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Kenneth Miller's and Barry Hall's challenge of Michael Behe

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Sean Pitman M.D.

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Apr 3, 2003, 12:59:50 PM4/3/03
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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.

"… 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.

unread,
Apr 3, 2003, 2:03:37 PM4/3/03
to

"Sean Pitman M.D." wrote:

"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
滴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

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Apr 3, 2003, 1:43:32 PM4/3/03
to

Sean Pitman M.D. wrote:

[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

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Apr 3, 2003, 3:44:18 PM4/3/03
to

"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.
>
> ". Foghorn would be walking along, notice a dollar bill or some other
> 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

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

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Apr 3, 2003, 3:56:46 PM4/3/03
to

"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

unread,
Apr 3, 2003, 4:43:58 PM4/3/03
to

"Sean Pitman M.D." wrote:

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.

unread,
Apr 3, 2003, 4:48:05 PM4/3/03
to

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
滴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

unread,
Apr 3, 2003, 5:31:43 PM4/3/03
to

"C.J.W." <watt...@bellatlantic.net> wrote in message
news:3E8CACCE...@bellatlantic.net...

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

unread,
Apr 4, 2003, 1:26:53 PM4/4/03
to
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?

> 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

unread,
Apr 4, 2003, 2:02:27 PM4/4/03
to

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

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Apr 4, 2003, 2:06:18 PM4/4/03
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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

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Apr 4, 2003, 4:22:41 PM4/4/03
to
G'Day All
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:

[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

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Apr 4, 2003, 9:24:55 PM4/4/03
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seanpi...@naturalselection.0catch.com (Sean Pitman M.D.) wrote in message news:<80d0c26f.03040...@posting.google.com>...

(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

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Apr 5, 2003, 11:12:01 AM4/5/03
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fn...@comcast.net (Frank J) wrote in message news:<38c5d0dd.03040...@posting.google.com>...

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

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Apr 5, 2003, 2:27:29 PM4/5/03
to
"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>

Sean Pitman

unread,
Apr 5, 2003, 3:05:02 PM4/5/03
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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. 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

www.naturalselection.0catch.com

Noelie S. Alito

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Apr 5, 2003, 7:57:05 PM4/5/03
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"Ian" <ibu...@NOSPAMaol.com> wrote in message
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

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Apr 5, 2003, 8:41:42 PM4/5/03
to

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

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Apr 5, 2003, 8:42:39 PM4/5/03
to
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.0304...@posting.google.com>...

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

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Apr 6, 2003, 6:34:22 PM4/6/03
to

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

unread,
Apr 7, 2003, 9:54:35 AM4/7/03
to
G'Day All
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

unread,
Apr 7, 2003, 3:32:27 PM4/7/03
to
seanpi...@naturalselection.0catch.com (Sean Pitman) wrote in message news:<80d0c26f.03040...@posting.google.com>...

> 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
> >
Snip:

>
> 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

unread,
Apr 8, 2003, 5:27:58 PM4/8/03
to

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 evol