All things obey the laws of physics. Including DNA. Why do columnar joints
form? Because the rock was simply obeying the laws of physics as it cooled. No
intelligent intervention required, no design, nada. Why does DNA do the vodoo
it does so well? It, like the basalt obeys the laws of physics.
>
>> What cock and bull story will you come up with next?
>
>You evidently do not seem to get the point of my argument. There is a
>naturalistic cause that easily and clearly explains both the formation
>of the crystaline structures as well as the formations at Devils
>Tower. No external intelligence or informational input was needed as
>the required information was self contained by the molecules and
>environment of the system itself.
And no external intelligence is needed for evolution.
It so refershing to see that you realize that natural phenomena don't require
an external intelligence, even ones which give the appearence of design.
Life only requires an external intelligence, in your view, because your
religious beliefs demand it.
These are basically examples of
>self assembly, no thoughtful mind required. This is not the case for
>honey comb formation. Bees are required.
Intelligence? But I already pointed out no intelligence was required for
colunmnar basalts. Only rules are required, and everything in the Universe
obeys the same rules.
So intelligence has nothing to do with it. Did you think nobody would notice
the not so subtle sleight of hand here?
Hmm. So creationist no longer argue that one of things separating men from the
animal world is our intelligence? I'll have to make a note of that.
We are making progess, whether you realize it or not.
This is not he case for the
>formation of my wristwatch, ID is required.
Paley's argument has been refuted so many times, that its a wonder creationist
keep making the this point and hope that nobody notices. Second, we know who
the desingers of wristwatches are. Nobody would posit a natural cause for them.
So you see, when there is
>no known naturalistic method of formation, a naturalistic cause cannot
>be an automatic default assumption.
We have a method to find a naturalistic cause. We have used it profitably. And
your assertion, that no naturalistic method is known is false.
In fact, in such a situation, ID
>is a very reasonable hypothesis.
3000 years ago, people didn't know why it rained, so they had a rain God,
didn't know why the moon went through phases so they had a moon God, etc..
ID has failed everywhere it's been tried. You have given no reason to suggest
that is no longer the case, other you wish it were so. ID has no method of
investigation.
You are truly unique, Dr. Pittman. Not everybody would use examples of
self-assembly in nature to argue that life can't self-assemble. That is highly
original.
Yes, indeed, you have really hit paydirt with that one.
Jason Cortina
I assure you I will lose no sleep over such a judgment from someone who
still does not seem to know the meaning of the concept of 'mechanism' and
considers our current ignorance in certain areas as a form of positive
evidence *for* something other than our current limitations.
--
Jason A Cortina
Meat is a terrible mechanism for transporting consciousness
across the vast emptiness of space.
catshark
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>catshark <cats...@yahoo.com> wrote in message news:<huilcv8p55jpshgks...@4ax.com>...
>
>> >> >For example, if I went to the moon and found a series of
>> >> >perfectly round 10kg rocks all arranged in a perfect geometric square
>> >> >measuring a mile on each side, it would be very reasonable of me to
>> >> >theorize that some sort of purposeful intelligence, above any sort of
>> >> >mindless naturalistic process, was at work here.
>> >>
>> >> Before or after I went to a beehive and saw "perfectly" hexagonal
>> >> honeycombs? Or are bees Intelligent Designers?
>> >
>> >A robot can be programmed to produce a beautiful work of art or to put
>> >together an intricate wristwatch.
>>
>> Ah, so sunsets are designed? God arranges the atmospheric conditions for
>> each beautiful sunset we see? Hurricanes are "intricate". Are those
>> designed?
>
>You seem not to be following my point very well.
Perhaps you are not explaining yourself well.
>The point is that
>just because a robot is not itself "intelligent" does not mean that
>the actions of the robot cannot be detected as being the result of a
>mindful intelligence. A robot can be programmed to put together a
>wristwatch. Does the fact that the robot is not intelligent mean that
>the wristwatch was formed without intelligent design? No. Certainly
>not.
If you are going to argue by analogy, can you at least try to keep them
consistent? You started out this thread by asserting that a regular
arrangement of rocks on the moon would be evidence of "purposeful
intelligence". I asked about regular features that occur in the natural
world and you now apparently concede that "Not all geometric shapes imply
intelligent design". Instead, you then switched to an analogy of a robot
creating art. I asked about "art" that occurs in nature and you concede
that "Mindless naturalistic processes can and do create or form some
amazing things, such as sunsets, rainbows, rivers, water falls, tornados,
super novas, volcanic explosions, snow flakes and etc." Now you switch to
a robot making (by common understanding) a humanly manufactured item. Do
try to make up your mind.
Now, let's take out the element of obvious human manufacture and, instead
of a "watch", just call it a "timepiece". How then do you explain
"chemical clocks"?
<http://www.faidherbe.org/site/cours/dupuis/oscil.htm>
Are they intelligently designed, even though they keep time by molecular
reactions that are "self-contained within the cause and effect actions of
the molecules and mindless forces of this solar system and planet"?
>
>Your suggestion that sunsets are the same level of complexity as the
>formation of honeycombs is misguided. The information needed to
>produce sunsets is self-contained within the cause and effect actions
>of the molecules and mindless forces of this solar system and planet.
>This is different from the formation of honeycombs in that bee's wax
>does not self-assemble to form honeycombs whereas sunsets do
>self-assemble.
But *bees* do self-assemble (we don't have to address any idea that the
"designer" assembles bees individually, do we?).
Please give a consistent and objectively verifiable way to distinguish
between the "level" of complexity involved in a chemical clock and that
involved in a living thing. Where is complexity "discontinuous"? At what
point does something become too complex for the "mindless forces" of the
universe?
>Honeycomb formation is actually on a higher level of
>complexity than is sunset formation in that outside information is
>needed for honeycomb formation.
This is nothing but a petitio principii and circular to boot. "The
existence of a 'higher' level of complexity proves there must be an
intelligent designer and we know it is higher complexity because it could
not exist without an intelligence to design it". Conveniently, you skip
the part about demonstrating discontinuous levels of complexity that
require an intelligence to breach.
>
>> >However, this ability was
>> >originally designed via some intelligent mind.
>>
>> I'm having trouble understanding your point. Because *some* things are
>> designed, all things are?
>
>No, not at all. Many phenomena have a purely naturalistic
>explanation. Mindless naturalistic processes can and do create or
>form some amazing things, such as sunsets, rainbows, rivers, water
>falls, tornados, super novas, volcanic explosions, snow flakes and
>etc. None of these phenomena require the input of information from an
>intelligent mind.
Good, we agree that complexity can arise from "Mindless naturalistic
processes". Now tell us what separates that complexity from the complexity
you say can't arise on its own . . . *without* using the equivalent of "I
know it when I see it".
>> >The same could be said
>> >of the honeybee's ability to make hexagonal compartments out of wax
>> >and put honey in them.
>>
>> You *could* say "the moon is made of green cheese". It would help if you
>> had evidence.
>
>Pardon me? The evidence is that no known mindless naturalistic
>process, outside of the workings of living things, like humans and
>honey bees, can form honeycombs, wristwatches, language systems, or,
>as I am arguing here, the language-like coded information written in
>the DNA of all living things.
Wait! Now you are all over the place. One moment "intelligent" was the
opposite of "mindless". Now something a low on the scale of intelligence
as a bee is all it takes to be opposite "mindless"? Why not an amoeba?
Are you proposing the "Intelligent Designer" can be an amoeba?
Joking aside, you are obviously having trouble explaining what separates
"intelligent" from "mindless". Please give a definition that isn't just
"life is the result of intelligence, everything else isn't".
>
>Many argue that just because no one has seen anyone design life or
>living systems that no intelligent designer can be reasonably
>hypothesized. However, if there is no naturalistic explanation or
>mechanism to explain the existence of life, then it is in fact quite
>reasonable to hypothesize an intelligent designer of life on this
>planet...
In order for this to have any persuasive power (outside personal
preference), you must first demonstrate that there *is* no naturalistic
explanation or mechanism, especially since you are making an extraordinary
claim in the face of the many successes naturalistic interpretations *have*
had in explaining what we see around us.
>especially when one considers that modern scientists are
>already manipulating the very codes of life and are creating "designer
>genes".
The absence of evidence is not evidence of absence.
A hundred years ago it was "impossible" that any human would ever fly, much
less go to the moon; the Earth supposedly couldn't be older than a few
hundred million years because we had no mechanism to explain its internal
temperature; and sickness was a "visitation from god". (Not to mention
that your argument just ignores what we *do* know about possible routes to
abiogenesis.)
As always, it is "god in the gaps". Do you really want to bet your beliefs
on science *not* discovering a naturalistic explanation for the beginning
of life? Of course, that is assuming that this argument *does* have
anything to do with your beliefs and isn't just a justification for what
you want to believe in the first place.
>Add to this the fact that, without an adequate naturalistic
>mechanism in place, no one has ever seen a mindless natural process
>create life either. So, since no one has seen any mindless process
>create life or change life forms to the degree that scientists, with
>the aid of intelligent minds, are able to change the codes of life, it
>is ridiculous to argue that science is incapable of hypothesizing
>design.
Hold it! Define "hypothesize". To this nonprofessional, a "scientific
hypothesis" means an idea for a program of *further* observation and
testing to discover empirical evidence. What program(s) of research and
testing has been proposed or implemented by Intelligent Design proponents?
If ID does not seek empiric evidence of this designer, how can it be
scientific?
Naturally, you are at a disadvantage here, since even you do not expect to
find any empiric evidence of this designer. But that just means you should
take your case to its proper realm, philosophy and religion.
>It is especially ridiculous to suggest this since the
>argument is based on a lack of observation of origin, which also holds
>true for any naturalistic explanation to date. Naturalistic mechanism
>have clearly failed to explain the existence of neutral genetic gaps
>that do in fact exist between various functional systems in living
>things.
But science will go on looking for the evidence. ID seems totally
uninterested in finding any.
>
>> >> And what would I do after I then went to Devil's Tower and saw the
>> >> hexagonal basalts? Volcanos are "purposeful"?
>> >
>> >Not all geometric shapes imply intelligent design.
>>
>> But bees do? Why?
>
>Again, no mindless naturalistic process can explain the creation of
>bees or even the honeycombs that bees make. The only process than can
>explain either one has its best explanatory power in the concept of
>intelligent design.
You keep *saying* this. Saying it is not evidence for it.
And what "explanatory" power does this proposed designer/god have? Does it
explain how the design was done, why it was done or how we can test for it
(except by mapping out the limits our own ignorance and stuffing he/she/it
in there)? Is there anything I can definitely say was *not* designed, even
your "mindless" naturalistic processes? Anything that exists, or could
possibly exist, could be the result of "design". How am I better off,
scientifically, *after* this designer is proposed than I am before? What
more do I *know* scientifically?
>
>> And DNA is what?
>
>DNA is nothing outside of the coded information that it contains. The
>ability to decode this information to create the phenotypic forms of
>various living things imbues DNA with power that is above and beyond
>its inherent molecular structure and natural ability.
Yes, ontogeny counts. Now demonstrate that anything more is *needed*
"above and beyond". You've left that part out . . . again.
>
>> >However, this self-contained information for assembly is not contained
>> >by many other systems of function, such as the parts to watch,
>>
>> Watches do not contain self-replicating molecules, that's true.
>
>Exactly. This is a major point.
If so, it is eluding me. Such a major difference between watches and
living things sinks you analogy qua analogy. You'll have to redo it yet
again, unless you think living things are watches that have to be
manufactured or that nature is incapable of anything human beings cannot do
right this moment. No great loss though, it wasn't very good when Paley
came up with it (and, no, I don't want to get into *that* endless argument
- one is enough.)
>
>> >or the
>> >code for a bacterial flagellum,
>>
>> Which "code" are you talking about?
>
>The coded information contained in the DNA of the bacterium that makes
>a flagellum. The information to make this flagellum is in fact coded
>information that is decoded from the strand of DNA contained by that
>bacterium. DNA works very much like a blueprint. Something must be
>written on the blueprint and then something else must be able to read
>or decode what has been written before the house that was coded by the
>blueprint can be built. The same thing happens with the decoding of
>information from DNA. Something sensible must first be written in the
>DNA sequences and then something else must be able to read and
>"understand" or "decode" the message contained in the DNA before the
>flagellum can be built.
Frankly, you'll have to go play with the "information theory gurus" about
this. Try Wilkins, who does a nice understandable job with it. I have
neither the time to dig out one of his old posts nor the inclination to
delve deeply enough into this myself to do it justice. Simply put, though,
once a self-replicator has arisen, the environment, along with mutation and
variation, supplies all the "information" necessary to explain evolution.
>
>> >or the letters and word sequences in a
>> >book or in this paragraph.
>>
>> Oh? Are you just a robot designed to write paragraphs? That would seem to
>> follow from your example about robots and art.
>
>No, I am the designer of these paragraphs.
So you can develop beyond your original design. Good.
Now, what stops the rest of life? And if life can develop, how can you
assert knowledge about how *much* it can develop, especially when you know
nothing about the supposed designer?
>However, I could program a
>computer to write out these same paragraphs over and over again.
>However, just because a mindless computer is now printing these
>paragraphs does not mean that these paragraphs could arise via the
>mindless processes of this computer. Obviously, these paragraphs, no
>matter the source of their subsequent production, where obviously
>purposefully designed. This quality of purposeful design can also be
>detected by the scientific method.
Ever hear of Turing Machines? I suppose those are "impossible" too.
>
>> >Many such phenomena give clear evidence of
>> >higher intelligent input in their formation that is beyond the
>> >mindless processes naturalistic mechanisms.
>>
>> Nice assertion. Why should I accept it?
>
>Why shouldn't you? You accept it every day when you read a book, when
>you look at the clock to see the time, when you see a sky scraper, or
>when you hear a foreign language being spoken or when you see Egyptian
>hieroglyphic writing that you cannot read or understand. How do you
>recognize design in these cases?
By knowing what *humans* do. If I was on another planet with intelligent
life forms, there is no reason to assume I'd recognize what they do as
intelligence driven.
>You assume design in such cases
>because you know that humans are capable of such creations, but you
>also know that naturalistic process are not capable of such creations.
*Only* because I recognize them *as* human activities.
> For example, when you see an amorphous rock, you do not automatically
>assume intelligent design even though a human could in fact have
>formed that very rock or natural landscape. So, since humans are
>capable of creating amorphous rocks, why not assume human design?
I do not assume an "Intelligent Designer" for rocks at all, because Occam's
Razor gives undefined, unknown and unknowable beings *awfully* close
shaves. As to whether humans have or have not made the rocks, I will
"assume" nothing, but I'll make a "first approximation" that the rocks I
find on a wild shore are probably not man-made. But I might well reverse
that when I see a rock inside a zoo cage, a museum diorama or a shopping
mall. In short, whatever my expectations may be, I'll wait for the
evidence.
>Because, naturalistic processes are also capable of producing
>amorphous rocks. You see then, you assume intelligent design as the
>most likely cause when no known naturalistic process could have
>produced a given phenomenon; especially when this phenomenon resembles
>other designed creations while, at the same time, not resembling any
>known creations produced by purely mindless naturalistic processes.
No, I look for evidence. Since we are talking about science, I look for
scientific evidence and since the only scientific evidence is empiric
evidence, *that's* what I look for. You are free, of course, to go outside
science but don't try to make me believe it *is* science.
>
>> >The origin of this
>> >intelligence does not need to be identified in order for it to be
>> >recognized.
>>
>> Yes it does. Hey, this assertion without proof thing is kinda easy, isn't
>> it?
>
>It seems to me that you are mistaken. There are only two known
>explanations for any given phenomenon. Either its origin or cause was
>designed with the use of a mindful intelligence or it was not designed
>and arose via a mindless naturalistic process. There is no other
>option. If there is no known naturalistic mechanism, then a
>naturalistic cause is NOT an automatic assumption. Without a known
>naturalistic cause or mechanism, the possibility of design clearly
>comes into play.
In philosophy or religion, perhaps. Science takes evidence.
>In fact, if the phenomenon at hand does in fact
>resemble other designed phenomena, then design is not only a possible
>explanation, but it is a likely explanation.
Speaking philosophically (just as you are), I disagree. I accept a
practical empiricism largely because science has a history of *working*.
It *explains* the universe in a incredibly successful and widely useful
manner. No other system of human though has such an extraordinarily track
record in opening up knowledge to humans. That is good enough for me to
not want to screw up that underlying process of science. No one is denying
you your philosophy or beliefs. I don't care if you want to believe this
stuff. I do, however, object to political attempts to inject it into
public schools at my expense, which is, as far as I can see, the one and
*only* activity that ID "researchers" have been engaged in.
>
>> >The inability for any known naturalistic process to
>> >produce a given phenomenon is itself evidence of intelligent design.
>>
>> You've found out how to prove a negative? Have you alerted the
>> philosophers and logitians yet? Do they give a Nobel for philosophy?
>
>No one every fully proves a negative. However, a negative can still
>be believed in and scientifically supported based on the preponderance
>of the evidence. Statistical negatives can be quite significant and
>reasonable indeed although never fully provable.
But this is an *extraordinary* claim. You are positing something you
cannot even *begin* to describe, much less explain, that nonetheless you
insist has a pervasive, even universal, unseen effect, operating by unknown
mechanisms and which is contrary to every other explanation we've
discovered through science, *all* of which have been naturalistic.
Extraordinary claims must have extraordinary evidence. You, on the
contrary, have *zero* evidence, other than pointing the empty sleeve of "we
don't know how to do it now".
>
>> >> J. Pieret
>> >>
>> >> The devil is in the details.
>> >> Science explains them.
>> >> Intelligent design explains them away.
>> >>
>> >> - Mark VandeWettering -
>> >
>> >Science or the scientific method certainly is a very powerful tool for
>> >the searching out of truth concerning the external world. In fact,
>> >there is no other method that I know of that can do as good a job as
>> >the scientific method. However, the scientific method does not
>> >pre-suppose only naturalistic causes as explanations for phenomena
>> >that occur in the external world. The a priori assumption of
>> >naturalistic causes is not in fact a scientific assumption. In fact,
>> >by using the scientific method, it is very reasonable to conclude that
>> >intelligent design was involved with the existence of many phenomena.
>> >The theory of ID can in fact be scientifically supported in many many
>> >undisputable cases and situations. Forensic science, for example, is
>> >based on this fact.
>>
>> So humans murderers aren't "naturalistic"?
>
>No. Humans are not "naturalistic" in that humans have minds that are
>intelligent.
Don't forget the bees!
Actually, humans are "naturalistic" in the same way a bee or an amoeba is.
We can know the full panoply of the abilities and limitations of humans
(unlike the case of your unknown designer) to a high degree of certainty.
While we cannot predict the exact actions of any individual human, neither
can we predict the actions of any individual amoeba. Unlike your designer,
we can predict with more-than-adequate precision the methods, means and
even motives of humans and empirically study them in depth.
>The processes of a mindless nature have no purpose or
>deliberate intelligence. Such mindless purposeless processes are
>supposed to have given rise to life as well as all the various life
>forms that we see around us. The current theory of evolution does not
>allow any intelligent processes to be involved. Any time human
>tampering is involved in the "change" of genes, this is not
>"evolution" because it is not "naturalistic" change. You do
>understand this point I hope because it is vital to my argument.
Yes, you are setting up your defense for when (and I think "when" is the
operative word here) science does demonstrate abiogenesis.
>
>> >So, to suggest that the origin of life must, by
>> >"a priori" definition, have a naturalistic cause . . . is really
>> >scientific heresy. Mark VandeWettering is obviously clueless, a
>> >devoted disciple of the religion of naturalism. If I were to propose
>> >ID as an explanation of the origin of the wristwatch on my arm, would
>> >that be "explain it away"? or would it be a scientific explanation of
>> >the evidence?
>>
>> No, the proposal of an *unknown* and *undescribable* manufacturer whose
>> methods and means of building watches is *unknown* and (apparently)
>> *unknowable* (since no one has proposed any way of investigating the ID
>> "designer") is *not* a scientific explanation, anymore than proposing to an
>> ME that a ghost killed someone is. And yes, saying god created your watch
>> *would* be explaining it away.
>
>No, it wouldn't. You need not know the identity of a designer at all
>to reasonable know that intelligent design was involved in its
>formation. No one need propose that the Christian God created life,
>or my wristwatch to know that SOMEONE with an intelligent mind did
>create both life and my wristwatch. I need not know who, exactly, did
>it to know that some mindful intelligence was in fact involved in its
>formation.
Where have I heard this before? Oh yes, this is the nth time you've said
this. It is also the nth time you've failed to provide evidence.
>To require direct knowledge of the actual identity of the
>designer before one might be able to propose design is a ridiculous
>argument. I have no idea why it is such a common argument. How on
>earth can the SETI scientists be looking for signs of intelligent life
>in outer space if they don't know the identity of the origin of these
>signs of intelligence when they find them?
Because we are looking for aliens who would do what *humans* do. Ones who
would use technology just like ours to send electrical/magnetic signals
into space just like we do. Any *other* intelligent alien, not using that
technology for that purpose, will be invisible to SETI. It is *just* like
looking for an unknown murderer. We know what type of being, with a
specific set of abilities and limitations, even if we don't know the exact
individual. If that murderer happens to be a ghost, we'll never catch him.
>
>> >But really, they are only helping to
>> >delude you into thinking that you are being rational when you are
>> >actually contradicting yourself. The devil really is in the details
>> >and science does search them out, but science does NOT always come up
>> >with a naturalistic explanation as the most reasonable explanation.
I see you made an unmarked snip of your ad hominem against me.
Too bad you couldn't have done as much for the one you made against Mark
VandeWettering.
>>
>> Ah, "reasonable" . . . as in the one you *prefer*, even if you don't have
>> evidence for it.
>
>The evidence is clear. It seems that your own preferences might be
>blinding you to the correct meaning of the evidence, but bias is a
>problem for everyone to one degree or another.
So everyone who disagrees with you is biased? Does it even *occur* to you
that it *could* be the other way around?
>
>> >To say that this must be the case is to be either misinformed or
>> >deliberately insane.
>>
>> Damn, funny how many insane people keep getting those research grants,
>> Nobel prizes in science and all the rest, isn't it? . . .
>
>Isn't it though ; ) But, this is an argument based on the authority
>and supposed understanding of others, not on your own ability to know,
>understand or explain the evidence.
Nonsense! All I was doing is pointing out one of those statistical facts
you cited with approval above. The *vast* majority of scientists find it
perfectly possible to do perfectly good science without once positing "non
naturalistic" forces or agents. For you to indiscriminately call *all* of
them "insane" cannot help but raise issues of *your* bias, at the very
least, if not bring up images of the kooks who insist that only *they* have
the real scientific truth [TM], hidden right underneath their tin foil
hats.
>You are basically saying, "How
>can so many brilliant scientists be wrong and you, an ignorant nobody,
>even hope to have any concept of what might be going on?" This is a
>lame authority-based argument that really has no explanatory value.
Oh, well, in for a penny . . .
"A man does not attain the status of Galileo
merely because he is persecuted;
he must also be right."
--Stephen Jay Gould
>
>> >Sean
>>
>> And if you like that last sig, you'll *love* this one!
>>
>> ---------------
>> J. Pieret
>> ---------------
>>
>> SETI is based on the simple assumption that nature
>> operates elsewhere the same way it does here.
>> ID is based on the assumption
>> that nature doesn't even work here.
>>
>> - Bobby Bryant -
>
>SETI is based on the ability for scientists to detect ID. SETI is all
>about ID. There is no separation of the terms. Both SETI and ID are
>based on the assumption that purposeful mindful intelligence works
>elsewhere as it works here and that mindless natural processes also
>work elsewhere as they work here. Bobby Bryant seems not to
>understand either ID or SETI. The fact is, nature does not work here
>in the way that modern science is proposing that it does work.
>Evolutionary scientists say that a mindless nature works on this earth
>in a way in which they have no evidence to show how this work actually
>happens. ID works on this earth in a way that can at least approach
>an explanation for life while no known naturalistic process even comes
>close.
No it isn't. Yes he does. You haven't demonstrated that in any way,
merely asserted it. They have lots of evidence that no amount of
handwaving will make go away. You've given no explanation of how life
*works*. And I'm tired of chasing after you as you run around as fast as
you can, hoping no one will see that you are going nowhere. Your argument,
no matter how many times you repeat it, all boils down to this: "if you
can't demonstrate I'm wrong, it must have been goddidit".
>
>Sean
---------------
J. Pieret
---------------
The political motivation behind the Wedge Strategy:
"Religion is the opiate of the masses . . .
and that is a _good_ thing."
-- Bobby Bryant --
Hiero5ant
"catshark" <cats...@yahoo.com> wrote in message
news:s4mocv86n07qemcav...@4ax.com...
> On Wed, 21 May 2003 20:18:09 +0000 (UTC),
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
<snip>
Don't forget
http://www.talkorigins.org/origins/postmonth/apr01.html
<snip remainder>
Mark Isaak
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote, among
other things:
>Many argue that just because no one has seen anyone design life or
>living systems that no intelligent designer can be reasonably
>hypothesized. However, if there is no naturalistic explanation or
>mechanism to explain the existence of life, then it is in fact quite
>reasonable to hypothesize an intelligent designer of life on this
>planet.
That's a logical fallacy. It is the same as saying, "We have natural
explanations for most UFO's, but not for all of them (because not all
have been studied to the same degree). Therefore it is quite
reasonable to hypothesize an intelligent designer for the unexplained
UFOs."
>DNA is nothing outside of the coded information that it contains.
But RNA certainly is. And since most abiogenesis proposals have RNA
preceding DNA, DNA is irrelevant to the origin of life.
>Obviously, these paragraphs, no
>matter the source of their subsequent production, where obviously
>purposefully designed. This quality of purposeful design can also be
>detected by the scientific method.
Yes, science can and does detect design all the time. Please explain,
then, why we should say life is designed when life looks undesigned.
>You see then, you assume intelligent design as the
>most likely cause when no known naturalistic process could have
>produced a given phenomenon; especially when this phenomenon resembles
>other designed creations while, at the same time, not resembling any
>known creations produced by purely mindless naturalistic processes.
Completely false. I assume intelligent design as the most likely
cause when the results look like the effects of intelligent design I
have seen in the past. That's why I say life is not designed. It
doesn't look designed.
Incidentally, I have observed phenomena which no known naturalistic
process produces, which resemble other designed creations at least as
much as DNA does, and which do not resemble any known creations
produced by purely mindless naturalistic processes. I concluded they
were entirely natural, and I stand by that conclusion. Concluding
design would have been insanity.
>It seems to me that you are mistaken. There are only two known
>explanations for any given phenomenon. Either its origin or cause was
>designed with the use of a mindful intelligence or it was not designed
>and arose via a mindless naturalistic process. There is no other
>option.
Other options: it could have arisen via a mindless supernatural
process. Or a mindful intelligence could have created it entirely by
accident. Or it could have arisen from a combination of processes.
And don't forget, the mind itself could have arise via a mindless
naturalistic process. And probably did.
>No. Humans are not "naturalistic" in that humans have minds that are
>intelligent.
So do ants. Are ants not part of nature?
>SETI is based on the ability for scientists to detect ID. SETI is all
>about ID. There is no separation of the terms. Both SETI and ID are
>based on the assumption that purposeful mindful intelligence works
>elsewhere as it works here and that mindless natural processes also
>work elsewhere as they work here.
In other words, ID demands that God be naturalistic. Or at least as
naturalistic as ants.
--
Mark Isaak at...@earthlink.net
Don't read everything you belive.
Ron Okimoto
To improve your impression all you have to do is take the best piece
of evidence for your alternative and compare it to the evidence that
we have that tells us something else. All you have to acknowledge is
that the evidence for the scientific explanation is so much better
than anything that you have that your position is laughable. You can
poke at bits like the Neandertal data, but you can't ignore the vast
majority of molecular data that says that the Neandertal example
amounts to nothing by comparison. The only reason that you are
unimpressed is that you are willfully ignorant of the data. As long
as you don't know how bad your arguments are, you consider that a
plus.
If you were really interested in what the best arguments are you need
to start reading some science texts instead of the creationist
propaganda rags that you immerse yourself in. You know for a fact
that you can't trust creationist material, but that is all that we see
out of you. How is that learning anything about the issue except it
tells you how bad the creationist arguments are. Present the honest
creationist argument that you claim exists somewhere. Who are these
honest creationists and what is the evidence for their beliefs of what
we see in nature. I've requested this several times because you keep
telling us that these people exist and that they have valid arguments,
but we never see any names or any valid arguments.
Ron Okimoto
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
Following up myself to correct some errors
On Wed, 21 May 2003 14:30:06 +0000 (UTC), "Ian Musgrave & Peta
O'Donohue" <reynella_R...@werple.mira.net.au> wrote:
[snip]
>Even in a case where it looks like 9 substitutions are required to
>convert melamine deaminase to the functionally quite different
>atrazine dehalogenase (a synthetic halogenated triazine herbicide not
>found in nature), this occured in the wild in under 40 years (however,
>all these gene substitutions look selective rather than neutral).
It was 30 years (atrazine was introduced in the '60s, and the first
mutants found in '91), and the key mutation is Asp328 which determins
dehalogenation, the other 8 are fine tuning.
[snip]
>And complex functions are usually carried out by bunches of simple
>enzymes, or a large protein that is a fusion of a bunch of small
>enzymes (like the AABB casette ATPases, which are basically a fusion
>of a number of small duplicated proteins,
Blast, that's AAA casette ATPase. For a nice discussion of this, which
is directly relevant to ID issues see
Beware of line wrap, some assebly may be required.
Cheers! Ian
Sean Pitman
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03052...@posting.google.com>...
> > roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.0305...@posting.google.com>...
> It looks like I quit too soon. I do screw up later on so I have to
> continue.
Welcome back . . .
> The Hemoglobin citation is on page 63 of the 1981 version of Stryer
> second edition Biochemistry. I too Biochem in 78-79 and I don't
> remember the phrase "nine positions are nearly invariant." There is a
> table with the nine amino acid residues, so I don't know why I
> remember it as a lower number of invariant amino acids. It could be a
> change between the first edition and the second, or I could just be
> misremembering.
It probably was a misread, although I do not have that addition of
Stryer readily available to me. The reason why I think this is that
when considering the heme pocket region alone as only part of the
hemoglobin molecule (adult human hemoglobin of course consists of 2
alpha sub-units of 141 residues each and 2 beta sub-units of 146
residues each), there are around "43 amino acids" that are "invariant
in 60 species". The stated reason for this is that "Mutations in
these regions interfere with normal cooperative O2 binding." Other
references go as low as "48 residues" as invariant, but none of them
go as low as "nine positions are nearly invariant" as you suggest.
Cytochrome C also seems to have a fair percentage of invariant amino
acids in its structure. Out of the usual 104 amino acids that make up
cytochrome c humans differ from bread mold by only 44 amino acids.
Even so, even with these differences, the various cytochrome c
sequences are basically the same, having essentially the "same 3D
topology." Furthermore, in vitro studies have shown that the
cytochrome c sequences from any species can integrate themselves
correctly with the other elements of the oxidation processes of all
other creatures using cytochrome c. In other words, all the varieties
are interchangeable because they are basically identical in 3D
structure and function. In order to maintain this specificity, other
studies that compared sequences of 40 species have shown that at least
"35 of the 104 amino acids are invariant." "Furthermore, at another
40 sites, only 2 or 3 amino acids occur, and at each of those sites,
the pairs of triplets are always very similar in chemical
character-i.e., they are either hydrophilic, hydrophobic, or neutral
with respect to water. At only a very few sites can radically
different amino acids occur. Why might this be? Presumably,
mutations occur at all sites. However, changes at some sites
presumably destroy the function of the molecule, whereas at other
sites, some change is tolerable, and at a few sites, major changes
don't seem to be of much consequence. Subsequent detailed studies of
molecular structure confirmed these premises. Many of the invariant
sites are critical in causing the molecule to fold itself
properly--changes at these sites would completely disrupt the
molecule's function."
So you see Ron, by in large, many if not most proteins are quite
specific molecules. It is quite amazing that 30% or 40% of a given
protein cannot change to any other amino acid at all. Then, consider
that yet another 30 or 40% can only change between a group of 2 or 3
amino acids out of the 20 available. These proteins are starting to
get quite rigid indeed. In fact, there are only a very "few" protein
positions that actually have any sort of freedom to change among just
any of the 20 amino acids. This is in fact very similar to the
workings of the human language system. Take a given sentence such as,
"Methinks it is like a weasel." Several of the letters could be
changed and one would still be able to make out what it was saying.
For example, I could change the sentence to read, "Methinkz it is like
a weasel." Obviously this is a misspelling, but the function of the
sentence is not destroyed. However, if I were to change a different
letter like, "Methinks it is like a teasel", the entire meaning of the
sentence has dramatically changed. The very same thing happens with
proteins. Many of the amino acids can be changed, but these changes
are generally quite limited and rigid in nature. This means that
there are far fewer functional options to pick from when one
approaches a random pile of proteins of a given length (at least from
the perspective of a given life form in a given environment).
http://www.botany.ubc.ca/biol201/p3201.htm
http://sc1.cc.kochi-u.ac.jp/~iwaim/publication/Suzuki%20et%20al.,%202000.pdf
http://www.nslc.wustl.edu/courses/Bio3501/2002/oct14.pdf
< snip >
> > > They are likely small for any one sequence, but there are a lot of
> > > sequences and a lot of possible functions, and when you change a
> > > sequence you change its functional potential. You can't just look at
> > > the potential functions of any single extant proteins, but you have to
> > > look at the potential function of all the molecules that you can get
> > > by changing just 1 to 3 amino acid positions. You know that this is
> > > possible. If you make one or two changes you can significantly change
> > > the landscape for any function, can't you?
> >
> > Yes, but you do not seem to understand the problem. You are thinking
> > that there are so many potential beneficial functions out there that
> > just about any change in bound to evolve at least one of them.
>
> No, what we see is that for anything that we can think up a selection
> for we can get that activity randomly changing the sequence of the
> variable region of the antibody.
Actually not. There are many functions that you could think up that
you could not get by randomly changing the sequences of the variable
regions of antibodies. The functions that are obtained in this manner
are universally simple enzymatic type functions that require a
relatively short amino acid sequence contained in a single protein.
And, even this sort of relatively simple "evolution" is still quite
difficult for many types of life forms. Hall's experiment
demonstrates this difficulty nicely. The lactase function is a
relatively simple enzymatic type function. In all likelihood, one
would expect that there would be a relatively larger percentage of the
total number of possible amino acid sequences out there that for other
more complex functions. Perhaps one out of every trillion amino acid
sequences of 1000aa or less would have at least some lactase function?
Given this relative abundance of potential lactase enzymes, it seems
quite strange then that certain of Hall's E. coli bacteria would have
much problem evolving at least one of these sequences. Perhaps the
lactase function is more complicated and requires more specificity
than one in a trillion 1000aa proteins? Perhaps the ratio is more
like 1 in a trillion trillion? Or, perhaps the E. coli just do not
have enough free genetic real estate to undergo random walk? Gene
duplication also has its limits as an adequate explanation for several
reasons. One reason is that the maintenance of non-functional DNA or
extra DNA that does not give an immediate selective advantage, is
expensive. It costs energy to maintain non-functional DNA. This is
actually a selective disadvantage. Nature would select to get rid of
it far before it would be able to drift along and arrive at any
significantly new and beneficial function. Besides this problem,
there are other problems that I have detailed earlier for you.
> > The
> > problem is that even though there are a lot of potential functions out
> > there as far as an absolute number goes, this number is very tiny
> > indeed when compared to the total number of potential sequences out
> > there. For example, there may be a billion potential lactase enzymes
> > out there of 4,000aa or less (The approximate length of the lacZ and
> > ebg lactase enzymes). Is a billion a large number? Well, yes it is
> > until one compares it with a 1 with 5,200 zeros after it (the total
> > number of potential proteins of this length). So you see, the "large"
> > number of potential functional sequences is really an illusion of
> > bigness. Such "big" numbers are really small in comparison to the
> > bigness of the total number of possibilities. In other words, no
> > matter which direction that a sequence "drifts" in its random walk, it
> > is unlikely that it will come across any other beneficial function,
> > from the perspective of a given organism, in short order. And, this
> > problem becomes more and more significant with increasing functional
> > complexity . . . especially when we start talking functions that
> > require multiple proteins all working together at the same time . . .
> > like in bacterial motility etc.
>
> Like I said before 10^12 is such a minute fraction of the possible
> sequences that there is something wrong with your evaluation of the
> system.
I doubt it. 10e12 are the number of selective tests involved, but the
field to choose from for each test involves millions of not billions
or trillions of amino acid sequences. Still, compared to 10e5,200
this is still quite a tiny fraction of the total possible sequences.
However, you seem not to understand my suggestion that the lactase
function, as well as many other such single protein enzymatic type
functions, is most likely a relatively simple function that may have a
relatively high fraction of the total number of sequences with at
least some lactase activity. It is like a 3-letter word in the
English language system. It is relatively simple. Perhaps the
fraction of the total pile of 10e5,200 sequences with at least some
lactase function is on the order of one in a trillion or even a
trillion trillion trillion. Relatively speaking, these would be
pretty high percentage ratios. However, even with such high ratios,
it might still be pretty hard for even a sizable bacterial colony to
come up with even one of these sequences, given the limited genetic
real estate available to this colony for random walk through the
"trillion trillion" or so non-functional sequences for this level of
function. This problem only gets worse as the complexity of the
situation increases. With more complex functions requiring longer and
still longer sequences, or even multiple sequences, the average length
of the random walk increases as an exponential rate.
There are of course those like Ian Musgrave who suggest that
increasing complexity is not an issue because it only requires the
addition of small functional sequences onto previously functional
sequences. He uses the example of adding cat to hat to bat to get
something like, "cat hat bat." What Ian forgets is that the order and
integration of even separate protein sequences is important. Really
now, what does "cat hat bat" mean? Each of the words by themselves
does in fact have a recognizable function, but the order in which they
are put together is also important for a collective "higher" or more
"complex" word function. Not just any order will do. Just as not any
order of amino acids will make a functional protein, so, not just any
order of individual proteins will make a higher collective function
either. The same problems apply. Certainly, there are certain
functions that work very much like cascading systems, where the
function as a whole is not irreducibly complex. Take one part away,
and the rest of the cascade will continue to function just fine . . .
like a series of dominos. However, many functions in living systems
are not like cascades. Behe describes many of these. A flagellum is
a great example. All of the 60 or so parts in a flagellum are needed
to be in the right place at the right time all working together at the
same time (not in a series like a cascade), in order for the
collective function of motility to be realized. Take any one part
away, and the function of motility will not be there at all, not even
a little bit. There are those, such as Ian, who suggest that the
various parts in the flagellum do in fact have other functional jobs
within the cell, but how do these other jobs help with the collective
evolution of bacterial motility? For example, the individual words,
"cat and hat and bat" each have an independent function within the
English language system, but that doesn't make them any closer to a
collective function when put together. You see, the non-organized
dumping of a bunch of individually functional parts into the same area
will not make them self assemble to form a more complex collective
function the same as dumping a bunch of fully formed amino acids into
a vat is not going to mean that they will self assemble into anything
functional at all.
> Explain how function is obtained in so few trials if you are even
> close to being correct in your inferences. This isn't some fluke, but
> is done routinely. Do a PubMed search on Abzymes.
And not surprising in the least as I have tried to explain over and
over again. . .
I can do it in less time with the English language. For example,
there are only 17,576 possible 3-letter words in the English language.
Of these potential sequences, a relatively large percentage have
actually been defined by the English language system as having some
function within the language system. All I would have to do is to
fill a bag will all the potential 3-letter sequences and then stick my
hand into this bag pulling out random sequences until I came across
one that was defined by the English language system as having
function. It might take me a few tries, but I would quickly pull out
a defined sequence. Then, lets say that I was to pull out a sequence
with a specific function, such as a word that has the meaning of an
animal. Well, there are fewer words with such specificity, but there
are at least more than one or two. For example, the words cat or dog
or pig would all work. Of course, it would take me a lot longer to
find one of these words, but it could still be done in relatively
short order. However, lets say that the desired function was a
meaningful sentence of at least five three letter words or less. Now,
I am sure that there are literally thousands of such sentences out
there, but when compared to the total number of possible sentences,
the ratio is far less than 1 in 17,000. The time involved to get any
one of these more complex sentences at random quickly shoots up in an
exponential fashion. For example, consider the 5-word sentence, "You
are a fat cat." The idea or function contained by this sequence
cannot be easily reduced. It requires a longer sequence than just
3-letters to communicate this idea or function. It is made up of 5
words that are each 3-letters or less in size. However, collectively,
these five words make up a much more complex sentence that is 17
characters (including spaces) long. There are far far fewer 17
character sentences out there that make any sense at all compared to
the total number of 17-character sentences (
2,153,693,963,075,557,766,310,747 or ~ 2 trillion trillion) that make
any sense whatsoever in the English language system. This means that
the gap between meaningful 19-character sequences is much wider than
the gap that exists between meaningful 3-letter sequences. The same
problem holds true for more and more complex functions in the genetics
of living things.
> > Dawkins tried to do it, somewhat, with his "Methinks it is like a
> > weasel" computer evolution experiment. However, where Dawkins went
> > wrong is that each of his generations of phrase evolution were
> > meaningless. He selected phrases of gibberish that were closer in
> > *spelling* but not in *meaning* to "Methinks it is like a weasel."
> > You do see the problem here don't you? There are a lot more
> > meaningless sequences of 28 characters in length than there are
> > meaningful sequences of this length. This poses a problem, as it did
> > for Dawkin's experiment, in that there simply is no path of function
> > from one sentence of this length to very many other meaningful
> > sentences, although there may in fact be millions of them, of similar
> > lengths. This same problem exists in genetic evolution experiments.
> > Natural selection is simply powerless without a change in function
> > with each change in genetic spelling.
>
> Um, it was an analogy and it is only used as something to get you to
> understand the power of selection. You do understand that don't you?
> It has limited biological relevance.
Actually, it is much more than a simple analogy. . . even for
Dawkins. Many brilliant people have taken this analogy quite
literally and have been convinced by it as explaining how evolution is
supposed to work. And, in fact, this really is the closest that
anyone has ever come at trying to explain how evolution is suppose to
work. However, the fatal flaw with this analogy is there although not
always clear to many people. Those who proposed the "million monkeys
typing away for millions of years to produce all the works of
Shakespeare" made a very similar mistake in their reasoning. The
problem with the typing monkeys is the same problem with Dawkins
weasel algorithm. It is a problem neutral gaps. There is no
selection if there is no corresponding change in function with each
change in symbolic code. Neutral gaps destroy the power of the
selector or the "head monkey". Without the power of a selection
mechanism, naturalistic Darwinian-style evolution is clearly in
trouble if not completely destroyed.
> > > Explain the antibody results if you are correct. Why is the
> > > impossible, possible for antibodies? Why do you only have to score
> > > 10^12 events before you find the activity that you select for?
> >
> > Because, as I have explained multiple times already, the activity that
> > was "selected for" was a relatively simple enzymatic type activity.
> > It is like throwing all the possible 3-letter sequences for English
> > words into a bag and asking me to pick out one of them that has a
> > particular function. It might take a while, but not very long
> > comparatively speaking because I am basically looking for a short
> > sequences with a simple function that has relatively high odds of
> > success.
>
> Lactase is pretty simple. So you have given up on the bogus use of
> the Halls work.
Not at all. Hall's experiments are very relevant because his
experiments show that even relatively "simple" functions such as the
enzymatic functions of various single, relatively short, proteins . .
. are still often quite difficult to evolve. If such a simple
function takes millions of generations to evolve, how many generations
might be needed to evolve something with a bit more complexity?
> > > By the
> > > early 1990's they had already produced over 70 different enzymatic
> > > activities using antibodies. I think that they have their own name,
> > > now, and they are called abzymes. If you do a PubMed search you will
> > > likely find references to a whole lot more enzymatic activities by
> > > now.
> >
> > Certainly true, and not suprising in the least. This is only to be
> > expected as many enzymatic activities are relatively simple protein
> > functions.
>
> This is pretty tragic. What have you spent months arguing?
Honestly, I don't know how to be any clearer. If you don't get my
position at this point perhaps you never will. . .
> > > > But, there is something hopeful about your hypothetical suggestion.
> > > > The very fact that you proposed such a hypothetical solution to the
> > > > problem means that you might actually recognize the problem, which is
> > > > a significant step. In any case, I remain most interested in your
> > > > thoughts and struggles with this issue.
> > >
> > > It is not an explanation for a problem, but for what we observe
> > > occuring in nature.
> >
> > You only observe this in nature as it relates to relatively simple
> > functions that are only very short neutral distances from what is
> > already there. The problem, as detailed over and over again above, is
> > far greater than this.
>
> That is what we were talking about for lactase function, weren't we?
Again, the lactase function is dependent upon relatively short
sequences contained in a single protein. The ratio of such potential
lactase sequences to the total number of possible sequences is most
likely relatively high. This is not the case as one move up the
ladder of function complexity.
> > > That is what is wrong with
> > > your argument. Our only problem seems to be trying to explain why it
> > > seems to be so easy to get function from a protein sequence.
> >
> > No . . . the problem is that with the increasing complexity of protein
> > function comes a vast increase in the average neutral gap that must be
> > crossed. Simple functions have smaller gaps. More complex functions
> > have larger gaps. That is the problem. How does a given life form
> > evolve such functions of higher complexity?
>
> Demonstrate that this is true. You have to first demonstrate that the
> gaps exist. This is just assertion without evidence. Take a complex
> system and show us where the gaps are and how you determined that
> these gaps exist.
If the gaps exist, and they do, with such simple functions as the
lactase function, then obviously as the functions become more and more
complex, the gaps must increase in size. It is ludicrous to think or
suggest that the gaps would remain the same size or get smaller!
Hall's experiments proved that there are in fact gaps between even
such relatively simple enzymatic-type functions and the current
genetic real estate of a large population of bacteria observed over
the course of many thousands of generations.
> > > A better
> > > argument for you and one that the ID people use is that since we don't
> > > have a good explanation for how we evolve these functions that some
> > > designer must be responsible for guiding these mutations and making
> > > the results happen.
> >
> > Uh . . . that is my argument.
>
> No, because we see it happening in nature. If you want to claim
> divine intervention, demonstrate that it is happening in the systems
> that these researchers are studying. Your argument is that it
> happened in the past because we obviously do not have any evidence
> that it is happening now.
Yes, my argument is that some sort of intelligent designer was in fact
involved in the origin of various life forms sometime in the past. I
also agree that I do not see evidence of the activity of intelligent
design, outside of human intelligence, acting to change life forms at
the present time. Also, I am not arguing for "divine" intervention
here, but for the actions of some sort of intelligent involvement from
someone in the origin of various life forms . . . not necessarily the
Christian God, although He may very well have been involved. Again,
the evidence for the position can be found both in lack of any
naturalistic explanation of the neutral gaps between various functions
that do in fact exist, and the close similarity of genetics and
genetic codes to other designed coded systems, such as human language
systems and computer codes.
> > > The problem with the ID argument is that it is
> > > stupid. Just try and find some evidence to support it.
> >
> > LOL - Ok . . . it is very easy to say that something is "stupid"
> > without giving any reasonable explanation as to why it is "stupid."
> > You are just spouting off without any basis for support of your
> > position whatsoever. I have been giving you the "evidence" to support
> > this ID argument all along. You seem to vaguely understand the
> > arguments, but you are so stuck in your rut of "naturalism explains
> > everything" that you are too blind to admit that there just might be
> > something to ID.
>
> You are just laughing at ID and yourself. Where is this evidence? It
> is the same stupid bull that the ID people are spouting, but if it
> were real evidence they would have published by now and they would
> have had something to teach in Ohio. What was the reason that they
> could not present a single thing about ID that they could support
> teaching if they had real evidence backing up their assertions? They
> were asked what they could teach about ID and the answer was nothing.
Not so. There is plenty to teach about ID, such as everything I have
been discussing here. Of course, there are many people who believe in
ID without really knowing why or how to defend their position. The
discussions in Kansas and Ohio have not been the best. Of course,
these school boards are up against a huge amount of naturalistic bias
which is in fact a religious position based on the philosophy of
naturalism. The evidence truly is in favor of ID, but the religion of
naturalism is so deeply rooted that it is very difficult to get anyone
to even consider any other alternative to naturalistic explanations,
especially when the topic in question is the origin of life.
Darwinism has been come like a sacred dogma, a church of popular
scientific culture if you will. It is a belief system the interprets
the evidence in its own favor, often by putting spins on the evidence
that are not warranted or even reasonable . . . just as many religious
fundamentalists do to protect their own religious faiths. The
evidence for the origin of life is there for everyone to study for
themselves and come to their own conclusions. . . and there really is
a very reasonable way to interpret it other than to invoke the power
of naturalism. You just don't like that.
> Verify this evidence. What good is it if you can't verify that it
> means anything?
You know Ron, I have been "verifying" the evidence all along here.
This is what we are talking about in this thread . . . the evidence
for ID. Part of that evidence comes in the form of neutral gaps. You
seem to recognize this or you would not be arguing so ardently that
these gaps do not exist. You seem to realize, deep down, that these
gaps, if you were to admit that they actually do exist, would present
significant evidence that would in fact destroy your position. Your
attempts to dismiss the evidence that I have presented thus far have
been feeble indeed, almost laughable. You do on occasion present some
very interesting points, but by in large, you seem to blow a lot more
hot air than anything else. You are just a big blustering wind trying
to find any scrap of nonsense to save your cherished religion.
> The ID people know this or they would have presented
> some of it as teachable. Isn't it stupid to claim that you have a
> viable argument when you know that it isn't viable, and you can't put
> it forward as being presentable without looking like a fool or being
> shown to be a liar?
LOL - What a lot of nonsense! Do you know how ridiculous this sounds?
ID is not based on wishful thinking, but on the evidence that is
really overwhelming. It seems incredible to me that you can actually
make statements like this and be serious. You and many other
scientists teach that humans and other life forms evolved from
bacteria without even being able to present a decent mechanism as to
how this might have been possible. And yet, this theory is presented
in all seriousness. What a crock.
> What is your explanation for ID's failure to present anything
> teachable in Ohio? Where was all this great evidence? The Discovery
> Institute Reps were there and there were supposedly University Profs
> on the side of teaching ID, so why didn't a single one of them come
> forward with something to teach when it was requested of them? The ID
> proponents know their limits or one of them would have been stupid
> enough to put something forward. This tells you something about ID
> proponents, but it isn't something good.
This is a ridiculous argument. Besides, we are not talking about
other ID supporters here, but about my ideas of ID. I have put many
"evidences" forward in this thread in support or to explain ID that is
"teachable." You are talking to me here, not some people in Ohio. If
I were there I would certainly have been able to argue in favor of ID.
Not a problem. You would no doubt disagree, but that is simply your
opinion, as misguided as I think it is.
< snip >
> > Yes, Hall did use the proper system to identify the mutants. You
> > simply do not seem to understand the experiment . . . probably because
> > you haven't read anything more than the abstracts. (As discussed
> > above)
>
> As I have discussed above Hall's system is not the system you can
> select for multiple mutations in because it is a single step
> selection. Can you get three mutations in 5 or 6 generations starting
> from a single bacterium? If you are lucky you might see one mutation
> if you plate enough bacteria.
You are wrong again. Please, read the paper. You have been wrong so
many times on this point that I don't know why you keep at it. You
initially said that Hall's experiments were based on "lethal"
selection. Of course, you were wrong. You are wrong again here.
Hall's system can in fact select for multiple mutations if they were
to ever occur in a way that produced a beneficial function in the
environment used by Hall for selection (i.e., lactose in this case).
In fact, Hall has isolated a double mutant using his selection media.
Also, Hall has selected for multiple mutations of 5 or 6 where each
individual mutation was beneficially functional. Again, any time the
lactase function evolves in Hall's set up, Hall would be able to
detect it, even after many generations.
> > > Just tell us one thing, if you are right about how difficult it is to evolve
> > > function in a protein would antibodies be able to evolve the novel enzyme
> > > functions in less than 10^12 trials? Yes or no.
> >
> > Again, it depends on the complexity of the function in question.
> > Simple functions would be easier to evolve since the gaps between
> > simple functions would obviously be smaller than gaps between more
> > complex functions. Abzymes are in fact relatively simple functions
> > that generally require one protein sequences of a relatively small
> > length. So yes, such functions would not be surprising to see
> > evolving in various life forms (also discussed above).
>
> If you look at the sequences of Abzymes you see that they are spread
> quite a distance around the molecule and not just in a short sequence.
>
> You still do not get how this makes your Hall argument irrelevant.
> Lactase is a simple enzymatic function.
Uh. . . yes. Lactase is a relatively simple enzymatic function. And
yet, Hall showed that E. coli have a tough time evolving even this
admittedly simple function given their available genetic real estate,
huge populations, and thousands of generations. That makes Hall's
experiments very relevant.
> > > You can claim anything else about these results that you want, but the plain
> > > fact is that these results demonstrate that your reservations are bogus.
> >
> > LOL - Actually, the results of these experiments only support my
> > position. They in no way counteract my reservations in the least.
>
> Demonstrate that this is true. You admit that it is trivial to evolve
> new functions, but for some reason your Hall argument is still
> relevant. Explain the relevance.
Can you demonstrate that it is not true? I don't think so. At least
you haven't done a very good job yet.
In any case, again and again I have explained this point and you are
still clueless. Hall's experiment is relevant because it shows that
even relatively small gaps between certain relatively simple enzymatic
type functions, such as the lactase function, do in fact place
significant road blocks in the path of evolution. If simple functions
are difficult to evolve because of the existence of relatively small
gaps in function, try imagining how the evolution of vastly more
complex function might proceed in a reasonable amount of time. . .
get it?
> > > Let's
> > > see you admit that simple fact. How many trials would it take to create new
> > > function if you were right? Why does it only take less than 10^12?
> >
> > It depends on the level of complexity involved with the function? How
> > many amino acids, at minimum, would be required? How many sequences
> > of a given length would have this particular function? What is the
> > ratio of potentially functional sequences as compared to the total
> > number of potential sequences? You see, the evolution of some simple
> > enzymatic type function really isn't the issue here. Such
> > demonstratable evolution is not the salvation of the theory of common
> > descent of all life forms. Hopefully you can begin to recognize this
> > problem, but I am beginning to have my doubts. Your logical abilities
> > seem to be quite blinded by your naturalistic philosophy.
>
> We don't care, all we care about is that it is possible. You have
> been claiming that it is highly improbable or impossible, but now it
> is trivial and you can still claim that your argument still stands.
> How can a 180 degree reversal support your original argument?
There was no 180-degree reversal. I never ever said that the
evolution of simple enzymatic type functions were "impossible." I
only said that with increasing neutral gaps in function come
exponentially increasing average times to make the crossing. Nothing
is "impossible", but many things are extremely unlikely, to the point
of impossibility as the ladder of increasing complexity is climbed.
You think that you have proven evolution when you get one little
simple function to evolve. You haven't proven anything. The neutral
gaps involved in your examples are nothing compared to the neutral
gaps involved with more and more complex functions. It is like those
scientists who found that they could produce a few organic
molecules/amino acids with a few chemicals and some electricity. What
they did was barely touch the tip of the iceberg. The real problems
come when the one start to try to climb above the first or second rung
of the ladder of complexity.
> > > You also can't seem to get it through your misperceptions that there is no
> > > goal.
> >
> > Yes, there is a "goal" for evolution. You are clearly mistaken here.
> > The goal of genetic evolution is the goal of new beneficial functions,
> > whatever they may be. That is the goal. The goal is NOT the
> > evolution of just any random set of genetic sequences. Evolution must
> > evolve functional sequences that are actually beneficial at the same
> > time. This means that there is some specificity to evolution. And,
> > this creates a problem for evolution which gets larger and larger to
> > the point of impossibility as the level of functions increases.
>
> There is no goal that we can observe. Things just happen. If you can
> see some goal for the random mutations that create abzymes you could
> become famous.
This is nonsense. Evolution proposes to explain the diversity of
*functional* life forms. This is the GOAL of the theory of evolution.
Things don't "just happen" without a cause. The theory of evolution
proposes to explain the occurrence of increased functional diversity
in living things. This functional diversity is in fact the goal
because it affects survival. Actually, I suppose you could say that
survival is the goal. The "selfish gene" hypothesis is a hypothetical
goal. Out competing one's peers is the goal of evolution. Trying to
give your offspring better functions than the next guy. That is the
goal. Certainly, there is a goal for evolution. This argument of
yours is just another spout of hot air.
> > > For some reason you are stuck with your bogus analogy of fixing broken
> > > windows. Lactase function was just a quirk that the bug found gave it some
> > > advantage. Without lactase function the bacteria was dividing happily in some
> > > mammal's guts. It didn't have to evolve lactase function to survive.
> >
> > Actually, it did have to evolve the lactase function if it wished to
> > use the potential energy source of the surrounding lactose for some
> > advantage.
>
> But it didn't have to and many bacteria didn't.
LOL - and how does this help you?
The fact that many bacteria do not evolve the lactase enzyme means
nothing as far as an explanation of evolution. In fact, this
phenomenon supports my position much more than it supports yours. To
say that some bacteria do not evolve something does not explain how
others do evolve new functions. That is your goal here. You are
suppose to explain how new functions can evolve naturally over time.
For you to argue then non-evolution somehow helps to explain how
evolution happens is certainly a stretch that I have yet to be able to
understand. The fact that many bacteria never evolve any lactase
functions despite being exposed to a lactose rich environment over the
course of thousands of generations cannot be explained except to say
that there must be something that is blocking the normal evolutionary
process. Because, if these bacteria actually could evolve the lactase
function in such an environment, it would certainly be to their
benefit and they would certainly outperform their peers. This is in
fact what happened in Hall's E. coli experiments when they evolved the
ebg gene to produce a lactase enzyme with a single point mutation.
They suddenly started outperforming and outgrowing their peers. The
same thing would happen with other types of bacteria in a lactose rich
environment . . . if in fact they were ever able to stumble across the
proper genetic sequence.
> > The window analogy is not "bogus" at all. It shows that
> > some "functions" simply have no naturalistic explanation while others
> > do have such explanations. A broken window has a naturalistic
> > explanation while a fixed window has no naturalistic explanation
> > outside of deliberate design.
>
> Demonstrate this in nature.
I have been demonstrating this throughout this entire thread over and
over again, but still just don't seem to get it . . . or at least you
will not let yourself even consider such a possibility. Again though,
neutral gaps in function, as the complexity of the various functions
increase, become less and less explainable with naturalistic processes
alone. They quickly reach a point that is wide enough to make their
crossing statistically impossible, even in an evolutionary time frame
of 4 billion years. The window here is a given complex function.
Breaking this function is like breaking a window in a house. This can
be explained with mindless naturalistic mechanisms alone. However,
once this function is shattered, putting it back together again cannot
be explained outside of ID since there is no known mindless
naturalistic process that can make such a repair. In fact, like a
window in a house, there is no known naturalistic process to explain
the formation of certain biological systems of function, such as
bacterial motility via flagellum or some other process of motility,
nor its existence in its current location (i.e., in a bacterium) when
it is fully functional.
So you see, the broken window analogy is not "bogus" but is in fact a
very helpful analogy to explain how ID can be detected even without
the knowledge of who the intelligent agent was.
> What is a broken window? What is a fixed window? Give examples. How
> does this demonstrate design?
Broken window = Lost bacterial motility or lactase function or some
other function.
Fixed window = The gain of the lost function.
Some windows are relatively easy to fix, such as the broken windows of
relatively simple single-protein enzymes. Occasionally, even random,
mindless, naturalistic processes can even fix such small windows.
However, with increasing complexity, the comparison with windows might
include a stained glass window, or a multipaneled window. Such
windows are not as easily fixed by intelligent design much less a
mindless nature. Likewise, with increasing genetic complexity,
naturalistic mechanisms simply take too long to fix or recreate these
functions and nature soon runs out of time even in evolutionary time
frames.
> > The same situation aplies to genetic
> > functions. If no naturalistic explanation exists to explain the
> > variety or level of certain genetic functions that exist in various
> > life forms, the only logical explanation available to explain their
> > obvious existence is ID.
>
> Only in ID fantasy.
Repeating this over and over doesn't help explain anything and it does
make ID any less true. Please, come up with some reasons besides
making such blatantly "just so" statements all the time with nothing
to back yourself up.
> If this were true, why can't they demonstrate it
> and support it with enough evidence to teach it to children?
Again, you make this "just so" statement without anything of substance
to back it up. You say there is no evidence for ID, but clearly there
is and it can be taught in quite a logical fashion. I myself have
explained ID to many people from a wide ranging of educational
backgrounds. Just about everyone is able to quickly grasp the concept
and logic behind ID especially if they do not come to the table with
preconceived naturalistic biases. In fact, this whole debate is about
how to interpret the evidence. I use the same evidence that you use,
but explain it in favor of ID. You try to explain it in favor of
naturalism. However, to say that there is no evidence against
naturalism or for ID is such a blind and short-sighted statement that
it is laughable.
You know, I could say the same thing about naturalistic evolution
being taught in schools. In my opinion, our children, high-school,
college and graduate students are being taught a bunch of baseless
just-so-stories with little solid evidence to back them up. Much of
the education on evolution consists of statements like, "Then this
evolved into that." but not much is said as to how, exactly, this
evolution could have taken place. Oh, yes, random mutation and
natural selection are terms that are slung around the classroom
without any real understanding on how they might really work when it
comes to genetic changes since many genetic functions are separated by
huge gaps of non-function. What happens now? What explanation is
given for how these gaps were crossed? Natural selection no longer
works here and random mutation takes too long. But, no one seems to
want to talk about that. Evolution must have happened, so don't
question how it happened. Ridiculous!
> The fact
> is that it is only good enough evidence to fool people like you into
> thinking that there is a valid argument in there somewhere. Where is
> this valid argument? Does the fact that the ID proponents admit that
> it isn't valid by their own inaction count for anything?
No ID proponents admit that they have an "invalid" argument and many
of them are in fact taking a lot of action. Behe, for example is
neither stupid, ignorant, or inactive. You make such generalizing
statements that they come off as rather desperate. What do you call
me? Am I stupid? Do I have a lower IQ than you do? How are you more
capable of rational thought that I am, and how do you know for sure
that it is not you who are the crazy one believing the scraps of
evidence and twisted interpretations that naturalism throws your way,
when the huge mountain of evidence sits squarely on the side of ID?
You ask me to "prove" ID, which I have been trying to do all along
here, but where is your evidence for a naturalistic cause? What
naturalistic evidence do you have to explain the existence of complex
genetic functions?
I know, it helps to be in the camp that seems to have most of the
intellectuals agreeing with you, but that doesn't make you right or
smarter than those who do not see things the way that you see things.
And, it does not automatically mean that you have a better
understanding of the evidence either. Perhaps then, the best you can
do is to avoid the evidence and try to support yourself by saying that
your opponents are stupid. Well, if that makes you feel better . . .
> > > What is one of the ways mosquitos evolve
> > > resistance to DDT? Isn't it gene duplication?
>
> > No. It is not gene duplication in the vast majority of cases. Such
> > resistance-type evolution is almost always the result of single point
> > mutations in target proteins or the like. It works much like the
> > evolution of many types of antibiotic resistance. For further
> > discussion of this, I have written a paper on various types of
> > antibiotic resistance at:
> >
> > http://naturalselection.0catch.com/Files2/antibioticresistance.html
>
> We're not talking about antibiotics, but of the case of DDT and
> multiple copies of genes and their influence on resistance to that
> pesticide.
In this case, the multiple copies of the gene did not evolve into
something else, but only increased the production of the same product.
This is not gene duplication for the purpose of gaining extra genetic
real estate for the evolution of new functional genes or proteins. No
new genes or functions evolved here. The same genes and the same
products were simply upregulated. This is just a production issue,
not the evolution of any new function. Upregulation is also
relatively easy. Not something very complex at all. . . not a
problem.
> > > Isn't this a favorite
> > > creationist misdirection ploy about evolved resistance? "It is only gene
> > > duplication."
> >
> > Not at all. If it is, it is not a very good argument as it really
> > explains very little. I certainly don't use such an argument.
>
> You are right it wasn't a very good argument. If you want evidence
> for gene duplication in the history of life look up the DDT papers and
> look at the glutothione related genes.
Again, gene duplication for the purpose of upregulating a given
product does not help to explain the evolution of new genes with new
functions. Also, as described above, gene duplication for the purpose
of creating extra genetic real estate where one copy undergoes random
genetic drift while the other copy maintains previous function, is
expensive and will be selected against by nature. The gene
duplication hypothesis for the evolution of new functions is very
limited indeed.
> > > Apparently lifeforms can survive happily with these duplications
> > > and if we look at genomes many of these gene duplications have evolved novel
> > > functions. We have evidence that this evolution is possible. What do you have
> > > to claim that it isn't possible?
> >
> > Most of the literature that suggests certain functions arose via gene
> > duplication are not based on any direct experimental evidence or
> > observation, but only on a "just-so-story of what must have happened.
> > Very few if any of these "examples" are based on any sort of real time
> > experiments. Such suggestions are based on certain similarities that
> > exist between various genes with different functions, but such
> > similarities could just as easily have been designed, again, with the
> > use of the principle of "conservation of design." You see,
> > similarities do not automatically support the theory of common
> > evolutionary origin over the concept of ID. The support of the theory
> > must be found in an explanation of the differences, not the
> > similarities. The similarities can equally be explained by both
> > theories, but the differences cannot. So, it is in the differences
> > where one must find evidence for or against naturalistic evolution vs.
> > intelligent design.
>
> Demonstrat that you can account for the data equally well with your
> model.
Why don't you demonstrate that your model can account for the data
better than my model. My model explains the differences and how the
neutral gaps between very complex functions can be crossed. Your
model explains little if anything as far as the existence of such
complex functions and huge genetic gaps in function. Your model is
capable of explaining the similarities among life forms, but not very
many of the differences. That is where my model comes into play.
> Remember the nested pattern of changes. When a gene
> duplicates it starts changing relatively independently. We see
> nesting within nesting in the successive duplication events of these
> large families of genes. Explain the nesting in your model and why it
> mimics biological evolution. I'd like to see you do this.
I have discussed this issue extensively with you before and have
written a paper on this as well:
http://naturalselection.0catch.com/Files2/geneticphylogeny.html
Nesting supports my model much better than it does your model.
Sequences are nested according to their functions and the functional
needs of their owner. Non-functional or neutrally functional
sequences are quickly scrambled by random mutations over time (Since
such sequences are not maintained by natural selection). So, to say
that some ancient protein sequences, such as cytochrome C, are nested
according to evolutionary relationships is illogical. The variations
in cytochrome C must be related to function, not necessarily
evolutionary relationships so much as the various needs of the owners.
The differences are in fact more easily explained as functional
differences. If they were not functional differences, but neutral
differences, then these neutral differences would be scrambled beyond
recognition in a relatively short time. . . and would no longer be
"nested". Neutral nesting does occur, but it only lasts for a
relatively short time. It can only be used as a common descent gage
for relatively recent diverging families, not for the determination of
potentially ancient relationships.
> > As detailed above, either the gaps may have been wider than this or
> > the E. coli didn't have enough free genetic real estate to undergo
> > random walk.
>
> This is where I screwed up and the first two changes were only
> believed to be neutral until they were studied in more depth.
Well, almost . . . except that Hall knew that the first two mutations
were not neutral from the beginning.
> So selection may have played a roll in getting the three mutations.
> We are stuck with no examples of 3 mutations needing to be bridged to
> get function. In those terms your argument is now even worse.
Actually not. This is exactly what my argument predicts will happen.
Each step in the crossing from one function to another must be
functionally beneficial or else the time required starts to increase
exponentially.
> Nature
> found a way to use selection to get the three changes. You claim that
> neutral changes are needed, but we can't find them.
I claim that more and more neutral changes are needed as functional
complexity increases. The changes in function that Hall described as
taking three successive mutations where actually extremely closely
related enzymatic type functions that involved the hydrolysis of very
similar sugar bonds. In fact, Hall explained these steps as being
basically the same function with different levels of activity. I
would actually call each step a new function, but the fact is that
each of these new functions were extremely similar, requiring a single
mutation for each step. Also, each of these functions was relatively
simple. It is very much like the evolution of 3-letter words (i.e.,
cat to hat to bat to bad to big to dig to dog). In other words, the
simpler the functions, the more likely that a few or several of them
will be clustered in their sequencing very close together, like a
little island in the sea of non-function. However, as the complexity
of the functions in question increase, so does the average space
between these functions. For example, bacterial motility cannot be
achieve with a single average length protein sequence . . . period.
Multiple proteins are required for any sort of bacterial motility to
be achieved. There might be many different ways that this motility
function could be achieved, but on average, all of these ways are
surrounded by oceans of non-functional sequences that are far far
wider than the relatively small gaps that surround the more simple
single protein enzymatic type functions (i.e., lactase, nylonase,
lipase, etc).
> Demonstrate that even three neutral changes would be needed for any
> system that you chose. You can't just claim that it is obvious. This
> example demonstrates that it takes a lot of hard work to determine
> these things and what was thought to be neutral really had some
> selective advantage even if they missed it initially.
The thing is, this assertion that increasing complexity results in
wider and wider neutral gaps in function is in fact very intuitively
obvious. You cannot or at least have not been able to explain how I
might be wrong. You need to do some demonstration to support your
assertion that I am wrong. My demonstration can be found in the fact
that no one has ever demonstrated the evolution of anything of the
level of complexity of say, bacterial motility, which involves
multiple interacting parts all working together simultaneously. I use
the argument of neutral gaps between functions to explain this limit
to the evolution of increasingly complex functions. You have not been
able to explain why such evolution doesn't seem to happen much less
how such evolution could happen. You even have difficulty explaining
the lack of evolution of the relatively simple lactase function in
Hall's experiments. How then can you possibly hope to explain the
evolution of anything more complex than single protein enzymes? You
are basically stuck trying to present feeble examples of the evolution
of relatively simple enzymatic type functions, which are always
realized with just one or two point mutations. It really is deceptive
and underhanded to try and pass these examples off as adequate proofs
of Darwinian-style evolution when they explain practically nothing.
In fact, you can't even come up with anything that even works on paper
much less in real life. Your position has very little explanatory
value since you can't explain more than the evolution of the simplest
of protein-based functions.
> Ron Okimoto
Sean
catshark
Ohh! Very nice. Thanks for pointing it out.
---------------
J. Pieret
---------------
Science, as a practice, process, or institution,
has no metaphysics other than the assumption
that if you can measure it you can study it . . .
- John Wilkins -
catshark
<vze4...@verizon.net> wrote:
Ohh! Very nice. Thanks for pointing it out.
---------------
J. Pieret
---------------
Cogito sum, ergo sum, cogito.
- Robert Carroll -
Sean Pitman
> > Thanks for the note. However, I'm not really here to convince anyone
> > of anything. . . although I don't mind if I end up sparking some
> > question of doubt concerning current evolutionary dogma. Basically
> > though, I'm really here for my own interest and benefit to see what
> > the best arguments are from those who ardently believe in evolution
> > and the doctrine of naturalism. So far, I'm less than impressed.
> >
> > Sean
>
> To improve your impression all you have to do is take the best piece
> of evidence for your alternative and compare it to the evidence that
> we have that tells us something else.
That's what I'm doing . . .
> All you have to acknowledge is
> that the evidence for the scientific explanation is so much better
> than anything that you have that your position is laughable.
This sentence is kinda mixed up, but I do get your point. However, I
do believe in the "scientific explanation." I just don't believe in
your view of science or in the popular views of many scientists.
However, just because my position is unpopular does not mean that it
is not scientific or that it is wrong. You can say, "You're wrong
you're wrong you're wrong . . . " until the cows come home, but simply
saying something over and over again doesn't make it so. You have a
habbit of spouting off great statements like this without a shred of
evidence to back yourself up.
> You can
> poke at bits like the Neandertal data, but you can't ignore the vast
> majority of molecular data that says that the Neandertal example
> amounts to nothing by comparison.
There are no mountains of molecular data that explain how naturalistic
molecular evidence happend or is happening. The evidence is actually
strongly in favor of ID. Similarities do not support naturalistic
common descent any more than they support ID. The differences are
what are important here and these differences in many wide ranging and
very complex functions within life forms simply have no reasonable
naturalistic explanation.
> The only reason that you are
> unimpressed is that you are willfully ignorant of the data. As long
> as you don't know how bad your arguments are, you consider that a
> plus.
Actually, it seems to me that you are ignorant of much of the data in
your own camp. You spouted off about Neanderthal papers that you had
never read and suggested explanations for molecular clock hypothesis
that other evolutionary scientists were calling hog-wash. Then, here
in this thread, you have spouted off about Hall's experiments without
first having read anything more than a few abstracts. Please! I read
quite a bit on this subject from main line science journals and text
books. I am certainly not up on every aspect of this topic, but I
still read a great deal about it. You should know this. I have
quoted many journals and papers written by evolutionists. This whole
thread right now is basically one that is discussing the work and
experiments of B.G. Hall . . . someone who you have yet to read aside
from a few abstracts. Again, a lot of hot air a smoke screens comming
from someone who is sounding more and more desperate by the post.
> If you were really interested in what the best arguments are you need
> to start reading some science texts instead of the creationist
> propaganda rags that you immerse yourself in.
What a bunch of BS! You for one should know that I read a great deal
of scientific texts as well as popular scientific propaganda. My
problem is just that I think for myself and am not so much impressed
with someone who calls themself a scientists or a "brilliant mind." I
must understand for myself before I accept it. And, so far, the
theory of evolution simply makes no sense to me as it stands. I am
not ignorant of its claims or of the evidence that it often used to
support it, I just do not see this evidence as really supporting the
theory of evolution at all. . . but rather the theory of ID.
> You know for a fact
> that you can't trust creationist material, but that is all that we see
> out of you.
This is also ridiculous. There is a lot of ID material out there that
is very good and trustworthy. You just have to be critical of all
material that you read, to include popular mainline scientific
material with is often just as badly biased and poorly thought out as
the worst that comes from the YEC camp.
> How is that learning anything about the issue except it
> tells you how bad the creationist arguments are.
Actually, man YEC arguments are extremely good. Such generalizations
aren't very convincing.
> Present the honest
> creationist argument that you claim exists somewhere.
I have been presenting such arguments. My own questions here are my
own and they are honest questions on my part. So, here is your answer
. . .
> Who are these
> honest creationists and what is the evidence for their beliefs of what
> we see in nature.
I am an honest creationist. There are also many more. I work with a
lot of them here at Loma Linda University. Leonard Brand, a geologist
here, is another very intelligent and honest creationist. I would say
that Michael Arct, geologist, and Prof. Javor, biochemist, are a
couple more. Behe is probably another. However, I can only really
speak for myself. It doesn't really matter to me if all other's in my
own camp are idiots or liars (and most of them are not), I am at least
being honest for myself and that is what really matters.
For more of a list see:
http://www-acs.ucsd.edu/~idea/scidoubtevol.htm
> I've requested this several times because you keep
> telling us that these people exist and that they have valid arguments,
> but we never see any names or any valid arguments.
This is total BS. I have mentioned many names before, to include the
names listed above. I have also listed many evolutionists as being
honest and intelligent and I discuss many of their ideas and papers.
You evidently have either a very limited or a very selective memory.
You simply do not agree that these ID scientists have good points, but
that is rather a matter of opinion. You haven't got anything, as far
as I can see, to argue effectively against these ID arguments. . .
> Ron Okimoto
Sean
howard hershey
Ron Okimoto wrote:
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03052...@posting.google.com>...
>
>>roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.0305...@posting.google.com>...
>>
>
> Snip:
>
> It looks like I quit too soon. I do screw up later on so I have to
> continue.
>
> The Hemoglobin citation is on page 63 of the 1981 version of Stryer
> second edition Biochemistry. I too Biochem in 78-79 and I don't
> remember the phrase "nine positions are nearly invariant." There is a
> table with the nine amino acid residues, so I don't know why I
> remember it as a lower number of invariant amino acids. It could be a
> change between the first edition and the second, or I could just be
> misremembering.
It involved a comparison between 20 (I am sure that more are available
now) different species (from lamprey to human). Stryer states, "A
comparison of these seqeunces shows considerable variability at most
positions. However, there are nine positions in the sequence that
contain the same amino acid in all or nearly all species studied thus far."
Note that *even* these nine amino acids are not necessarily *invariant*,
and that there is *considerable variability* at most positions.
Comparing human alpha chain, human beta chain, and whale myoglobin (only
3 sequences), all of which form similar 3-D structures and bind oxygen
through heme, we find only 24 out of 141 sites being identical.
>>>>The problem is that, relatively speaking, these islands of function
>>>>are quite small indeed. When compared to the total number of
>>>>completely non-functional sequences out there in the ocean of
>>>>non-function, those sequences that have any function whatsoever (from
>>>>the perspective of a given life form in a given environment), make up
>>>>only the tiniest of fractions, especially when you start talking about
>>>>functions that require amino acid sequences that average more than one
>>>>enzymatic-type protein in length. When functions require multiple
>>>>proteins totaling several hundred, thousand, or even tens or hundreds
>>>>of thousands of amino acids in length, then your little islands with
>>>>their little impressions don't come near close enough to avoid the
>>>>random drift problem.
Remember that the current multiplicity of sequences all perform at close
to roughly the same level of functionality. Presumably there are just
as many, if not more, seqeuences that are sub-optimal wrt current
function. Selection, of course, is a matter of going from such a
sub-optimal level of functionality to *an* optimal level (any of the
current sequences would do, but of course only one such sequence was
*the* ancestral sequence which arose from a sub-optimal precursor).
Once we have the original optimized ancestral sequence, selection works
to preserve those components necessary for function (allowing only
neutral changes, small modifications to optimize to local conditions,
and, more rarely, a slightly deleterious change). It is this last
process that we are examining when we follow changes in, say, hemoglobin
in lineages.
>>>They are likely small for any one sequence, but there are a lot of
>>>sequences and a lot of possible functions, and when you change a
>>>sequence you change its functional potential. You can't just look at
>>>the potential functions of any single extant proteins, but you have to
>>>look at the potential function of all the molecules that you can get
>>>by changing just 1 to 3 amino acid positions. You know that this is
>>>possible. If you make one or two changes you can significantly change
>>>the landscape for any function, can't you?
>>
>>Yes, but you do not seem to understand the problem. You are thinking
>>that there are so many potential beneficial functions out there that
>>just about any change in bound to evolve at least one of them.
>
>
> No, what we see is that for anything that we can think up a selection
> for we can get that activity randomly changing the sequence of the
> variable region of the antibody.
Besides, organisms do not *need* nearly as many functions as Sean
thinks. Cells did not *need* to generate multicellularity. When
multicellularity was generated it was beneficial to some organisms in
some local conditions. It is a *necessity* to be multicellular to
produce humans, but that doesn't make multicellularity a function
*necessary* for life. Life existed for billions of years before
multicellularity appeared. In the yeast, S. cerevisiae, only about 1500
genes are *necessary* for even that relatively advanced organism.
That doesn't mean that organisms cannot take advantage of any 'luxury'
function that happens to be advantageous in a local environment.
>
> The
>
>>problem is that even though there are a lot of potential functions out
>>there as far as an absolute number goes, this number is very tiny
>>indeed when compared to the total number of potential sequences out
>>there. For example, there may be a billion potential lactase enzymes
>>out there of 4,000aa or less (The approximate length of the lacZ and
>>ebg lactase enzymes). Is a billion a large number? Well, yes it is
>>until one compares it with a 1 with 5,200 zeros after it (the total
>>number of potential proteins of this length). So you see, the "large"
>>number of potential functional sequences is really an illusion of
>>bigness. Such "big" numbers are really small in comparison to the
>>bigness of the total number of possibilities. In other words, no
>>matter which direction that a sequence "drifts" in its random walk, it
>>is unlikely that it will come across any other beneficial function,
>>from the perspective of a given organism, in short order. And, this
>>problem becomes more and more significant with increasing functional
>>complexity . . . especially when we start talking functions that
>>require multiple proteins all working together at the same time . . .
>>like in bacterial motility etc.
>
>
> Like I said before 10^12 is such a minute fraction of the possible
> sequences that there is something wrong with your evaluation of the
> system.
Most 'new' functionalities arise as modifications of old, already
present functionalities rather than arising out of completely random
sequences. So Sean's assuming that all new functionalities arise out of
the entire potential population of completely random sequences is a
problem with *his* argument. The real question is how far any of the
10^12 possible sequences with optimal functionality (and the probably
much greater number that have suboptimal functionality) are from any of
the *existing sequences* (or combinations of sequences, since new
activities often seem to arise via new combinations of protein motifs
via transposition or errors in recombination) in an organism. Sean
persists in the creationist argument that new genes usually appear *de
novo* by magic from random garbage in order to make his calculation.
That, and he continues to overestimate the number of amino acids that
need to change before *any* functionality related to the selectively
important function appears.
Unlike English words, where a single change of letter often produces
complete garbage, in the language of proteins, most changes do not
produce complete garbage.
I wonder why Sean doesn't see that saying that many enzymatic activities
are relatively simple protein functions destroys his argument?
Your definition of "neutral gap" is what is strange. Apparently you
think there is a huge gap of changes which must occur before there is
*any* selectable functionality in the protein. That is, a protein is
like an arch, in which you cannot place a keystone until all the other
stones are present, but you get no arch activity until the keystone is
in place. Wrt real proteins, this is an absurdist argument unrelated to
how proteins work. But in the creationist world where all new protein
functionalities arise from completely random sequences (or get poofed by
a magician) it might make some sense.
>
> Demonstrate that this is true. You have to first demonstrate that the
> gaps exist. This is just assertion without evidence. Take a complex
> system and show us where the gaps are and how you determined that
> these gaps exist.
To do this, you must show both that each change is necessary and that no
order of occurrence produces a protein with even partial activity that
has selective value. Otherwise, if even one order of change does have
intermediates with partial activity, the evolution of the system does
not have the gaps you need. Most evolutionary change probably results
from an initial change producing a suboptimal functionality, with
subsequent secondary mutations enhancing that initial functionality.
There exist, of course, many mutants (both intra- and inter-genic) whose
function is to "enhance" or "suppress" the effect of another mutation.
>
>
>>>A better
>>>argument for you and one that the ID people use is that since we don't
>>>have a good explanation for how we evolve these functions that some
>>>designer must be responsible for guiding these mutations and making
>>>the results happen.
>>
>>Uh . . . that is my argument.
>
>
> No, because we see it happening in nature. If you want to claim
> divine intervention, demonstrate that it is happening in the systems
> that these researchers are studying. Your argument is that it
> happened in the past because we obviously do not have any evidence
> that it is happening now.
The ID does seem to be rather absent in the present day wrt generating
the various antibiotic and pesticide resistance systems of various
organisms that have acquired new 'functionalities' against chemicals
that have only been made recently.
>>>The problem with the ID argument is that it is
>>>stupid. Just try and find some evidence to support it.
>>
>>LOL - Ok . . . it is very easy to say that something is "stupid"
>>without giving any reasonable explanation as to why it is "stupid."
>>You are just spouting off without any basis for support of your
>>position whatsoever. I have been giving you the "evidence" to support
>>this ID argument all along. You seem to vaguely understand the
>>arguments, but you are so stuck in your rut of "naturalism explains
>>everything" that you are too blind to admit that there just might be
>>something to ID.
Did the ID independently create the various genes that permit resistance
to antibiotics and pesticides used by the creature he favors above all
others? Seems like he has a strange way of showing his love.
Why didn't you include the mechanism of resistance of cancer cells to
methotrexate in your examples? That certainly is a form of resistance
of some relevance to a physcian?
>>
>>>Isn't this a favorite
>>>creationist misdirection ploy about evolved resistance? "It is only gene
>>>duplication."
>>
>>Not at all. If it is, it is not a very good argument as it really
>>explains very little. I certainly don't use such an argument.
>
>
> You are right it wasn't a very good argument. If you want evidence
> for gene duplication in the history of life look up the DDT papers and
> look at the glutothione related genes.
Or look up methotrexate and dihydrofolate reductase activity and what
happens when you select for methotrexate resistance in cells in culture
or in humans.
>
>
>>>Apparently lifeforms can survive happily with these duplications
>>>and if we look at genomes many of these gene duplications have evolved novel
>>>functions. We have evidence that this evolution is possible. What do you have
>>>to claim that it isn't possible?
>>
>>Most of the literature that suggests certain functions arose via gene
>>duplication are not based on any direct experimental evidence or
>>observation, but only on a "just-so-story of what must have happened.
>>Very few if any of these "examples" are based on any sort of real time
>>experiments. Such suggestions are based on certain similarities that
>>exist between various genes with different functions, but such
>>similarities could just as easily have been designed, again, with the
>>use of the principle of "conservation of design." You see,
>>similarities do not automatically support the theory of common
>>evolutionary origin over the concept of ID. The support of the theory
>>must be found in an explanation of the differences, not the
>>similarities. The similarities can equally be explained by both
>>theories, but the differences cannot. So, it is in the differences
>>where one must find evidence for or against naturalistic evolution vs.
>>intelligent design.
Not in the case of methotrexate resistance nor DDT (and several other
pesticide) resistance. In that case, we have the intermediates with the
relevant duplicated genes.
This is indeed Sean's key problem. He has no evidence that there are
any systems that require evolution by a 'keystone' (no function until
the last step is put in) mechanism that involves more than one to three
steps. Nor does he present any evidence that any of these putative
systems arose from completely random sequences that were more than two
or three steps away from selectable functionality. He posits distances
of many amino acids until the 'keystone' amino acid that instantly
produces full functionality from zero functionality, but never points
out any actual system that requires such distances.
>
> Snip:
>
> Ron Okimoto
>
Mark Isaak
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>I just do not see this evidence as really supporting the
>theory of evolution at all. . . but rather the theory of ID.
What theory of ID? To the best of my knowledge, no theory of ID has
ever been published.
I will grant that there exists a highly informal "theory" that says,
pretty much in its entirety, "life looks designed." But that theory
is falsified by data.
Sean Pitman
> On Wed, 21 May 2003 20:18:09 +0000 (UTC),
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
> >The point is that
> >just because a robot is not itself "intelligent" does not mean that
> >the actions of the robot cannot be detected as being the result of a
> >mindful intelligence. A robot can be programmed to put together a
> >wristwatch. Does the fact that the robot is not intelligent mean that
> >the wristwatch was formed without intelligent design? No. Certainly
> >not.
>
> If you are going to argue by analogy, can you at least try to keep them
> consistent? You started out this thread by asserting that a regular
> arrangement of rocks on the moon would be evidence of "purposeful
> intelligence". I asked about regular features that occur in the natural
> world and you now apparently concede that "Not all geometric shapes imply
> intelligent design". Instead, you then switched to an analogy of a robot
> creating art. I asked about "art" that occurs in nature and you concede
> that "Mindless naturalistic processes can and do create or form some
> amazing things, such as sunsets, rainbows, rivers, water falls, tornados,
> super novas, volcanic explosions, snow flakes and etc." Now you switch to
> a robot making (by common understanding) a humanly manufactured item. Do
> try to make up your mind.
Evidently you do not yet understand the difference between my initial
analogy of unnatural geometric patterns and your use of naturally
occurring geometric patterns. So, I will try and explain my position
again.
The difference between my example and yours is that all naturally
occurring geometric patterns have the ability to self-assemble. No
outside informational input is needed. The information is completely
contained in the mindless system itself. Your example of honeycombs
is not such an example however because bee's wax does not have an
inherent ability to self assemble in hexagonal patterns. This can be
tested. Bee's wax never self-assembles in this way. So, when we find
such a geometric pattern made with bee's wax, we can assume that
something else, outside of the inherent power of bee's wax, acted upon
this wax in a way unnatural to the wax's own abilities to change.
Even if we never saw any bees making a honeycomb before in our lives
and even if we never heard of a honeycomb, given our previous
experience with wax, once we saw a honeycomb, we would not be able to
logically propose a purely non-directed naturalistic mechanism of
assembly. The most logical explanation would have to fall to ID in
the form of the action of some sort of life form or programmed agency
that has its origin in ID (i.e., such as a robot or a computer).
Devil's Tower, on the other hand, is not like bee's wax. Our
experience with the materials that form Devils Tower show us that no
outside informational input is needed to form the geometric shapes
found there. The same can be said for snow flakes and other
crystallized structures where our previous experience with these
elements makes it clear that such structures contain all the necessary
information for self-assembly within themselves.
So you see, if you were to go to an alien planet and find perfectly
round, polished, 1kg granite rocks all made out of the same material
and all being the same shape, size, and weight, and all being arranged
in a perfect geometric pattern, with each rock separated by a one
meter distance, forming a perfect square one mile on each side . . .
would you really assume a mindless naturalistic cause? You might say
that you would here, for the sake of argument or to save face, but in
reality, I highly doubt that you would. You would assume ID because
your past experience with granite rock tells you that granite never
self assembles itself into such a pattern. Outside directed
information is needed.
Also, when I used the term "art" before, I was doing so in a more
narrow sense, such as a painting of the Mona Lisa or some other
similar pattern as my hypothetical alien rock pattern described above.
Something where paint and canvas (with the help of mindless,
non-living, forces of nature) simply do not ever self-assemble
themselves to produce anything comparable. Certainly mindless
naturalistic forces can act on paint to form unique and very
interesting patterns, but such patterns can easily be distinguished
from purposeful paintings of the character of the Mona Lisa or other
such classical works. Of course, intelligent minds can and have given
rise to some types of "modern art" that is very similar to what
naturalistic processes can and do produce. In such cases, ID could
not be adequately supported as a cause. In order to hypothesize ID, a
given phenomenon must be determined to be outside of the realm of
known naturalistic processes.
> Now, let's take out the element of obvious human manufacture and, instead
> of a "watch", just call it a "timepiece". How then do you explain
> "chemical clocks"?
>
> <http://www.faidherbe.org/site/cours/dupuis/oscil.htm>
>
> Are they intelligently designed, even though they keep time by molecular
> reactions that are "self-contained within the cause and effect actions of
> the molecules and mindless forces of this solar system and planet"?
Again, the workings of the chemicals in this situation is entirely
self-contained or self-assembled. No outside directed intelligence is
needed because all of the information for the operation or "workings"
of these chemicals is entirely self-contained. This is nothing like a
wristwatch were the component parts never self-assemble without the
guidance of an outside force that is backed by a deliberate
intelligent mind. You even quote me here, but you don't seem to
understand the quote. The workings of anything where the individual
parts can automatically self-assemble themselves, cannot be said to be
definitely intelligently designed (although it could have been).
However, when one finds a collection of parts performing a function or
creating a pattern where this pattern or function is beyond the
self-assembly potential of the parts involved, then, ID can be
reasonably hypothesized.
> >Your suggestion that sunsets are the same level of complexity as the
> >formation of honeycombs is misguided. The information needed to
> >produce sunsets is self-contained within the cause and effect actions
> >of the molecules and mindless forces of this solar system and planet.
> >This is different from the formation of honeycombs in that bee's wax
> >does not self-assemble to form honeycombs whereas sunsets do
> >self-assemble.
>
> But *bees* do self-assemble (we don't have to address any idea that the
> "designer" assembles bees individually, do we?).
Bees do not self-assemble. The assembly of bees requires pre-existing
strands of DNA with a coded blueprint for bee assembly. The various
parts of a bee do not simply form *themselves* into a bee. There is a
coded message that has to be decoded by code reading processes that
are also coded for in the bee's DNA blueprint. For example, if
scientists were to build a robot that had a program that told it how
to make more copies of itself . . . this robot could self-replicate.
However, the robots that this original robot made, could not be said
to have "self-assembled" because they were in fact designed by
purposeful intelligent minds in the beginning. The offspring of the
original robot were not designed by the original robot either, but by
the original design of the intelligent designers. So you see, you are
wrong to say that bee parts actually "self-assemble" because they
don't unless they are in an extremely specific arrangement that has
always been there. I can give you all the bee parts that you want. I
can give you all the atoms and molecules to make a bee. If you stuff
them all together randomly, they will not get together of their own
accord and produce a bee. Higher informational input is needed here
to get the parts to "know" where to go. The parts do NOT naturally go
to the right places to make a bee.
> Please give a consistent and objectively verifiable way to distinguish
> between the "level" of complexity involved in a chemical clock and that
> involved in a living thing. Where is complexity "discontinuous"? At what
> point does something become too complex for the "mindless forces" of the
> universe?
If in your experience, you can demonstrate how rocks or chemicals or
atoms can self-assemble themselves in a given mindless and lifeless
environment to produce a given phenomena, then you will remove the
concept of ID as the only reasonable hypothesis to explain such a
phenomenon.
> >Honeycomb formation is actually on a higher level of
> >complexity than is sunset formation in that outside information is
> >needed for honeycomb formation.
>
> This is nothing but a petitio principii and circular to boot. "The
> existence of a 'higher' level of complexity proves there must be an
> intelligent designer and we know it is higher complexity because it could
> not exist without an intelligence to design it". Conveniently, you skip
> the part about demonstrating discontinuous levels of complexity that
> require an intelligence to breach.
Actually I didn't skip anything. Wax can be experimentally
demonstrated to never form honeycombs by itself. Period. This is
different from the formation of a sunset where all the parts to a
sunset do self-assemble themselves on a regular basis. Wax never
does.
> >> >However, this ability was
> >> >originally designed via some intelligent mind.
> >>
> >> I'm having trouble understanding your point. Because *some* things are
> >> designed, all things are?
> >
> >No, not at all. Many phenomena have a purely naturalistic
> >explanation. Mindless naturalistic processes can and do create or
> >form some amazing things, such as sunsets, rainbows, rivers, water
> >falls, tornados, super novas, volcanic explosions, snow flakes and
> >etc. None of these phenomena require the input of information from an
> >intelligent mind.
>
> Good, we agree that complexity can arise from "Mindless naturalistic
> processes". Now tell us what separates that complexity from the complexity
> you say can't arise on its own . . . *without* using the equivalent of "I
> know it when I see it".
The ability of self-assembly.
> >> >The same could be said
> >> >of the honeybee's ability to make hexagonal compartments out of wax
> >> >and put honey in them.
> >>
> >> You *could* say "the moon is made of green cheese". It would help if you
> >> had evidence.
> >
> >Pardon me? The evidence is that no known mindless naturalistic
> >process, outside of the workings of living things, like humans and
> >honey bees, can form honeycombs, wristwatches, language systems, or,
> >as I am arguing here, the language-like coded information written in
> >the DNA of all living things.
>
> Wait! Now you are all over the place. One moment "intelligent" was the
> opposite of "mindless". Now something a low on the scale of intelligence
> as a bee is all it takes to be opposite "mindless"? Why not an amoeba?
> Are you proposing the "Intelligent Designer" can be an amoeba?
Yes, I am. ID can be expressed through the programmed workings of the
object that was designed. Again, if I make a robot and program it
with the ability to make a honeycomb, was the resulting honeycomb made
by the mindless robot or by me?
> Joking aside, you are obviously having trouble explaining what separates
> "intelligent" from "mindless". Please give a definition that isn't just
> "life is the result of intelligence, everything else isn't".
All life forms do something that inanimate matter cannot do. There is
something special about all living things. Life forms all have
programming that is far above the sum of their parts . . . like
computers or robots. This programming that is behind all life forms
is what naturalistic explanations cannot explain. There is no
mindless force in inanimate nature that can explain how such DNA
programming and the resulting variation in the functions of various
life forms, could have been produced by the workings of a undirected,
unprogrammed, mindless nature. Random mutations and natural selection
are both mindless forces that really do exist outside of any life form
or intelligent mind. They are indeed powerful forces, but only these
can be used to explain the existence and variations of living things.
This has yet to be done in any sort of reasonable way.
> >Many argue that just because no one has seen anyone design life or
> >living systems that no intelligent designer can be reasonably
> >hypothesized. However, if there is no naturalistic explanation or
> >mechanism to explain the existence of life, then it is in fact quite
> >reasonable to hypothesize an intelligent designer of life on this
> >planet...
>
> In order for this to have any persuasive power (outside personal
> preference), you must first demonstrate that there *is* no naturalistic
> explanation or mechanism, especially since you are making an extraordinary
> claim in the face of the many successes naturalistic interpretations *have*
> had in explaining what we see around us.
Actually, you are asking me to absolutely prove a negative. You are
suggesting that in order for you to believe that natural forces cannot
produce the Mona Lisa, that I have to do an infinite number of
demonstrations where natural forces did not produce the Mona Lisa. Of
course, this is impossible. However, with each demonstration of
failure, the weight of evidence builds higher and higher in favor of
ID.
Really, you and popular scientists are the ones who are making an
extraordinary claim. You are claiming that the most fabulous machines
that we know of, machines and systems of function that far outshine
the very best that we humans have been able to produce with our most
brilliant efforts, arose through mindless naturalistic processes.
What an extraordinary and counterintuitive claim! But where is the
evidence? It's almost funny how nature is referred to as a "bind
watchmaker". The comparison of a mindless nature to the workings of
an intelligent watchmaker is quite intriguing . . . but where is the
evidence that nature can and does do things that are just as
impressive and even more so than the workings of our best human
watchmaker?
> >especially when one considers that modern scientists are
> >already manipulating the very codes of life and are creating "designer
> >genes".
>
> The absence of evidence is not evidence of absence.
Actually it is. Of course, no one can absolutely prove a negative,
except in the light of eternity, but a belief in a negative can still
be scientifically supported. The existence of a true negative is
hypothesized based on the current weight of negative evidence. This
weight of negative evidence after repeated tests starts to create
predictive power concerning future tests. The scientific method is
all about predictive power, not about the absolute proof of anything.
In fact, the basis of science is disproof since absolutely NOTHING
except a disproof can be fully proven.
> A hundred years ago it was "impossible" that any human would ever fly, much
> less go to the moon; the Earth supposedly couldn't be older than a few
> hundred million years because we had no mechanism to explain its internal
> temperature; and sickness was a "visitation from god". (Not to mention
> that your argument just ignores what we *do* know about possible routes to
> abiogenesis.)
Again, the evidence for all hypothesis, is the lack of disproving
evidence or "absence of evidence" to contradict the prevailing
paradigm. A hundred years ago it was perfectly reasonable and even
scientific to hypothesize some of the notions that you mention here.
As long as there was a "absence of evidence" to disprove such
hypothesis, they stood as "true." They were in fact falsifiable
however, and one day they were falsified and they lost their
predictive power. Now, we have more hypothesis and theories that have
very good predictive power, for now. But they may also be disproved
in the future when more evidence comes to light. You see, no
hypothesis, theory, or even law that is based on the scientific method
is eternally safe from challenge or potential falsification. So, to
suggest that just because there were ideas in the past that turned out
to be wrong does not mean that current scientific positions are
correct. You say you "do know about possible routes to abiogenesis"
but this is ridiculous. You don't *know* anything of the sort. You
cannot even begin to explain abiogenesis, even on paper.
> As always, it is "god in the gaps". Do you really want to bet your beliefs
> on science *not* discovering a naturalistic explanation for the beginning
> of life? Of course, that is assuming that this argument *does* have
> anything to do with your beliefs and isn't just a justification for what
> you want to believe in the first place.
Yes. The evidence for ID can clearly be found in the gaps. "Not"
finding something is very important in science. The absence of
evidence is actually evidence as described above.
> >Add to this the fact that, without an adequate naturalistic
> >mechanism in place, no one has ever seen a mindless natural process
> >create life either. So, since no one has seen any mindless process
> >create life or change life forms to the degree that scientists, with
> >the aid of intelligent minds, are able to change the codes of life, it
> >is ridiculous to argue that science is incapable of hypothesizing
> >design.
>
> Hold it! Define "hypothesize". To this nonprofessional, a "scientific
> hypothesis" means an idea for a program of *further* observation and
> testing to discover empirical evidence. What program(s) of research and
> testing has been proposed or implemented by Intelligent Design proponents?
> If ID does not seek empiric evidence of this designer, how can it be
> scientific?
Again, as described above, the scientific method proposes some
explanation to explain a given phenomenon, a hypothesis. This
hypothesis must make certain predictions about the future that can be
tested. If the predictions hold, the predictive power of the
hypothesis is strengthened but it is never fully confirmed this side
of eternity. The more and more predictions that are confirmed, the
greater and greater grows the predictive power of the hypothesis until
it is declared to have reached the level of theory. The same thing
happens with a theory until it is declared to have reached the level
of law. Even then, a law is not above question as nothing is in
science.
ID is a theory that does make testable/falsifiable predictions . . .
as I have been doing in this thread when I predict various outcomes of
experiments done with bacteria or explain what I think is happening or
will happen with the experiments of others, such as the E. coli
experiments of Barry Hall. ID is certainly well within the realm,
workings, and evaluation of the scientific method.
> Naturally, you are at a disadvantage here, since even you do not expect to
> find any empiric evidence of this designer. But that just means you should
> take your case to its proper realm, philosophy and religion.
You don't seem to understand the scientific method or how scientific
hypothesis and theories can be and are formed. If you did, you
wouldn't make such statements as this. Perhaps this is because you
have had little chance to learn about and deal with the scientific
method consciously, although we all use the scientific method everyday
on a rather subconscious level without realizing it.
> >It is especially ridiculous to suggest this since the
> >argument is based on a lack of observation of origin, which also holds
> >true for any naturalistic explanation to date. Naturalistic mechanism
> >have clearly failed to explain the existence of neutral genetic gaps
> >that do in fact exist between various functional systems in living
> >things.
>
> But science will go on looking for the evidence. ID seems totally
> uninterested in finding any.
Not so. The goal of science is to disprove positions. This is the
power of science. The efforts to disprove some position only
strengthen that position if no evidence can be found to challenge its
testable predictions. ID theorists are very interested in finding as
much evidence as possible. Because, it is in the repeated testing and
challenge of the predictions of ID that ID is more firmly established.
The problem for the theory of evolution is that many of its most
important predictions are not falsifiable or at least no one has
thought of a way to make them falsifiable. For example, the idea that
bacteria-like creatures can evolve novel functions on the order of
multipart systems of function where all the parts work together
simultaneously, such as is the case with all systems of bacterial
motility, cannot be experimentally tested. There are those, many of
whom are posting to this thread, who propose that the evidence for the
evolution of various single protein enzymes, such as lactase and
nylonase enzymes, is enough evidence to support the theory that even
more complex systems of function did evolve in like manner. However,
I for one, am quite skeptical of this because the statistics involved
say something entirely different. The statistical hurdles are simply
too great as one moves up the ladder of system complexity.
> >> >> And what would I do after I then went to Devil's Tower and saw the
> >> >> hexagonal basalts? Volcanos are "purposeful"?
> >> >
> >> >Not all geometric shapes imply intelligent design.
> >>
> >> But bees do? Why?
> >
> >Again, no mindless naturalistic process can explain the creation of
> >bees or even the honeycombs that bees make. The only process than can
> >explain either one has its best explanatory power in the concept of
> >intelligent design.
>
> You keep *saying* this. Saying it is not evidence for it.
If you would read the my first post in this thread and several of my
subsequence posts dealing with Hall's E. coli experiments, you would
find the evidence for this statement.
> And what "explanatory" power does this proposed designer/god have? Does it
> explain how the design was done, why it was done or how we can test for it
> (except by mapping out the limits our own ignorance and stuffing he/she/it
> in there)? Is there anything I can definitely say was *not* designed, even
> your "mindless" naturalistic processes?
Detecting ID is far different from detecting the absence of ID. I
don't believe that the absence of deliberate design is as easy to
detect as the presence of ID.
> Anything that exists, or could
> possibly exist, could be the result of "design".
Certainly, but not just anything that exists could be produced without
ID. You see, your statement here is certainly true, but the reverse
statement is not.
> How am I better off,
> scientifically, *after* this designer is proposed than I am before? What
> more do I *know* scientifically?
You would be able to predict the future better. That is the goal of
the scientific method. . . to predict the future.
> >> And DNA is what?
> >
> >DNA is nothing outside of the coded information that it contains. The
> >ability to decode this information to create the phenotypic forms of
> >various living things imbues DNA with power that is above and beyond
> >its inherent molecular structure and natural ability.
>
> Yes, ontogeny counts. Now demonstrate that anything more is *needed*
> "above and beyond". You've left that part out . . . again.
Take a bunch of amino acids and mix them together. They will not make
anything. The "above and beyond" can be found in their non-random
arrangement that actually contains coded information that is not
inherent to the molecules themselves. The information is attached to
these molecules arbitrarily. It is like the human language system.
The letters of the alphabet mean nothing by themselves. They are
simply meaningless characters on a page. Only as they have been
arbitrarily assigned higher meaning by an outside source of
information or code are they able to perform the higher function of
information transmission that they perform.
> >> >However, this self-contained information for assembly is not contained
> >> >by many other systems of function, such as the parts to watch,
> >>
> >> Watches do not contain self-replicating molecules, that's true.
> >
> >Exactly. This is a major point.
>
> If so, it is eluding me. Such a major difference between watches and
> living things sinks you analogy qua analogy. You'll have to redo it yet
> again, unless you think living things are watches that have to be
> manufactured or that nature is incapable of anything human beings cannot do
> right this moment. No great loss though, it wasn't very good when Paley
> came up with it (and, no, I don't want to get into *that* endless argument
> - one is enough.)
Living systems of function are very much like watches, only vastly
most complex. In fact, Dawkins himself compared living things to
watches in his book, "The Blind Watchmaker." The only real
differences then between living things and watch is that living things
far outshine the best watch ever produce by human intelligence.
The fact is, mindless processes of sand, wind, rain, sea, lightening,
heat and the like could never produce a wristwatch. So, what on earth
is there that allows a mindless nature to produce even more complex
life forms?
> >> >or the
> >> >code for a bacterial flagellum,
> >>
> >> Which "code" are you talking about?
> >
> >The coded information contained in the DNA of the bacterium that makes
> >a flagellum. The information to make this flagellum is in fact coded
> >information that is decoded from the strand of DNA contained by that
> >bacterium. DNA works very much like a blueprint. Something must be
> >written on the blueprint and then something else must be able to read
> >or decode what has been written before the house that was coded by the
> >blueprint can be built. The same thing happens with the decoding of
> >information from DNA. Something sensible must first be written in the
> >DNA sequences and then something else must be able to read and
> >"understand" or "decode" the message contained in the DNA before the
> >flagellum can be built.
>
> Frankly, you'll have to go play with the "information theory gurus" about
> this. Try Wilkins, who does a nice understandable job with it. I have
> neither the time to dig out one of his old posts nor the inclination to
> delve deeply enough into this myself to do it justice. Simply put, though,
> once a self-replicator has arisen, the environment, along with mutation and
> variation, supplies all the "information" necessary to explain evolution.
Not so. This is the whole point. Try it with a computer program and
you will see. Computers can easily be programmed to self-replicated
software programs as well as to insert random mutation into these
programs over time. And yet, no matter what function based selection
mechanism is used, computers will never be able to evolve their own
software. Why? because the selection mechanism is *function based*.
Most genetic mutations are not functionally different from the
sequences that came before. Because of this, these mutations are
called "neutral" mutations. Neutral mutations are purely random,
outside of any selectibility by nature. And, because they are random,
neutral mutations drift around aimlessly until they come to some new
function that can be selected by nature. The problem is that this
neutral drift requires greater and greater amounts of time as the
complexity of functions increase. In fact, the time required expands
exponentially until billions and trillions upon trillions of years
pale into insignificance.
Really, if you are not interested in "delving" into this particular
issue, then there really is no need for us to continue to talk. This
is THE issue. This is where the rubber meets the road. If you do not
understand this concept, you will never understand the real problem
with naturalism and common descent.
> >> >or the letters and word sequences in a
> >> >book or in this paragraph.
> >>
> >> Oh? Are you just a robot designed to write paragraphs? That would seem to
> >> follow from your example about robots and art.
> >
> >No, I am the designer of these paragraphs.
>
> So you can develop beyond your original design. Good.
>
> Now, what stops the rest of life?
Neutral gaps in genetic function. The intelligent mind can evolve,
learn and grow over time. The information in DNA, being mindless and
being "guided" by a mindless nature, cannot evolve. It is very
similar to the information code in computers. Computers use a code of
zeros and ones. However, mutations and functional selection to this
code over time will never be the basis for creating new computer
software.
> And if life can develop, how can you
> assert knowledge about how *much* it can develop, especially when you know
> nothing about the supposed designer?
Life forms can evolve new functions, but these functions are
statistically simple to evolve. It is the statistical size of the
neutral gaps that determines "how much" life forms can evolve with the
use of naturalistic processes alone.
> >However, I could program a
> >computer to write out these same paragraphs over and over again.
> >However, just because a mindless computer is now printing these
> >paragraphs does not mean that these paragraphs could arise via the
> >mindless processes of this computer. Obviously, these paragraphs, no
> >matter the source of their subsequent production, where obviously
> >purposefully designed. This quality of purposeful design can also be
> >detected by the scientific method.
>
> Ever hear of Turing Machines? I suppose those are "impossible" too.
Turing machines are not "impossible." What is your point here? How
do you think a Turing Machine is relevant here?
> >> >Many such phenomena give clear evidence of
> >> >higher intelligent input in their formation that is beyond the
> >> >mindless processes naturalistic mechanisms.
> >>
> >> Nice assertion. Why should I accept it?
> >
> >Why shouldn't you? You accept it every day when you read a book, when
> >you look at the clock to see the time, when you see a sky scraper, or
> >when you hear a foreign language being spoken or when you see Egyptian
> >hieroglyphic writing that you cannot read or understand. How do you
> >recognize design in these cases?
>
> By knowing what *humans* do. If I was on another planet with intelligent
> life forms, there is no reason to assume I'd recognize what they do as
> intelligence driven.
Yes you would, especially if what you saw was at all similar to
something that "humans do" as well as what nature "doesn't do." The
coded nature of the information in DNA is in fact very similar to what
"humans do." Humans make very similar coded systems all the time . .
. in the form of human languages, writing, and computer codes.
> >You assume design in such cases
> >because you know that humans are capable of such creations, but you
> >also know that naturalistic process are not capable of such creations.
>
> *Only* because I recognize them *as* human activities.
AND because you have never seen anything in a mindless non-living
nature produce anything even close.
> > For example, when you see an amorphous rock, you do not automatically
> >assume intelligent design even though a human could in fact have
> >formed that very rock or natural landscape. So, since humans are
> >capable of creating amorphous rocks, why not assume human design?
>
> I do not assume an "Intelligent Designer" for rocks at all, because Occam's
> Razor gives undefined, unknown and unknowable beings *awfully* close
> shaves. As to whether humans have or have not made the rocks, I will
> "assume" nothing, but I'll make a "first approximation" that the rocks I
> find on a wild shore are probably not man-made. But I might well reverse
> that when I see a rock inside a zoo cage, a museum diorama or a shopping
> mall. In short, whatever my expectations may be, I'll wait for the
> evidence.
Actually, you do assume natural causes in most cases. You do not
actually assume "nothing" as you claim. Your "first approximation" is
your initial hypothesis, your initial assumption. You will continue
to hold this initial hypothesis as "true" until you actually find some
evidence to the contrary. Occam's Razor suggest that the most simple
explanation is usually the best. This is a reasonable start. . . and
you take it. The same can be said for the theory of ID. I have never
seen anything evolve naturally that compares to the workings of even
the most simple of life forms. I have seen intelligent designers
make things that are at least somewhat similar. I hypothesize ID for
the origin of life. I hold this as true until further evidence comes
along to challenge my hypothesis. So far, no further evidence against
this initial hypothesis has been forthcoming. My hypothesis has only
been strengthened over time by the repeated challenges and tests that
have come against it.
> >Because, naturalistic processes are also capable of producing
> >amorphous rocks. You see then, you assume intelligent design as the
> >most likely cause when no known naturalistic process could have
> >produced a given phenomenon; especially when this phenomenon resembles
> >other designed creations while, at the same time, not resembling any
> >known creations produced by purely mindless naturalistic processes.
>
> No, I look for evidence.
This is evidence. You must make an initial hypothesis. You do not
simply have "no opinion" when you come across such phenomena. You are
basically suggesting that you will reserve opinion until you can find
evidence to support a naturalistic explanation. That is not
scientific. That is philosophy.
> Since we are talking about science, I look for
> scientific evidence and since the only scientific evidence is empiric
> evidence, *that's* what I look for. You are free, of course, to go outside
> science but don't try to make me believe it *is* science.
Again, you don't understand the way science works.
> >> >The origin of this
> >> >intelligence does not need to be identified in order for it to be
> >> >recognized.
> >>
> >> Yes it does. Hey, this assertion without proof thing is kinda easy, isn't
> >> it?
> >
> >It seems to me that you are mistaken. There are only two known
> >explanations for any given phenomenon. Either its origin or cause was
> >designed with the use of a mindful intelligence or it was not designed
> >and arose via a mindless naturalistic process. There is no other
> >option. If there is no known naturalistic mechanism, then a
> >naturalistic cause is NOT an automatic assumption. Without a known
> >naturalistic cause or mechanism, the possibility of design clearly
> >comes into play.
>
> In philosophy or religion, perhaps. Science takes evidence.
Again, I suggest some reading on how the scientific method works.
> >In fact, if the phenomenon at hand does in fact
> >resemble other designed phenomena, then design is not only a possible
> >explanation, but it is a likely explanation.
>
> Speaking philosophically (just as you are), I disagree. I accept a
> practical empiricism largely because science has a history of *working*.
Science is not limited to proposing mindless naturalistic
explanations. Period.
> It *explains* the universe in a incredibly successful and widely useful
> manner.
Yes it does, but we disagree on exactly what *science* is saying. The
scientific method for me gives evidence of ID. So yes, we both agree
that science is a very powerful tool to help us to understand this
universe that we live in. We just disagree on exactly how science
works and what it says about this universe.
> No other system of human though has such an extraordinarily track
> record in opening up knowledge to humans. That is good enough for me to
> not want to screw up that underlying process of science. No one is denying
> you your philosophy or beliefs. I don't care if you want to believe this
> stuff. I do, however, object to political attempts to inject it into
> public schools at my expense, which is, as far as I can see, the one and
> *only* activity that ID "researchers" have been engaged in.
You see, I believe that science is on my side. You think that it
supports your beliefs. We both must have "faith" in our own beliefs
about what the scientific method is telling us. Interpretation is
necessary when using the scientific method. This means that human
passion and bias comes into play. Human theories are no more than
interpretations of the evidence. They are in fact belief systems or
systems of faith. We both think we have the "correct" interpretation.
However, to say that philosophical and religious truths are beyond
the reach of science is simply mistaken. The search for all forms of
truth can in fact employ the scientific method and can therefore be
"scientific."
> >> >The inability for any known naturalistic process to
> >> >produce a given phenomenon is itself evidence of intelligent design.
> >>
> >> You've found out how to prove a negative? Have you alerted the
> >> philosophers and logitians yet? Do they give a Nobel for philosophy?
> >
> >No one every fully proves a negative. However, a negative can still
> >be believed in and scientifically supported based on the preponderance
> >of the evidence. Statistical negatives can be quite significant and
> >reasonable indeed although never fully provable.
>
> But this is an *extraordinary* claim. You are positing something you
> cannot even *begin* to describe, much less explain, that nonetheless you
> insist has a pervasive, even universal, unseen effect, operating by unknown
> mechanisms and which is contrary to every other explanation we've
> discovered through science, *all* of which have been naturalistic.
> Extraordinary claims must have extraordinary evidence. You, on the
> contrary, have *zero* evidence, other than pointing the empty sleeve of "we
> don't know how to do it now".
LOL - Again, saying that I have "zero" evidence over and over again
does not make it so. It seems obvious to me that you have little idea
about how the scientific method operates. You propose again and again
that the existence of a negative cannot be supported by science, but
this is really what science is all about. Scientists believe in the
existence of many negatives, based on the lack of evidence of the
corresponding positive . . . which is testable. Please, I really
cannot imagine how your mind works. Your "logic" is beyond me.
> >> >> J. Pieret
> >> >>
> >> >> The devil is in the details.
> >> >> Science explains them.
> >> >> Intelligent design explains them away.
> >> >>
> >> >> - Mark VandeWettering -
> >> >
> >> >Science or the scientific method certainly is a very powerful tool for
> >> >the searching out of truth concerning the external world. In fact,
> >> >there is no other method that I know of that can do as good a job as
> >> >the scientific method. However, the scientific method does not
> >> >pre-suppose only naturalistic causes as explanations for phenomena
> >> >that occur in the external world. The a priori assumption of
> >> >naturalistic causes is not in fact a scientific assumption. In fact,
> >> >by using the scientific method, it is very reasonable to conclude that
> >> >intelligent design was involved with the existence of many phenomena.
> >> >The theory of ID can in fact be scientifically supported in many many
> >> >undisputable cases and situations. Forensic science, for example, is
> >> >based on this fact.
> >>
> >> So humans murderers aren't "naturalistic"?
> >
> >No. Humans are not "naturalistic" in that humans have minds that are
> >intelligent.
>
> Don't forget the bees!
Exactly. . .
> Actually, humans are "naturalistic" in the same way a bee or an amoeba is.
> We can know the full panoply of the abilities and limitations of humans
> (unlike the case of your unknown designer) to a high degree of certainty.
> While we cannot predict the exact actions of any individual human, neither
> can we predict the actions of any individual amoeba. Unlike your designer,
> we can predict with more-than-adequate precision the methods, means and
> even motives of humans and empirically study them in depth.
Humans have an intelligent mind that can manipulate nature in a way
that mindless natural processes cannot act. That is the difference.
Humans are in fact capable of ID while a mindless nature is not. How
you can even TRY to argue this point is beyond me. If human
scientists alter the genetic information in another life form, or even
in their own bodies, this alteration was the result of ID, not a
mindless naturalistic process.
> >The processes of a mindless nature have no purpose or
> >deliberate intelligence. Such mindless purposeless processes are
> >supposed to have given rise to life as well as all the various life
> >forms that we see around us. The current theory of evolution does not
> >allow any intelligent processes to be involved. Any time human
> >tampering is involved in the "change" of genes, this is not
> >"evolution" because it is not "naturalistic" change. You do
> >understand this point I hope because it is vital to my argument.
>
> Yes, you are setting up your defense for when (and I think "when" is the
> operative word here) science does demonstrate abiogenesis.
What? If humans direct the formation of molecular structures to form
some variation of a life form, this would not be "evolution" but ID.
Don't you understand this?
> >> >So, to suggest that the origin of life must, by
> >> >"a priori" definition, have a naturalistic cause . . . is really
> >> >scientific heresy. Mark VandeWettering is obviously clueless, a
> >> >devoted disciple of the religion of naturalism. If I were to propose
> >> >ID as an explanation of the origin of the wristwatch on my arm, would
> >> >that be "explain it away"? or would it be a scientific explanation of
> >> >the evidence?
> >>
> >> No, the proposal of an *unknown* and *undescribable* manufacturer whose
> >> methods and means of building watches is *unknown* and (apparently)
> >> *unknowable* (since no one has proposed any way of investigating the ID
> >> "designer") is *not* a scientific explanation, anymore than proposing to an
> >> ME that a ghost killed someone is. And yes, saying god created your watch
> >> *would* be explaining it away.
> >
> >No, it wouldn't. You need not know the identity of a designer at all
> >to reasonable know that intelligent design was involved in its
> >formation. No one need propose that the Christian God created life,
> >or my wristwatch to know that SOMEONE with an intelligent mind did
> >create both life and my wristwatch. I need not know who, exactly, did
> >it to know that some mindful intelligence was in fact involved in its
> >formation.
>
> Where have I heard this before? Oh yes, this is the nth time you've said
> this. It is also the nth time you've failed to provide evidence.
Again, for the umteenth time, read the discussions about B.G. Hall's
E. coli experiments for the "evidence" that you say I'm not providing.
> >To require direct knowledge of the actual identity of the
> >designer before one might be able to propose design is a ridiculous
> >argument. I have no idea why it is such a common argument. How on
> >earth can the SETI scientists be looking for signs of intelligent life
> >in outer space if they don't know the identity of the origin of these
> >signs of intelligence when they find them?
>
> Because we are looking for aliens who would do what *humans* do. Ones who
> would use technology just like ours to send electrical/magnetic signals
> into space just like we do. Any *other* intelligent alien, not using that
> technology for that purpose, will be invisible to SETI. It is *just* like
> looking for an unknown murderer. We know what type of being, with a
> specific set of abilities and limitations, even if we don't know the exact
> individual. If that murderer happens to be a ghost, we'll never catch him.
Yes, and what would you call the coded information contained in DNA if
not something very similar to what "humans do"?
> >> Ah, "reasonable" . . . as in the one you *prefer*, even if you don't have
> >> evidence for it.
> >
> >The evidence is clear. It seems that your own preferences might be
> >blinding you to the correct meaning of the evidence, but bias is a
> >problem for everyone to one degree or another.
>
> So everyone who disagrees with you is biased? Does it even *occur* to you
> that it *could* be the other way around?
Of course I am biased. All humans are biased in one way or another.
It just amazes me that that there are actually those who feel that
they are purely rational in their thinking, above all biases or human
weaknesses. Bias is simply part of us, but at least we can be aware
of such personal biases.
> >> >To say that this must be the case is to be either misinformed or
> >> >deliberately insane.
> >>
> >> Damn, funny how many insane people keep getting those research grants,
> >> Nobel prizes in science and all the rest, isn't it? . . .
> >
> >Isn't it though ; ) But, this is an argument based on the authority
> >and supposed understanding of others, not on your own ability to know,
> >understand or explain the evidence.
>
> Nonsense! All I was doing is pointing out one of those statistical facts
> you cited with approval above. The *vast* majority of scientists find it
> perfectly possible to do perfectly good science without once positing "non
> naturalistic" forces or agents.
Yes, but I disagree. I do not think that the vast majority of
scientists are correct in their thinking.
> For you to indiscriminately call *all* of
> them "insane" cannot help but raise issues of *your* bias, at the very
> least, if not bring up images of the kooks who insist that only *they* have
> the real scientific truth [TM], hidden right underneath their tin foil
> hats.
I'm not saying that all of them are insane. Many of them are quite
brilliant indeed. I may in fact be the insane one. However, that
possibility does not help me to understand what the "vast" majority of
scientists claim to understand. I am doing my own thinking and I am
not going to "just believe" something because it is a majority
opinion. You may take great faith and comfort in the notion that you
are with the majority of scientists here, but that just doesn't do it
for me.
> >You are basically saying, "How
> >can so many brilliant scientists be wrong and you, an ignorant nobody,
> >even hope to have any concept of what might be going on?" This is a
> >lame authority-based argument that really has no explanatory value.
>
> Oh, well, in for a penny . . .
>
> "A man does not attain the status of Galileo
> merely because he is persecuted;
> he must also be right."
>
> --Stephen Jay Gould
Yes. . . finally a quote I can agree with. Time will tell.
Yes I have. You just haven't taken the time to read it.
> And I'm tired of chasing after you as you run around as fast as
> you can, hoping no one will see that you are going nowhere. Your argument,
> no matter how many times you repeat it, all boils down to this: "if you
> can't demonstrate I'm wrong, it must have been goddidit".
That is the scientific method. If the hypothesis is testable, and yet
you cannot demonstrate that it is wrong, then it gains in predictive
power. The conclusion follows that with each test that fails to
counteract the hypothesis, the "correctness" of the hypothesis
remains.
> >Sean
>
> ---------------
> J. Pieret
> ---------------
>
> The political motivation behind the Wedge Strategy:
>
> "Religion is the opiate of the masses . . .
> and that is a _good_ thing."
>
> -- Bobby Bryant --
Yes, especially if one's particular religion is found in the, "search
for truth."
Sean
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
On Thu, 22 May 2003 22:14:02 +0000 (UTC),
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
[snip]
>There are of course those like Ian Musgrave who suggest that
>increasing complexity is not an issue because it only requires the
>addition of small functional sequences onto previously functional
>sequences.
Me, and those who professionally study enzyme structure and function.
Davidson JN, Peterson ML. Origin of genes encoding multi-enzymatic
proteins in eukaryotes. Trends Genet. 1997 Jul;13(7):281-5.
>He uses the example of adding cat to hat to bat to get
>something like, "cat hat bat."
The example was "cat sat mat"
>What Ian forgets is that the order and
>integration of even separate protein sequences is important.
No, I and the other biologists who study protein structure and
function haven't forgotten it, because not often is it actually
important. There are a wide range of enzyme multi unit structures
where the order of units is unimportant. There are also a number of
multi unit systems where the order and integration evolved after they
agglomerated (the ion channel super family is an example). The there
is the AAA atpases, where the order evolved first from simpler
subunits, and these already ordered subunits fuse.
Beware of line wrap, some assembly may be required.
And sometimes, banging together two unrelated protein sequences in any
old order generates a novel function, sdic, the sperm specific dynenin
gene is a good example of this.
>Really now, what does "cat hat bat" mean?
Using the real example "cat sat mat", the meaning is obvious, "cat mat
sat" will work just as well. As I said introducing the original
example, I'm using Indonesian grammatical rules as they more closely
reflect the flexibility of the protein language.
"cat hat bat" would likely be more like "the cat is on the hat over
the bat" in English. The meaning is somewhat ambiguous*, just like the
original fusion of two half barrels made an alpha/beta barrel protein
that could synthesize parts of both the histidine and tyrptophan
pathway, and later duplication and mutation established the separate
HisA and TyrF enzymes.
*(unless you grew up in the tropics, like I did, and bats and their
interaction with cats is exceedingly obvious, especially after you
have captured a pesky bat in a handy hat)
>Each of the words by themselves
>does in fact have a recognizable function, but the order in which they
>are put together is also important for a collective "higher" or more
>"complex" word function. Not just any order will do. Just as not any
>order of amino acids will make a functional protein, so, not just any
>order of individual proteins will make a higher collective function
>either. The same problems apply.
Try repeating this to you self several times. "Biochemistry is not
English". The rules are _far_ more flexible than you think. And many
rearrangements of biochemical systems that you would intuitively
expect to produce nonsense produce novel functions, the Sdic genes is
an excellent example of this.
(biochemistry is more like Shakespearian English, where spelling was
an optional extra (people would commonly spell the same word two or
more ways in the same document) and grammar far more flexible. But
even then the flexibility of biochemical systems is much greater)
>Certainly, there are certain
>functions that work very much like cascading systems, where the
>function as a whole is not irreducibly complex. Take one part away,
>and the rest of the cascade will continue to function just fine . . .
>like a series of dominos.
And there are many examples of cascade system that work just fine with
smaller numbers of pieces, see the article on evolving immunity at
www.talkdesign.org
>However, many functions in living systems
>are not like cascades. Behe describes many of these.
Actually, he describes only two, one, the cilia, is readily shown to
work with whole chunks missing.
>A flagellum is a great example.
Yes it is, have you read my article on it
http://www.health.adelaide.edu.au/Pharm/Musgrave/essays/flagella.htm
(I promise to finish the new version with all the new info on
archebacteria and gliding motility systems Real Soon Now)
>All of the 60 or so parts in a flagellum are needed
>to be in the right place at the right time all working together at the
>same time (not in a series like a cascade), in order for the
>collective function of motility to be realized.
Not even vaguely true (many systems have fewer or more than the
canonnical 60), a huge chunk of that 60 is the "plug and play"
chemosensing system, which turns up in all manner of other systems
(including, tantalizingly, the secretion-based gliding motility
system, could it just be possible the eubacterial secetion-based
swimming motility system evolved from a secretion-based gliding
motility system which in turn evolved from a simpler secretion system,
like the archebacterial flagella did?).
Bacteria without the chemosensing system do just fine. They also do
fine without the turning mechanism. You can get rid of the ATPase and
bacteria swim happily. Get rid of the motor proteins (MotAB, which are
related to a range of proteins which energise secretion) and the
flagella stops (but it still continues secreting, and anchoring to
substrates via contact ahesion, two of the flagellas OTHER important
functions), get rid of the flagella filament, and the bacteria doesn't
swim (but they DO continue secreting one of flagellas other important
functions).
The core of the flagella is the rivet secretory system (which is made
up of a number of duplicated proteins, which can function
independently as a secretory system just fine. All the other bits are
independent proteins "bolted on" later, which could be "bolted on" in
any order.
>Take any one part
>away, and the function of motility will not be there at all, not even
>a little bit.
As we have just seen, this is just not true.
>There are those, such as Ian, who suggest that the
>various parts in the flagellum do in fact have other functional jobs
>within the cell, but how do these other jobs help with the collective
>evolution of bacterial motility?
See my article above, but briefly, adding the MotAB secretion
energizing system to a simple secretory system will energise better
secretion, adding the flagellal whip improves delivery of secreted
products (which is why several of the virulence secretory systems have
them), a few mutations make the whip move jerkily, which is great for
swarming/gliding motility (which flagella are still involved in) and
later fine tuning provide swimming. The Che chemosensing system can be
bolted on at any time.
>For example, the individual words,
>"cat and hat and bat" each have an independent function within the
>English language system, but that doesn't make them any closer to a
>collective function when put together. You see, the non-organized
>dumping of a bunch of individually functional parts into the same area
>will not make them self assemble to form a more complex collective
>function the same as dumping a bunch of fully formed amino acids into
>a vat is not going to mean that they will self assemble into anything
>functional at all.
Strangely enough, you are completely wrong about this,
Ron Okimoto
>
> > > Thanks for the note. However, I'm not really here to convince anyone
> > > of anything. . . although I don't mind if I end up sparking some
> > > question of doubt concerning current evolutionary dogma. Basically
> > > though, I'm really here for my own interest and benefit to see what
> > > the best arguments are from those who ardently believe in evolution
> > > and the doctrine of naturalism. So far, I'm less than impressed.
> > >
> > > Sean
> >
> > To improve your impression all you have to do is take the best piece
> > of evidence for your alternative and compare it to the evidence that
> > we have that tells us something else.
>
> That's what I'm doing . . .
Before I go to the trouble of answering the long post let's clear up
some points here.
You obviously do not know what an honest argument is or what evidence
for your position is. The evidence that you put up is so lame that it
doesn't count as serious evidence. Just think about what you put up
as evidence. They are just assertions backed up by nothing. You
can't just say there are 60 proteins in a flagellum so that is proof
that there are 30 gaps you have to cross. You have to demonstrate
that there are gaps. You never do this. You never present a single
gap that is neutral that had to be crossed. Why should anyone believe
that there are 30 if you can't present one with evidence backing it
up?
I can't believe that you are an MD. How do you make a diagnosis? Do
you use evidence that lame to make a diagnosis or do you just look up
the symptoms in a book and let someone else tell you what is wrong.
If you thought about it you do not use lame evidence like you present
to make a diagnosis. If you did you would be a fool. You have to
verify things. Do tests, get results etc.
You can use estimates like these to give yourself a general direction
to head, but you have to verify the inference before you cut someone
up. How do you function if you think that the stuff you come up with
is really evidence of enough value to do anything with? You are as
bad as Nowhere man. He doesn't know what evidence is either. He just
thinks that whatever sounds reasonable to him is evidence. Evidence
is something that anyone can use to evaluate a problem, no matter what
their bias. Bias only affects the interpretation of the evidence, but
the evidence should be something that anyone can check out and see
that it is true. Where are three consecuative neutral gaps that have
to be there in the evolution of the flagellum. You know that they
have to be consecuative because once they become selectable you have
to start over. I'd settle for just one verified neutral gap and the
method that you determined that it had to be neutral.
Your evidence is bullshit. Demonstrate that it is not.
>
> > All you have to acknowledge is
> > that the evidence for the scientific explanation is so much better
> > than anything that you have that your position is laughable.
>
> This sentence is kinda mixed up, but I do get your point. However, I
> do believe in the "scientific explanation." I just don't believe in
> your view of science or in the popular views of many scientists.
> However, just because my position is unpopular does not mean that it
> is not scientific or that it is wrong. You can say, "You're wrong
> you're wrong you're wrong . . . " until the cows come home, but simply
> saying something over and over again doesn't make it so. You have a
> habbit of spouting off great statements like this without a shred of
> evidence to back yourself up.
If you don't know what evidence is how can you claim to believe in the
scientific explanation?
You can demonstrate that I am wrong by just presenting one piece of
evidence for your model, that I can't demonstrate is worse than the
evidence that we have for biological evolution. Your neutral gap
evidence is so lame that it doesn't even count as evidence. Just the
succession of lifeforms in the fossil record is so much better than
that lame piece of evidence that you should be ashamed to put it
forward. You can't even demonstrate that the neutral gaps exist. We
have real fossils, and the original order of the fossils was put
together by creationists and guess what the order hasn't changed much
since then.
>
> > You can
> > poke at bits like the Neandertal data, but you can't ignore the vast
> > majority of molecular data that says that the Neandertal example
> > amounts to nothing by comparison.
>
> There are no mountains of molecular data that explain how naturalistic
> molecular evidence happend or is happening. The evidence is actually
> strongly in favor of ID. Similarities do not support naturalistic
> common descent any more than they support ID. The differences are
> what are important here and these differences in many wide ranging and
> very complex functions within life forms simply have no reasonable
> naturalistic explanation.
Yes, every laboratory experiment that is mutation analysis. We
constantly verify that the types of changes that we see between
species occur regularly in the lab. This is so much better than any
evidence that you have that it didn't happen, that it should make you
wonder about your position, but since you are so brain dead about this
subject you will just blow off the fact that we observe these changes
happening. There is no evidence that mutations were different in the
past. There is a mountain of data that is consistent and verifies
that the changes that we see could have happened. What equivalent
evidence do you have that things happened the way that you think?
Present this evidence.
It is not the similarities that support common descent over ID it is
the specific pattern of similarity that demonstrates that certain
lifeforms preceded others in a specific pattern that basically
conforms to other data that we have from the fossil record and
morphological comparisons. The only ID model that this is consistent
with is the one that Dembski and Behe support that common descent
happened and that life has a long history and that some designer is
tweeking it from time to time, even if we can't see any tweeking at
the momment.
Both Behe and Dembski claim what you claim about complex systems, but
there is one problem, they are full of baloney. You can demonstrate
that this is not true by showing us where either of them or any ID
proponent has ever verified that assertion. ID is a basket case
psuedo science because the people spouting it can't do anything to
verify what they claim. If you think that this isn't true, just
present the verification.
>
> > The only reason that you are
> > unimpressed is that you are willfully ignorant of the data. As long
> > as you don't know how bad your arguments are, you consider that a
> > plus.
>
> Actually, it seems to me that you are ignorant of much of the data in
> your own camp. You spouted off about Neanderthal papers that you had
> never read and suggested explanations for molecular clock hypothesis
> that other evolutionary scientists were calling hog-wash. Then, here
> in this thread, you have spouted off about Hall's experiments without
> first having read anything more than a few abstracts. Please! I read
> quite a bit on this subject from main line science journals and text
> books. I am certainly not up on every aspect of this topic, but I
> still read a great deal about it. You should know this. I have
> quoted many journals and papers written by evolutionists. This whole
> thread right now is basically one that is discussing the work and
> experiments of B.G. Hall . . . someone who you have yet to read aside
> from a few abstracts. Again, a lot of hot air a smoke screens comming
> from someone who is sounding more and more desperate by the post.
Cross check those posts and retract this stupidity. I read those
Neandertal papers, I was the one that corrected you on them, remember?
You were the one that hadn't read them and you were using some
creationist claptrap web site for your information. I could be mixing
you up with AVE since both of you were farting around with the
Neandertal data, but I've read those papers.
I can't believe that you even claim something like this. You are
turning into someone that is really stupid or insane.
About Hall. Just give the reference where we find out that he used
the same selection procedures to find the first two mutations as he
used to find the next three that grew better. You won't be able to
come up with that reference because, just from the abstract I can tell
that he used different selection schemes to get those mutations.
Present the reference that demonstrates that I am wrong and I will
read it and retract if you are correct.
He used the color plate assay to get the first two, but the color
plate assay would be a useless waste of money once he had the first
two mutations that produced the white colonies. He stated in the
abstract that he started the experiment with the double mutant ebgab.
This means that all the bacteria in the experiment could metabolize
Lactose. There would have been no reason for him to use a clone of
this bacteria on the color plate assay unless he were looking for
reversion to no lactase activity.
>
> > If you were really interested in what the best arguments are you need
> > to start reading some science texts instead of the creationist
> > propaganda rags that you immerse yourself in.
>
> What a bunch of BS! You for one should know that I read a great deal
> of scientific texts as well as popular scientific propaganda. My
> problem is just that I think for myself and am not so much impressed
> with someone who calls themself a scientists or a "brilliant mind." I
> must understand for myself before I accept it. And, so far, the
> theory of evolution simply makes no sense to me as it stands. I am
> not ignorant of its claims or of the evidence that it often used to
> support it, I just do not see this evidence as really supporting the
> theory of evolution at all. . . but rather the theory of ID.
You could be the first one to ever present a scientific theory of ID.
Please do.
What does the fact that absolutely no one has come forward with a
scientific theory of ID tell you about your assertion above. If
someone had a scientific theory of ID why didn't they present it at
Ohio or Georgia or Kansas?
If you are just assuming that there is a scientific theory of ID you
are being misled. Even the Discovery Institute hasn't presented one
for evaluation, so where are you getting your scientific theory of ID
from?
The rubes on Ohio board went on TV and in the newspapers saying that
there was a scientific theory of ID that they were going to teach, but
once the Discovery Institute reps (Meyers, the head of that department
was one of these reps) came to town and gave their pathetic speel,
they had to change their claims.
What was sad was that after it was demonstrated not to be science,
some of the board memebers wanted to teach ID in the social science
class, and some wanted to change the definition of science so that
they could teach things like ID as science. The problem is that
voodoo and astrology would be considered science under the new
definition. ID would bring in some pretty good company with it. You
can't get anymore dishonest or pathetic than that.
>
> > You know for a fact
> > that you can't trust creationist material, but that is all that we see
> > out of you.
>
> This is also ridiculous. There is a lot of ID material out there that
> is very good and trustworthy. You just have to be critical of all
> material that you read, to include popular mainline scientific
> material with is often just as badly biased and poorly thought out as
> the worst that comes from the YEC camp.
Name some very good ID material. Really. Remember to include all
that evidence for there model.
>
> > How is that learning anything about the issue except it
> > tells you how bad the creationist arguments are.
>
> Actually, man YEC arguments are extremely good. Such generalizations
> aren't very convincing.
Present one YEC argument that you consider to be extremely good.
>
> > Present the honest
> > creationist argument that you claim exists somewhere.
>
> I have been presenting such arguments. My own questions here are my
> own and they are honest questions on my part. So, here is your answer
> . . .
Where are these honest arguments? Stupid honest questions are just
stupid honest questions. They don't mean anything except to
demonstrate that someone is ignorant enough to get sucked in by
someone elses dishonest arguments.
Where is that scientific theory of ID and who told you that it
existed? The claim that there is a scientific theory of ID may be an
honest argument, but it is stupid and it is wrong.
>
> > Who are these
> > honest creationists and what is the evidence for their beliefs of what
> > we see in nature.
>
> I am an honest creationist. There are also many more. I work with a
> lot of them here at Loma Linda University. Leonard Brand, a geologist
> here, is another very intelligent and honest creationist. I would say
> that Michael Arct, geologist, and Prof. Javor, biochemist, are a
> couple more. Behe is probably another. However, I can only really
> speak for myself. It doesn't really matter to me if all other's in my
> own camp are idiots or liars (and most of them are not), I am at least
> being honest for myself and that is what really matters.
There are a lot of honest religious scientists, but name any that
support your lame creationist arguments that understand the arguments
enough not to be fooled by the creationist scams. If they write these
scams they are either fools or dishonest creationists. Present one
honest creationist argument. I keep requesting it, but you never
present it. What creationist argument have you found to be honest?
You've been bashed up the side of the head with enough to know that
most of them are bogus, so give us the honest ones. We aren't talking
about honest arguments that are just wrong. Creationism is full of
guys like you that spout stuff because they don't know any better.
Just an honest valid argument. Have you ever found one?
You may be honest, but that only means that you are stupid. It can't
just be ignorance. You have to be pretty stupid to think that what
you consider to be evidence is any good. That is just a fact. Take
the best piece of evidence that you have presented and verify that it
means what you claim that it means.
I really can't believe that you think that the fact that there is 60
proteins in a flagellum that, that is evidence for the neutral gaps
that you claim are there. That is only evidence of your ignorance.
Really, just verify one neutral gap. What protein or protein
combination that it had to occur in and how you determined that it had
to be neutral.
>
> For more of a list see:
>
> http://www-acs.ucsd.edu/~idea/scidoubtevol.htm
>
> > I've requested this several times because you keep
> > telling us that these people exist and that they have valid arguments,
> > but we never see any names or any valid arguments.
>
> This is total BS. I have mentioned many names before, to include the
> names listed above. I have also listed many evolutionists as being
> honest and intelligent and I discuss many of their ideas and papers.
> You evidently have either a very limited or a very selective memory.
> You simply do not agree that these ID scientists have good points, but
> that is rather a matter of opinion. You haven't got anything, as far
> as I can see, to argue effectively against these ID arguments. . .
>
> > Ron Okimoto
>
> Sean
Where are the honest valid creationist arguments. I haven't seen any.
Refresh my memory and just present one. Why couldn't you present one
in this response? Is it so hard? You spent quite a bit of verbage
claiming that they exist, so why not present one? You are the one
that is BSing. If you had one you could just present it without all
the bullshit. If you really think that ID has any honest arguments,
why didn't they present anything to teach in Ohio when it was
requested of them. The fact is that they haven't got a single valid
argument. They know this, so anything that they claim that is
otherwise is dishonest.
You claim that things would have been different if you were in Ohio,
but the only thing that would have been different is your own side
would have bound and gagged you and run you out of town before you
made them all look like a bunch of fools. Once you make the specific
claim that you can teach something, you have to be able to support
those claims. Everyone else there would have more on the ball than
you and would have known that there wasn't anything that they could
support teaching. You only claim that these things exist because you
are either stupid or ignorant. I used to lean toward ignorance, but
since you are unable to understand the concept of evidence I'm
starting to lean toward stupidity.
What would you have taught about ID and how would you have supported
those assertions with evidence? Remember this is for a science class,
not theology.
You can do a google seach for ARN and bring up that ID board. There
was a thread a couple of weeks ago where someone asked what ID had
accomplished. The answer is basically nothing, but a bunch of new
buzzwords. IC, EF, a new law of thermodynamics etc. All
unverifiable. Just think what ID could have if they could verify a
new law of thermodynamics. What do you think of the guys that would
propose a new law of thermodynamics based on just about nothing? It
is just sad that they have as much evidence for a new law of thermo as
they do for anything else they are spouting.
Rereading this post, I'm probably too hard on you, but you are acting
pretty strange. You have no concept of what decent evidence is and
you are making mind boggling stupid assertions. If you don't think
that they are stupid defend them.
Ron Okimoto
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
On Thu, 22 May 2003 22:14:02 +0000 (UTC),
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>You see, the non-organized
>dumping of a bunch of individually functional parts into the same area
>will not make them self assemble to form a more complex collective
>function the same as dumping a bunch of fully formed amino acids into
>a vat is not going to mean that they will self assemble into anything
>functional at all.
But if you dry that solution out on a warm rock, the amino acids self
assemble into hydolases, phosphatases and a range of other enyme
activities.
Neat eh?
Ron Okimoto
> roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.03052...@posting.google.com>...
> > seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03052...@posting.google.com>...
> > > roki...@mail.uark.edu (Ron Okimoto) wrote in message news:<63afe69c.0305...@posting.google.com>...
>
> > It looks like I quit too soon. I do screw up later on so I have to
> > continue.
>
> Welcome back . . .
>
> > The Hemoglobin citation is on page 63 of the 1981 version of Stryer
> > second edition Biochemistry. I too Biochem in 78-79 and I don't
> > remember the phrase "nine positions are nearly invariant." There is a
> > table with the nine amino acid residues, so I don't know why I
> > remember it as a lower number of invariant amino acids. It could be a
> > change between the first edition and the second, or I could just be
> > misremembering.
>
> It probably was a misread, although I do not have that addition of
> Stryer readily available to me. The reason why I think this is that
> when considering the heme pocket region alone as only part of the
> hemoglobin molecule (adult human hemoglobin of course consists of 2
> alpha sub-units of 141 residues each and 2 beta sub-units of 146
> residues each), there are around "43 amino acids" that are "invariant
> in 60 species". The stated reason for this is that "Mutations in
> these regions interfere with normal cooperative O2 binding." Other
> references go as low as "48 residues" as invariant, but none of them
> go as low as "nine positions are nearly invariant" as you suggest.
Someone else gives the full citation from Stryer and it says what I
claimed. Your source is a botany course syllabus, and it looks like
they may be confusing similarity with "invariant" amino acids. The
study would also have to consider the 60 species used. If they were
all primates or all mammals all the molecules would be fairly closely
related. The fact is that hemoglobin molecules are more diverse than
this. You can pull up the drosophila sequence and compare it to
mammals and fish etc using Genbank. I've looked at the drosophila
sequence and it is difficult to even find where it could match
mammals. I was going to make the comparison, but with so little
similarity it would be too much work even with the programs that I
have in the lab.
I'll wait to answer the rest of this post once you cover evidence and
probably the first half of this post that you haven't gotten too.
If it is so hard to evolve these activities and if Lactase and the
flagellum were designed, why do you think the designer would make it
possible for the bacterium to steal food from babies and make
pathogens more effective. Maybe these things evolved when the
designer wasn't looking?
Ron Okimoto
Sean Pitman
> On Thu, 22 May 2003 22:14:02 +0000 (UTC),
> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>
> >There are of course those like Ian Musgrave who suggest that
> >increasing complexity is not an issue because it only requires the
> >addition of small functional sequences onto previously functional
> >sequences.
>
> Me, and those who professionally study enzyme structure and function.
>
> >He uses the example of adding cat to hat to bat to get
> >something like, "cat hat bat."
>
> The example was "cat sat mat"
Ok. . . So are you saying that my use of different words makes an
important difference here?
> >What Ian forgets is that the order and
> >integration of even separate protein sequences is important.
>
> No, I and the other biologists who study protein structure and
> function haven't forgotten it, because not often is it actually
> important. There are a wide range of enzyme multi unit structures
> where the order of units is unimportant.
Not when the units are different from each other. In such cases, the
order and regulation of the coded information for the production of
these various units is important for their correct assembly into a
joint complex with higher collective function.
> There are also a number of
> multi unit systems where the order and integration evolved after they
> agglomerated (the ion channel super family is an example). The there
> is the AAA atpases, where the order evolved first from simpler
> subunits, and these already ordered subunits fuse.
>
> http://www.google.com.au/groups?q=AAA+group:talk.origins+author:zosdad&hl=en&lr=&ie=UTF-8&selm=74227462.0201220501.25140dec%40posting.google.com&rnum=1
>
> Beware of line wrap, some assembly may be required.
You do this all the time. You make statements that seem to indicate
that the method of the evolution of such structures is a clear a
crystal, when in fact no such evolution has been observed and when
even on paper there are huge gaps. The link and the papers that are
referenced by it describe the *supposed* path of more complex AAA
ATPases as well as dynein motor units. However, no such experiments
detailing this supposed evolutionary scenario have ever been performed
and even the author of this paper admits that large gaps are still
unexplained and that his discussion is just a "general outline" of
some potential evolutionary path. In other words, the entire
discussion here was one big "just-so-story."
For example, the author comments that, "Some AAA ATPases are coded for
by six genes, arrayed next to each other along the chromosome. Six
copies of the gene can occur very simply by gene duplication; what is
interesting about this situation is that the duplication allows each
copy to evolve independently, and therefore to specialize to perform
nonuniform functions in the AAA ATPase ring."
I have a few questions at this point. First off, what good is a
"simple" ATPase for a bacterium that never needed an ATPase before?
What selective advantage would an ATPase, by itself, give to a
bacterium that happened evolve it? I mean, as I understand it, the
ATPase, by itself, doesn't do much. It must be connected to something
else that can use the energy provided by the break down of ATP, such
as the dynein complex. So, to evolve an ATPase apparatus by itself is
just part of the problem. Also, the evolution of just the first
ATPase gene for the first and most simple ATPase production, is not an
easy task. Even though only one gene and only one type of protein is
needed in such a scenario, even such a relatively simple gene still
has a fairly high degree of complexity, as we learned from Hall's
experiments with E. coli lactase evolution (i.e., many of Hall's E.
coli never evolved the relatively simple lactase enzyme despite high
selection pressures and thousands of generations).
Let's move on and look at the next steps suggested by the author. The
author made the statement that, "Six copies of the gene [the original
ATPase gene] can occur very simply." This statement is at least
supported by real time experiments . . . although I would question the
degree of commonality of such events suggested by the author's
statement. However, the author goes on to claim that each of these
copies will easy evolve independently and therefore specialize to
perform nonuniform functions in the AAA ATPase ring." Now, this is
quite another thing entirely. Where has this been experimentally
demonstrated in real life? From here on out the entire scenario is
just one big made-up story on how things "must have happened." There
is no real time research or actual laboratory experiments here showing
this sort of evolution. And yet, the author concludes, "If you
blinked, you might have missed it: we just moved from non-IC to IC
using very simple, well understood genetic processes." But, where is
the "well understood" genetic process in evolving each of the copied
genes to make an entirely different ATPase apparatus that is in fact
irreducibly complex? This is the entire issue and the author simply
makes a statement that it just happens. No explanation or
experimental data is given to support this statement for the case of
complex ATPase evolution.
Interestingly enough, the author then moves on to describe the next
step of dynein evolution. He writes, "So where does dynein come in?
Well, it turns out that the dynein heavy chain, which is coded by a
single large gene, has six AAA-like domains in it. This can be easily
explained if the genes of a six-gene, asymmetric ATPase were merged
into one huge gene. And once this has occurred, additional
complexities can evolve."
All this is just one huge just-so-story. Where has this phenomenon
ever been observed? Also, just because something is "like" something
else does not mean that they have the same function or that gaps of
neutral function are not involved in getting from one functional
structure to another structure that is "like" the first one. Again,
even if this could and did happen and an already evolved "asymmetric
ATPase merged into one huge gene", where is the evidence that all the
other differences in the dynein complex could or would have simply
evolved? Again another "trust me" statement without experimental
demonstration.
The author goes on to explain that, "In the dynein heavy chain, the
fusion of the six AAA modules into a single polypeptide has permitted
the hexameric assembly to evolve even greater structural and
functional asymmetry, including the acquisition of the two substantial
accessory structures that protrude from the motor unit. One of these
acquired structures, formed from the region of the dynein heavy chain
between D4 and D5, comprises the 100 A stalk with predicted
[alpha]-helica coiled-coil configuration that supports the
all-important ATP-sensitive microtubule binding site. The second is
formed by the approximately 1800 residue extension onto the N terminus
of D1 that comprises the tail component of the complete dynein heavy
chain. The substantial [alpha]-helical component in these accessory
structures suggests that they may both have evolved through a gradual
extension and specialization of the much shorter
coiled-coil/leucine-zipper structure often found in the N-terminal
region of AAA proteins. Interestingly, the microtubule binding domain
of katanin also involves an N-terminal extension from its AAA
structure. However, an alternative possibility is that the microtubule
binding stalk evolved by prolongation of helices H6 and H7, which form
a short leucine-zipper-like structure in the C domain of our present
models, where it has been inherited from the NSF-D2 template. In the
simple AAA ATPase, all of the 6 subunits could hydrolyze ATP. But
interestingly, in dynein, one of the former genes (now a single domain
of the six-domain dynein protein, labeled D1) has specialized to do
the ATP hydrolysis, and the other domains act to help transmit the
resulting mechanical energy to the power stroke of the stalk."
Again, the reference here suggests that the fusion of the six modules
into one polypeptide allowed for the evolution of two more
"substantial" units to add themselves. I'm just wondering, what
benefit is this fusion of the six modules unless the two substantial
units are already there waiting, fully formed? I mean, one of these
units is described as being "all-important" to dynein function. So,
where was the selective advantage for the initial fusion? This
problem and its explanation is rather quickly glossed over with
another statement of "Trust me. . . this is how it happened." Also,
no explanation is given as to how these two vital dynein structures,
with their own independent complexity, could have easily fused with
the six-module-complex even if they were already preformed somewhere
else in the genome. Again, the order and arrangement of even
preformed units is important, even in supposed scenarios such as this.
Over and over again the author and the authors of his references use
words and phrases like, "maybe, possibly, potentially, this suggests,
most likely." Where, I ask you, is this a demonstration of anything?
I am asked to believe whole-heartedly in a "maybe" without
experimental evidence? I mean, no explanation is given as to the
previous function of these "accessory structures" and yet their
independent complexity seems fairly high. In fact, it seems so high
that the author feels the need to try and give another story as to how
their independent structures might have evolved. He comments that,
"The substantial [alpha]-helical component in these accessory
structures suggests that they may both have evolved through a gradual
extension and specialization of the much shorter
coiled-coil/leucine-zipper structure often found in the N-terminal
region of AAA proteins." Of course, this evolution would have had to
happened before the ATPase evolution and fusion of the six modules
into one. Or, where would the beneficial function be for the complex?
You see, I fail to see that the author has adequately supported his
assertion that each required step here in beneficially functional.
And, he glosses over many steps in his leaps from one step to another,
much like the many demonstration of how Behe's mousetrap could have
evolved one functional step at a time.
The author goes on to note that, "Expression constructs lacking any of
the AAA modules, or even the region of the tail component adjacent to
D1 (residues 1400-1813), appear to show no ATPase activity [11, 46].
This requirement for structural integrity of the dynein motor unit
resembles that of other members of the oligomeric ATPase class and may
indicate that cooperative interactions of module D1 with the other AAA
modules play an essential role in transferring the energy made
available at the hydrolytic ATP binding site in D1 to the microtubule
binding site attached between D4 and D5."
Obviously then, here is an "irreducibly complex" system of function,
neatly evolved by Darwinian style evolution. What a crock! The
author has used fancy language to tell one tall tale while skipping
over vital aspects of the story. Also, where has this scenario or
anything even close to it ever been demonstrated in real time? I
mean, it seems so easy, so simple. I mean, if one didn't read through
this carefully, the author is trying to make it appear as if there are
really no significant gaps in function at all between the various
steps. But, I ask you, without significant gaps to slow things down,
why don't we see such a level of evolution in real time? The
experiments here should be very easy indeed. Such an evolutionary
scenario should proceed quite rapidly without the hindrance of neutral
gaps. It seems to me that it is not observed in real time because the
complexities involved with such a scenario are far greater than you or
this author seem to imagine. Very wide gaps in function just might be
the problem. I mean, if you and this author can use words like "maybe
and could be and most likely" as sufficient enough evidence to "prove"
your point, then so can I. So, "most likely" very limiting neutral
gaps are involved here.
The auther here goes on to summarize:
"Starting point: G --> P (a simple, stand alone ATPase)
Step 1: G --> PPPPPP (a hexamer ring of 6 identical subunits)
Step 2: GGGGGG --> PPPPPP (the genes have been duplicated sixfold)
Step 3: G1-G2-G3-G4-G5-G6 --> P1-P2-P3-P4-P5-P6 (the genes have
diverged, producing an IC machine with six necessary,
noninterchangable, and necessarily interacting and well-matched parts)
Step 4: D1-D2-D3-D4-D5-D6 --> 'proto-dynein' (could have the same
function as the protein in previous step; the 6 genes have been
concatenated into one big gene with six necessary domains,
specialization of the domains continues)
Step 5: D1-D2-D3-D4-X1-D5-D6-X2 --> dynein heavy chain (this is the
dynein heavy chain; two interdomain extensions have evolved) "
"So, we've got a reasonably good and detailed outline for the origin
of the dynein motor. It should be emphasized that the 'steps' are
really major stages [major understatement]; for example, the
duplication and diversification of G1-G6 genes could have occurred one
by one; one gene duplicates and diverges via point mutation, then
another. The genes could have been linked into domains one-by-one,
also, etc. So the number of discrete 'steps' would be very much
greater. But notice that no processes other than (a) gene duplication
and (b) gradual optimization via NS of small mutations needed to be
invoked. Certainly this is still just a general outline, and will need
much development and testing in further research."
I find this summary rather humorous. The author actually admits that
his steps are each really major changes (with major gaps in-between)
and yet he has the audacity to claim that he has clearly demonstrated
that gene duplication and gradual optimization via natural selection
of "small" mutations are all that are needed. Uh, where did I get
lost? How does the glossing over of huge gaps between functional
changes explain the evolution of anything with natural selection?
Humans can cross such gaps in real life and on paper, as this author
has done, but natural selection cannot make such great leaps. But, I
do agree with the author's closing line. Certainly MUCH more
development of his explanation and a great amount of further research
is needed before his very weak assertions become anything more than
wishful thinking.
> And sometimes, banging together two unrelated protein sequences in any
> old order generates a novel function, sdic, the sperm specific dynenin
> gene is a good example of this.
Please, if you can explain this assertion with testable evidence that
is any better than can be found in the reference you gave, I am all
ears.
> >Really now, what does "cat hat bat" mean?
>
> Using the real example "cat sat mat", the meaning is obvious.
Oh, so it is important exactly which three words are used in order to
have propper meaning? Interesting. What about the order of the three
words? Would it make any difference if the sequence went, "mat sat
cat"? or "sat cat mat"?
> "cat mat
> sat" will work just as well. As I said introducing the original
> example, I'm using Indonesian grammatical rules as they more closely
> reflect the flexibility of the protein language.
Let's pose a hypothetical situation in which a cat sat on a mat in
Indonesia and someone told his neighbor about it by saying the phrase,
"cat mat sat." Now, lets suppose that the neighbor actually
understood this statement to mean that his friend speaking to him
actually saw a cat sit on a mat. Certainly this would be one of many
of such potentially meaningful phrases, given this situation. But,
do you know just how many potentially meaningful and benefical phrases
would work here? as a fraction of the total number of possible
sequences of three, 3-letter words? Are you trying to say that just
any collection and order of three-letter words would have beneficial
meaning here? There are billions of possible sequences of this length
that could have been spoken here. What fraction of all these
possibilities would carry some sort of recognizable meaning for the
Indonesian neighbor in this situation?
Also, I fail to understand how protein language is nearly as flexible
as you are suggesting. As far as I understand protein language, the
grammatical rules are quite rigid indeed. For example, explain to me
the flexible nature of the cytochrome c protein amino acid sequence.
There are around 104aa in cytochrome c. Of these, about 40% are
invariant. Another 40% are only "variant" between just two amino
acids. So, just about 80% of cytochrome c is extremely rigid. Just
about any little change in any one of 80 or so amino acids will result
in a complete loss of function. Then, the majority of the rest of the
20% of this protein can only change between certain classes of amino
acids (i.e., hydrophilic vs. hydrophobic or acidic vs. basic). As it
turns out, only a handful of the total number of amino acids in this
protein are what anyone would call widely variant. The same situation
holds true for other protein based functions such as the oxygen
delivery function of hemoglobin. Such grammatical rules seem rather
strict to me . . . much more in line with English grammar rules than
the "Indonesian rules of grammar" that you are trying to use as a
comparison. However, even with your Indonesian rules, the levels of
complexity and specificity required to transmit information quickly
become quite complex, involving larger and larger nonsensical or at
least non-beneficial gaps between various meaningful phrases. You
will admit that not just any series of words, even in Indonesia, would
make beneficial sense in a given situation or "environment." I would
think that even Indonesians are capable of getting drunk and speaking
a lot of "gibberish" that makes no sense to anybody.
> "cat hat bat" would likely be more like "the cat is on the hat over
> the bat" in English.
Or, it could equally mean, "The cat got hit with the bat into the
hat." Or, "The cat is also my hat and I am using it to bat at flies
as they go by." Or, "The cat ate the fruit bat out of my hat." You
see, this could be interpreted in English in so many different ways
that it really has no consistent meaning or beneficial function.
Proteins really are not like this at all. They are generally very
specific and get more specific as the level of complexity increases.
In fact, I am quite surprised that you would even attempt to argue
this point.
> The meaning is somewhat ambiguous, just like the
> original fusion of two half barrels made an alpha/beta barrel protein
> that could synthesize parts of both the histidine and tyrptophan
> pathway, and later duplication and mutation established the separate
> HisA and TyrF enzymes.
Again, another just-so-story, but where is your experimental evidence
to back this lovely story up? Just because two genes or genetic
sequences in different systems of function seem similar or even
identical, does not necessarily mean that they evolved from the same
gene once upon a time. The differences are what are important here,
not so much the similarities. How are the differences explained? The
similarities could equally have been the result of either a
naturalistic type of common descent or common design. The explanatory
value of both hypothesis works equally well to explain the
similarities. However, the question is NOT if naturalism can explain
the similarities, but can it explain the differences? Certainly it
can explain some of the differences, but I fail to see how it can
explain anything more than the most simple of functional differences.
This is your job, but so far, I am getting nothing but story after
story. Where is the evidence?
> *(unless you grew up in the tropics, like I did, and bats and their
> interaction with cats is exceedingly obvious, especially after you
> have captured a pesky bat in a handy hat)
Actually, I did spend several years of my childhood in the tropics.
However, even in the tropics there are different meanings to the word
"bat" as well as "cat" and even "hat". There are also a huge number
of potential interpretations to the combination of these words (Also,
these are not the only three-letter word options that there are).
Specificity in such arrangements is minimal. Information transmission
is extremely vague at best. Also, do you realize the total number of
possible three word combinations? Again, given a particular scenario
or event, what are the odds that any three words spoken by an
Indonesian will be beneficially understood? Lets say that there are
5,000 defined 3-letter words. The total number of combinations is 125
billion. Of these, how many would be "beneficial" in a given
situation? What percentage of the total?
> >Each of the words by themselves
> >does in fact have a recognizable function, but the order in which they
> >are put together is also important for a collective "higher" or more
> >"complex" word function. Not just any order will do. Just as not any
> >order of amino acids will make a functional protein, so, not just any
> >order of individual proteins will make a higher collective function
> >either. The same problems apply.
>
> Try repeating this to you self several times. "Biochemistry is not
> English". The rules are _far_ more flexible than you think.
Try repeating this to yourself, "I need to give some evidence for this
statement besides a just-so-story."
> And many
> rearrangements of biochemical systems that you would intuitively
> expect to produce nonsense produce novel functions, the Sdic genes is
> an excellent example of this.
Again, these are single protein functions that are relatively simple.
Such examples are the same as the evolution of nylonase or lactase
enzymatic type functions. I mean, even a three-atom water molecule
has the ability to "hydrolyze" many different chemicals. How can such
a simple molecule have such a hydrolytic function in so many different
environments? Because, the function of hydrolysis for many molecules
is very simple. Other molecules require something more than water in
order to be cleaved in a reasonable amount of time. Lactose is one of
these. The nature of the molecular bonds in lactose requires
something more than any 3-atom enzyme to break them apart effectively.
The complexity of what is needed to hydrolyze lactose increases from
a very simple 3-atom molecule to a molecule that contains thousands of
atoms. And yet, this lactase enzyme still has a relatively simple or
common function . . . relative other vastly more complex cellular
functions. There are many different lactase enzymes of a given length
of minimum complexity. Perhaps, given the total number of potential
enzymes of 1,000aa or less (~1e1,300), there would be enough different
lactase enzymes to make a ratio of 1 in a trillion lactase vs.
non-lactase sequences. Of course, this would be a relatively high
ratio made possible because of the relatively commonality/simplicity
of the lactase function. However, this gap of 1 trillion that exists
between functional lactase enzymes is still a gap. This gap would be
able to be crossed in short order by a population of 1 trillion with a
3,000bp section of neutral genetic real estate, but still, it would
take some time. It is a real gap. Now, try moving up the ladder of
complexity. The time needed to cross growing gaps increases
exponentially with each neutral step in function.
> (biochemistry is more like Shakespearian English, where spelling was
> an optional extra (people would commonly spell the same word two or
> more ways in the same document) and grammar far more flexible. But
> even then the flexibility of biochemical systems is much greater)
Not so. Even Shakespearian English, with all its flexibility is too
rigid to allow easy naturalistic evolution of text. Using even these
more relaxed rules of spelling and grammar, you could not program a
computer to make any sort of significant phrase evolution using random
mutation and functional phrase selection. This is basically the same
argument that Dawkins was trying to make with his failed "Methinks it
is like a weasel" computer phrase evolution. You might be able to get
a bit farther with more relaxed rules, but still, the gaps are so much
wider than you seem to realize that very quickly they would block
further functional phrase evolution and you'd be stuck. Try it. Use
your more relaxed Shakespearian rules of spelling and grammar and see
just how far you can go with a meaningful phrase evolution of 30 or so
characters. How many functional phrases can you link together one
mutation at a time? Then, consider how many of these would be
beneficially functional? You see, even in Shakespearian times, there
was a lot more potential non-sense than sense.
> >Certainly, there are
> >functions that work very much like cascading systems, where the
> >function as a whole is not irreducibly complex. Take one part away,
> >and the rest of the cascade will continue to function just fine . . .
> >like a series of dominos.
>
> And there are many examples of cascade system that work just fine with
> smaller numbers of pieces, see the article on evolving immunity at
Yes there are. However, even in these examples, there is a limit
beyond which such systems cannot be reduced without a complete loss of
all function. Even the most simple of protein functions or cascading
systems of functions is irreducibly complex. IC is a given in all
systems of function. IC is also a continuum. Some IC systems of
function are very simple. Others are more complex, and others are
extremely complex. To demonstrate how the most simple IC systems can
evolve is not the issue. Statistically, the gaps between such systems
can be crossed in relatively short order with the power of random walk
alone. The problems come when one tries to explain more and more
complex systems of function that require the crossing of neutral gaps
that are growing exponentially in size.
> >However, many functions in living systems
> >are not like cascades. Behe describes many of these.
>
> Actually, he describes only two, one, the cilia, is readily shown to
> work with whole chunks missing.
Behe describes more than two IC systems, both in his book and later in
his papers. In any case, just because you can show that a cilia can
still work with "many chunks missing" does not mean that the function
of the cilia is not irreducibly complex. There comes a point where
you cannot reduce the parts in the cilia any further without a
complete loss in cilia function. For example, you cannot get cilia
function with just one protein of say 100 amino acids no matter which
arrangement you try. Even the most trimmed down version of a cilium
that you could possibly come up with would be composed of many
proteins all working together at the same time.
> >A flagellum is a great example.
>
> Yes it is, have you read my article on it
> http://www.health.adelaide.edu.au/Pharm/Musgrave/essays/flagella.htm
> (I promise to finish the new version with all the new info on
> archebacteria and gliding motility systems Real Soon Now)
Yes, I have read your article on it and it is just not much better
than the article you referred me to above. You make a lot of
just-so-statements and leaps of faith. You really have very little
experimental demonstration to back your assumptions up.
> >All of the 60 or so parts in a flagellum are needed
> >to be in the right place at the right time all working together at the
> >same time (not in a series like a cascade), in order for the
> >collective function of motility to be realized.
>
> Not even vaguely true (many systems have fewer or more than the
> canonnical 60)
Oh yeah? I am willing to consider the evidence you have on this
point. What is the evidence here? What is the minimum number of
different proteins that are needed to produce functional motility of
any type, not just flagellar type motility? I would be curious
though, how many different proteins would you suggest as necessary to
produce flagellar type motility? What is the most trimmed-down
version of a functional flagellum that is out there? No bells and
whistles, just the basics.
> A huge chunk of that 60 is the "plug and play"
> chemosensing system, which turns up in all manner of other systems
> (including, tantalizingly, the secretion-based gliding motility
> system, could it just be possible the eubacterial secetion-based
> swimming motility system evolved from a secretion-based gliding
> motility system which in turn evolved from a simpler secretion system,
> like the archebacterial flagella did?).
This is a fine story! Where is the evidence? Sorry, but you seem to
have a lot of gap-crossing to do before your stories will float.
> Bacteria without the chemosensing system do just fine. They also do
> fine without the turning mechanism. You can get rid of the ATPase and
> bacteria swim happily. Get rid of the motor proteins (MotAB, which are
> related to a range of proteins which energise secretion) and the
> flagella stops (but it still continues secreting, and anchoring to
> substrates via contact ahesion, two of the flagellas OTHER important
> functions), get rid of the flagella filament, and the bacteria doesn't
> swim (but they DO continue secreting one of flagellas other important
> functions).
Just because a particular setup has multiple functions does not say
anything about the complexity of any one given function, such as
motility. You can say that a collection of parts that is also needed
for flagellar-type motility also has other important functions, such
as a secretory function, but that doesn't help you when it comes to
the motility function. The question is, how many parts, at minimum,
is needed for the *motility* function of the flagellar apparatus? I
know I know, you try to use the other functions as a series of
beneficial steps on the road toward the motility function, but you
simply skip over far too many gaps in your discussion of how this is
supposed to happen. In any case, the fact of the matter is, the
motility function itself, by itself, is irreducibly complex. No doubt
about it. If you reduce the number of parts too much, the motility
function *suddenly* vanishes. And, if you replace the last required
part, the motility function *suddenly* appears. That is IC.
> The core of the flagella is the rivet secretory system (which is made
> up of a number of duplicated proteins, which can function
> independently as a secretory system just fine. All the other bits are
> independent proteins "bolted on" later, which could be "bolted on" in
> any order.
Again, list the minimum number of parts needed for the MOTILITY
function. Not for other functions, but for the motility function of
the flagellum. Now, if you could show that each of the other
functions formed a gapless series of small mutational changes to
arrive at the motility function of the flagellum, then you might have
something. However, you really have far too many gaps to make your
story convincing.
> >Take any one part
> >away, and the function of motility will not be there at all, not even
> >a little bit.
>
> As we have just seen, this is just not true.
Actually, we have not seen this at all. You have not explained in the
least how the motility function of the flagellum is not IC. You have
blown a lot of smoke into the air, but really, the motility function
of the flagellum is still IC.
> >There are those, such as Ian, who suggest that the
> >various parts in the flagellum do in fact have other functional jobs
> >within the cell, but how do these other jobs help with the collective
> >evolution of bacterial motility?
>
> See my article above, but briefly, adding the MotAB secretion
> energizing system to a simple secretory system will energise better
> secretion, adding the flagellal whip improves delivery of secreted
> products (which is why several of the virulence secretory systems have
> them), a few mutations make the whip move jerkily, which is great for
> swarming/gliding motility (which flagella are still involved in) and
> later fine tuning provide swimming. The Che chemosensing system can be
> bolted on at any time.
Exactly what mutations make it so that the MotAB to be added to a
simple secretory system? Then, exactly how is this flagellar whip
added? What mutations, exactly, would be needed to make this whip
move jerkily?
You have far too many gaps in your story. Also, there is no
experimental demonstration of any of this much less the evolution of
any motility system, not even of the flagellar type that you claim
would be so easy.
> >For example, the individual words,
> >"cat and hat and bat" each have an independent function within the
> >English language system, but that doesn't make them any closer to a
> >collective function when put together. You see, the non-organized
> >dumping of a bunch of individually functional parts into the same area
> >will not make them self assemble to form a more complex collective
> >function the same as dumping a bunch of fully formed amino acids into
> >a vat is not going to mean that they will self assemble into anything
> >functional at all.
>
> Strangely enough, you are completely wrong about this,
I'm sure you have some evidence to back this up? See below . . .
> >You see, the non-organized
> >dumping of a bunch of individually functional parts into the same area
> >will not make them self assemble to form a more complex collective
> >function the same as dumping a bunch of fully formed amino acids into
> >a vat is not going to mean that they will self assemble into anything
> >functional at all.
>
> But if you dry that solution out on a warm rock, the amino acids self
> assemble into hydolases, phosphatases and a range of other enyme
> activities.
Again, hydrolases, phosphatases, and a range of other single protein
enzymes that randomly self-assemble in this manner, and in other
documented ways, are universally very simple in structure and
function. Again, the 3-atom water molecule has hydrolytic activity on
many compounds. Why? Because this is a relatively simple function.
I am betting though, really putting myself out on a limb here, that
your warm rock proteins never self-assemble into a flagellar
apparatus, or any other such multi-protein complex with a motility
function or any other such function of comparable complexity. Why?
Because, the spectrum of function complexity is very wide. Some
functions can be performed by almost anything while others are far
more specific. For example, lets say that I want to hammer in a nail.
I can use a hammer or brick or a rock or a book or my hand. All of
these will in fact "work" in this situation to one degree or another
to give the desired function. Why? Because the desired function is
relatively simple. However, none of these will help me unlock my car
door if I forgot me car key. Why? Because the function of unlocking
my car door is far more complex than the function of hammering in a
nail.
Really, you do have your job cut out for you here. I am still quite
confused. . .
> Neat eh?
And simple. . . eh?
> Cheers! Ian
Cheers! ; )
Sean
catshark
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
>catshark <cats...@yahoo.com> wrote in message news:<s4mocv86n07qemcav...@4ax.com>...
>> On Wed, 21 May 2003 20:18:09 +0000 (UTC),
>> seanpi...@naturalselection.0catch.com (Sean Pitman) wrote:
[Metasnip]
This has become nothing but Argumentum ad Nauseam on your part and, having
a life myself and some consideration for others who might blunder on this
thread and be overcome by obfuscation induced coma before they can hit the
'skip to next unread message' button, I am going to recapitulate some of
your claims, without the welter of words to obscure the real import (though
I cannot help this being long, given your "scattershot" approach):
To begin, it appears that you are claiming that ID is scientific. At the
least, you try to equate it with forensic science and SETI. You also speak
of a 'design hypothesis,' as if ID is a legitimate part of science. But
many of your arguments appear (to me at least) to be clearly arguments from
philosophy (of a sort) or based on supposedly "common" sense, such as
geologic patterns discussed below. You may find these arguments
persuasive. I don't. In any case, they are not part of science. The
issues I intended to discuss are limited to whether such arguments are
properly scientific hypothesis and theories, derived from empiric evidence,
or whether you (and the rest of the IDers) are conflating science into, and
trying to infect it with, your theistic beliefs.
You claim that all "naturally occurring patterns have the ability to
self-assemble" but you nonetheless claim that rocks of a certain type
and/or arrangement ("perfect geometric pattern, with each rock separated by
a one meter distance, forming a perfect square one mile on each side . . .)
can be taken as designed.
It should first be noted that even Behe has more intellectual integrity
than to argue that. In _Darwin's Black Box_, p. 195-196, he discusses what
would happen if we went to an alien planet and found *steel rods*
(something that, in our limited knowledge of the vast universe, *only*
result from manufacture by humans) laying around a volcano. He says: " .
. . you would need more information before you could be sure that alien
geological processes - natural to that planet - had not produced the rods."
(Note: Yes, I am aware that Behe goes onto give other criteria *he* thinks
give rise to the design inference, but you have not included those in
*your* argument here.)
Secondly, as Stuart Weinstein has already pointed out, you are wrong about
such things as hexagonal basalts having "the ability to self-assemble."
The basalts actually attain such forms through the complex interaction of
matter and energy. It is your *contention* (which I will come back to)
that such interactions cannot result in living things. Simply *saying*
there is a difference between the basic forces and processes of the
universe that result in the assembly of hexagonal basalts and the forces
and processes that result in the formation of living things is *not*
evidence. It is, in fact, nothing but begging the question.
The argument over geologic formations is actually a trivial point (or more
correctly, a trivial argument on your part) except for the fact that it
demonstrates that you are applying a subjective standard to your argument
from design ("I know it when I see it") and continue to do so though out
your other arguments. If I am wrong, you will be able to demonstrate the
demarcation line between your proposed "perfect geometric pattern" and a
totally disordered geological arrangement. What if *one* rock is out of
alignment in your "perfect" arrangement by an inch? A foot? A meter?
What if *two* rocks are out by an inch . . . three rocks, and so on? When
does the ID "inference" stop because of less-than-perfect arrangements?
Does something that *looks* like a human face from space count as designed?
And if you are not treating the "Face on Mars" as *evidence* for design,
why not? More importantly, why should *science* (instead of philosophy,
religion or, more likely, pseudoscience) treat the "face" as evidence for
design, *before* we have a good knowledge of the local conditions?
Again trivially, such an arrangement of rocks would, of course, excite
science's interest and lead to further investigation. It is that
"investigation" part that is the important one. You and other ID adherents
vault over the investigation and go strait to conclusions unfettered by
inconveniences such as evidence.
You next say that bees wax does not "self-assemble" the way rocks do.
Again this is a trivial objection. Biochemistry and embryology deals at
length with the self-assembly of organisms. The point is that there are
many processes that result from the interplay between matter and energy and
you have not demonstrated, merely asserted, that there is a *fundamental*
difference between these forces and processes. Bees wax "forms" hexagons
because bees do the forming. Bees form because of the fundamental
processes of biochemistry, which operate by the same basic rules of
chemistry and energy that operate in every other reaction. You claim that
bees do not self-assemble because they need "pre-existing strands of DNA
with a coded blueprint for bee assembly." But they get those, as any
teenager knows, from the ordinary process of reproduction, including any
errors of copying. How those processes result in hexagonal honey combs (by
the laws of physics and chemistry resulting in imperfect copying which can
then be the subject of selection, i.e. evolution) and how they result in
hexagonal basalts (obeying the laws of physics in heating and cooling) are
different in detail but have *not* been demonstrated to be different in
"kind." They are not only well understood but, as far as we can determine
(in *science*) derive from the same basic forces, with no need to posit
"outside" intelligent action. This whole line of argument, is nothing more
than wasted time and example of your attempt to overwhelm those who
disagree with empty verbiage. Let's skip most of the rest (including your
insistence on a manufactured, non-living, non-replicating watch as an
analogy for living things) and get to your "real" argument, that
abiogenesis by natural forces cannot explain the first replicator.
When I asked you for a consistent and objectively verifiable way to
distinguish between the "level" of complexity involved in a chemical clock
and that involved in a living thing; a demonstration, in other words, that
complexity is somehow "discontinuous" at some point so that something
becomes too complex to be explained by the known forces of the universe,
you answered only:
"If in your experience, you can demonstrate how rocks or chemicals or
atoms can self-assemble themselves in a given mindless and lifeless
environment to produce a given phenomena, then you will remove the
concept of ID as the only reasonable hypothesis to explain such a
phenomenon.
Notice, first, that you did not even *try* to answer my question. For
instance, you smudged your premises (again) by introducing the concept of
"lifeless" without definition. It is simplicity itself to show that
hexagonal basalts form on their "own", as do amino acids, stars, weather
patterns and other complex phenomenon without aid from living things. That
addition of "lifeless" makes no sense, unless you are now claiming that
energy itself is the result of design. Conversely, it is also easy to
demonstrate that life as we know it operates by the same "blind" elemental
forces of chemistry and physics as do basalts and stars. And, while it is
less easy, because of the sheer volume of the evidence, it can also be
amply demonstrated that the differences in living forms are explained by
the selection by the environment of imperfectly reproduced living things.
The most you've done is *assert* that living things have "programming that
is far above the sum of their parts." Everything that science sees about
life is amply explained by reproducing life forms subject to selection.
Where is there empiric evidence that there is something more than the sum
of its parts? The development of "programming" is sufficiently
demonstrated (especially in the absence of evidence to the contrary) in
such places as this:
http://www.space.com/scienceastronomy/artificial_life_030507.html
That leaves you down, at best, to abiogenesis. Worse, for your side, that
formulation of "in your experience" reveals that yours is only an argument
from ignorance.
Indeed, this is all it comes down to, as shown where you say:
" . . .scientists are the ones who are making an extraordinary
claim. You are claiming that the most fabulous machines
that we know of, machines and systems of function that far outshine
the very best that we humans have been able to produce with our most
brilliant efforts, arose through mindless naturalistic processes.
What an extraordinary and counterintuitive claim!
Ignore the incorrect analogy between replicating life and
non-self-replicating machines; ignore the incorrect standard that, somehow,
humans must be able to do "better" than what nature does; ignore that you
are trying to raise negative evidence to a structural support for your
"hypothesis" instead of, at best, a demonstration that some particular
evidentiary claim is wrong; and just keep in mind that this is nothing but
an argument from incredulity that has no place in science. The
demonstration of abiogenesis will come or not (and there is much reason to
believe that it may come sooner rather than later or not at all) but that
is not important here. That you must rely on arguments of ignorance and
incredulity is enough to disqualify ID from science.
As long as scientists cannot describe exactly how abiogenesis works, Iders
will keep claiming that *that* is the point between "natural" and
"unnatural" complexity. Once it happens (and I think it will), you will
decamp and move to something else, probably a claim that any abiogenesis
experiment by humans, no matter how closely it follows natural conditions,
is ultimately the result of intelligence.
Now, can you demonstrate that there is such a barrier, by empiric evidence
and without an argument from ignorance or begging the question?
I am tired of this now. I have skipped over much poor argumentation on
your part but am not worried, I'm sure you will repeat it again.
---------------
J. Pieret
---------------
The peril of negative arguments is that they may rest on
our lack of knowledge, rather than on positive results.
- Michael J. Behe -