Re: [asa] Exaptation

From: Randy Isaac <>
Date: Wed Jun 24 2009 - 09:46:08 EDT

I ran out of time yesterday and didn't finish my comments on those Science
News articles I cited. Permit me to add a little more.

What the article on structure variants pointed out was that mutations
involving large numbers of nucleotides are more frequent than had been
thought previously. They estimated that human beings typically have on the
order of 50-60 single nucleotide mutations from their parents but also about
10 structure variants like copy number variations. Each of these can involve
as many as a million nucleotides. Gene duplication is one example but there
can be many other variations.

How "big" can a change be without being detrimental to reproductive success?
It seems we don't know enough to figure this out theoretically. We have no
idea a priori what the functional impact might be of a given genetic change.
Nor can we theoretically predict, given a particular structural or
functional variation, which genetic change is responsible. We can only
observe experimentally what occurs.

Take the example of polydactyly. It seems to be a fairly obvious and major
change stemming, apparently, from a single gene variation but it can be one
of several different genes. I don't know if this is a hereditary feature but
it seems to occur in about 1 out of 500 births worldwide. One case is
reported in 2 Samuel 21:20 (1 Chron. 20:6). In other words, we can observe
that rather obvious structural changes might be connected with "minor"
genetic changes while what we might consider "major" genetic changes aren't
visible at all.

Darwin had no knowledge of DNA but his prowess was careful observation. His
brilliant insight was to recognize the potential magnitude of changes that
could occur as the cumulative result of these observed small changes
occurring over a very long period of time. The primary criterion that sets
the bound of what change can occur in one generation is that the offspring
can survive and reproduce. Now with our discovery of DNA, we can see another
criterion is that the change is within reach in genetic phase space. That
is, you have to be able to get there from here with a genetic mutation
event. Darwin was hampered by a lack of understanding how such variations
could persist since he didn't know of Mendel's work and he didn't know about
DNA. In his day, traits were thought to average out so the persistence of
any change was problematic.

A more specific example was sent to me by Craig Story, a biology professor
at Gordon. He cites this from his own studies:
"FcRn, the antibody transport protein that I worked on in grad school is
quite obviously derived from a different structural family of genes (MHC
class I genes) that serve a totally different purpose and is a great example
of exaptation. It's encoded (it landed) in a different part of the genome
from its presumably ancestral proteins. The nearby genes are the same in
mouse, rat and human, more evidence that this gene "jumped" to its new
location in an ancestor shared by mouse and human (that's going back many
millions of years).

Reasons to think it is derived have to do with the fact that it retains the
overall fold structure but has lost a key component of the function of the
MHC proteins, namely, a groove into which peptides fit to be presented to T
cells. The groove in FcRn is closed, the two alpha helices that would
0therwise form the groove are still there, however.

Here the new function is binding antibody proteins, the old function was
binding T cell receptors. As one can see from normal process of antibody
protein production, a random process can indeed give rise to something
useful. The key concept is that it only has to happen one time, and even
incrementally (presumably). Once a new function is hit upon that gives an
advantage, transporting antibody from mother to young. The function can be
further tweaked and improved. Presumably the original FcRn worked mainly in
the yolk sac, and possibly also as an antibody "half life increaser" then
became more and more fine tuned by mutations which gave it a pH-dependent
binding via key Histidine amino acid residues.

Not hard for me to see how this happened. Now, a very similar story I am
sure can be told for myriad different genes. For example, pyruvate
dehydrogenase complex is a homologous set of genes with alpha-ketoglutarate
dehydrogenase. Molecular motor making ATP in mitochondria is a homologous
system as the molecular flagellar motor of bacteria, etc etc."

Net: your original question was whether there might be a theoretical or
conceptual problem with exaptation. I think from all the various responses,
it seems that this is not a concern.


----- Original Message -----
From: "Bill Powers" <>
To: "Randy Isaac" <>
Cc: <>
Sent: Tuesday, June 23, 2009 7:55 AM
Subject: Re: [asa] Exaptation

> Randy:
> I will try looking at some of the articles you reference.
> I take you to be saying that incrementalism on the genetic scale may
> produce "discontinuity" on the morphological scale.
> I suspected the same some 20 years ago when I first started studying
> evolutionary theory, which is why I thought at the time that we really
> don't know what a transitional species would look like.
> My experience with nonlinear and chaotic systems suggested to me that the
> same might be possible for biological systems.
> If this is the case, one ought to be at least suspect of any proposed
> transitional history since almost all are based upon morphological
> similarity, although I imagine the theory has begun to rely upon presumed
> ancestry.
> bill
> On Tue, 23 Jun 2009, Randy Isaac wrote:
>> Interesting point, Bill. I think we need to be careful about an argument
>> based on the a requirement of incrementalism. We still have so much to
>> learn about the quantization of descent with modification. In contrast to
>> Darwin's view of gradualism, the discovery of DNA led to a quantization
>> of changes at the molecular level but we still have so little awareness
>> of what that might mean macroscopically in the functional realm.
>> There have been several good articles in Science News recently that talk
>> about this. In January, an article showed some support for Conway
>> Morris's approach.
>> Molecular Evolution
>> Investigating the genetic books of life reveals new details of 'descent
>> with modification' and the forces driving it
>> By Tina Hesman Saey
>> January 31st, 2009; Vol.175 #3 (p. 26).
>> Even more relevant was a story in March on structure variants.
>> Jumping genes provide unexpected diversity
>> Mobile DNA elements help shape human genomes
>> By Tina Hesman Saey
>> March 14th, 2009; Vol.175 #6 (p. 16)
>> The above articles are too long to copy and post but most of you probably
>> have access to either paper or electronic copies.
>> The net is that incremental changes at the molecular level may be more
>> significant than we expected and the resulting functional impact may be
>> even greater.
>> Randy
>> ----- Original Message ----- From: "Bill Powers" <>
>> To: <>
>> Cc: <>
>> Sent: Tuesday, June 23, 2009 12:14 AM
>> Subject: [asa] Exaptation
>>> I'm continuing to think about Irreducible Complexity. A closely related
>>> concept is that of exaptation, wherein some biological structure or
>>> process
>>> used for one function is later used for a different function.
>>> Exaptation is apparently a well accepted doctrine and there a few
>>> carefully
>>> documented arguments to support the notion, including the development
>>> from the
>>> jaw bone for use in the middle ear, the bone spur of the panda
>>> developing into
>>> a thumb, and the development of feathers from thermal insulation into
>>> feathers
>>> for flight. The last two have problems in my mind conceptually, the
>>> first is
>>> perhaps the best.
>>> Nonetheless, exaptation appears to present theoretical problems, and
>>> here is why.
>>> It appears to me that Darwinian (random) evolution, not only presumes,
>>> but
>>> must be committed to a principle of incrementalism, whereby evolution
>>> sensibly
>>> proceeds according to small incremental changes.
>>> This principle appears necessary because of the random nature of the
>>> process.
>>> Significant, but random, changes are highly likely to be deadly,
>>> producing a
>>> non-survivable species. This is because it is likely that survival
>>> large
>>> changes are likely to be complex and highly integrated, but to expect a
>>> random
>>> process to be able to accomplish such a feat seems to ask far too much.
>>> On
>>> the other hand, small changes are more likely to leave the species still
>>> survivable. Such changes, while small, can be mildly advantageous,
>>> neutral,
>>> or even mildly disadvantageous.
>>> The principle of incrementalism presumes that in some sense that changes
>>> are
>>> near each other. But this nearness is not conceptual nearness,
>>> something
>>> utterly foreign to a blind process, but probablistic.
>>> Prima facie, exaptation violates this principle of incrementalism. This
>>> is so
>>> because the previous function is not probabilistically near the new
>>> function.
>>> It is conceptually near perhaps, but how can it be probabilistically
>>> near?
>>> Functionality is conceptual. I don't know how else to say it. In a
>>> sense the
>>> very notion of functionality is suspicious in a non-teleological
>>> process. But
>>> what then do we mean when we say in exaptation that an old function is
>>> used
>>> for a new one?
>>> To take, but one example, if one reviews, even in cartoon form the
>>> evolutionary development of the jaw bone into the middle ear, it appears
>>> to me
>>> to be miraculous if viewed as a random process. It only seems
>>> reasonable
>>> "conceptually," but not, to me, as a blind process.
>>> Can anyone help?
>>> thanks,
>>> bill
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Received on Wed Jun 24 09:46:54 2009

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