Re: Haldane's Dilemma and quantitative genetics

On Sat, 8 Jul 2006 00:05:21 -0400 (EDT),
Wirt Atmar <atmar@xxxxxxxxxxxxxxxxx> wrote:
ErikW writes:

[snip]

I even have thought myself that perhaps competition induces phenotypic
evolutionary stasis but have had no real reasons for it other than
intuitive ones and I still don't (but I have never persued it). This
is an area where I am rather open to ideas.

Let me first apologize for being so long getting back to this.

As for the idea that intense competition induces phenotypic
evolutionary stasis, let me say that I'm relatively quite convinced
that it's true.

The corollary is that intense competition produces perfectly adapted
species. Can you point to an example of a modern species that you think
is perfectly adapted and therefore not evolving? Could we test this by
looking to see if the species contains any variation?

[snip]

[As an aside, it always amazed me that SJ Gould would, due to his
Marixt leanings, argue so forcefully for the lack of the competition in
natural situations and its subsequent optimizations, and then argue so
eloquently for "punctuated equilibria," those long periods of
evolutionary stasis which he saw in the rock record. Those periods of
stasis are obviously governed by the attainment of points of optimality
and the competitive pressures that keep the phlyetic lineages there.]

That's not the argument that Gould makes. He does not claim that stasis
is due to perfect adaptation. (Eldredge, on the other hand, is sympathetic
to that idea.) Gould says that large populations dampen phenotypic change.

Gould knows about pulse turnovers but as a pluralist he recognizes other
possibilities.

Its just that thing about neutral mutations and population structure I
don't agree with. I detect population structure because I can detect
neutral molecular variation. One of two neutral variants will fix
sooner or later even across gene flow barriers, provided reproductive
isolation doesn't happen before that. I mean, I see the (presumably)
neutral variants so how can your argument be correct?

The question you're asking, I believe, is: "why am I seeing neutral
mutations in my populations if you're claiming they're so difficult to
establish?" Let me answer that question in a moment. First please allow
me to reiterate my claim.

By chance, Bruce Walsh (U Arizona) just very recently put up his notes
for a quantitative genetics class he taught earlier this year. They're
available at:

http://nitro.biosci.arizona.edu/workshops/Aarhus2006/notes.html

Chapter 7, "Genetic Drift," is the chapter of interest:

http://nitro.biosci.arizona.edu/workshops/Aarhus2006/pdfs/lecture07.pdf

We only need to look at his first figure illustrating the
"Wright-Fisher model of genetic drift," which is simply a Markov random
walk with two absorbing barriers, fixation and extinction.

Note that he starts his graph, as is standardly done, with the
frequency of the neutral allele being 50% in the population, thus it
has equal opportunity to walk to either fixation or extinction over
time. But this is far from realistic. A novel neutral allele begins
life just an iota off of the 0% axis, and as in any gambler's ruin
markovian process, must play against the "house," and is therefore
enormously more likely to go extinct than fixate, being initially just
a hair's breath away from the extincting absorbing barrier.

But in a geometrically distributed population, the situation is much
worse still. In Walsh's graph, the probability of increasing or
decreasing an allele's frequency is 50-50. But that's not true in a
geometrically distributed set of demes that are communicating with one
another. The probability isn't 50-50, but perhaps more akin to 80-20 in
favor of the "house" (the standard allele winning at each generation),
with the precise ratios being determined by the geometries.

Not only does the neutral allele ride right on the edge of extinction
initially, its odds of surviving to the next generation are very poor.

That's all very interesting but the molecular data shows that thousands
and thousand of neutral mutations become fixed in a population. Is this
as example of a nice theory being ruined by a nasty little fact?

How do *you* explain the fact that chimpanzee and human pseudogenes
are different? How do you explain the divergence of intergeic sequences?
It look like neutral alleles can be fixed with no problem.



Larry Moran


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