Re: Epistasis and Linkage - was: Ernst Mayr: Where Are We (1976)

Perplexed in Peoria <jimmenegay@xxxxxxxxxxxxx> wrote or quoted:
> "John Edser" <edser@xxxxxxxxxx> wrote in message news:d7q4jm$13ss$1@xxxxxxxxxxxxxxxxxxxxxx
> > "Perplexed in Peoria" jimmenegay@xxxxxxxxxxxxx
> > > JM:-

> > > ... it is an "empirically true fact" that epistatic gene fitnesses
> > > (as you seem to use this term) are not heritable.

[snip]

> > > JM:-
> > > The key issue in such models is the degree of linkage
> > > (segregation independence) between the two loci. [...]

> > JE:-
> > Linkage and fecundity rates (the rate of reproduction of sterile
> > immatures) determine the probability that two alleles at two different
> > loci may be inherited together within just a sterile immature body. When
> > a female tick, which can only reproduce itself once, mass produces about
> > 10,000 sterile immatures and then dies, many recombination events are
> > represented in these immatures. What matters is which of these 10,000
> > are raised to fertile adulthood and _exactly_ how is each gene is
> > actually selected in nature. In this species only about 2.something
> > sterile immatures are mostly raised to fertile adulthood, i.e. just a
> > tiny fraction of the fecundity rate. The mass of infertiles that die
> > along with their gene combinations are only subject to a process of sub
> > selection and not selection because they are only dependently and not
> > independently selectable. This means that high fecundity rates can be
> > advantageous because they allow the less costly act of sub selection of
> > the better epistatic gene combinations. Sub selection is more efficient
> > than selection because a selection of them would require immatures to be
> > raised to fertile adulthood so they acquire an independent fitness.
>
> You raise an interesting point here. I think that your analysis is wrong
> but I would appreciate comment from someone who understands the issues
> better.
>
> The population of fertile fecund female ticks (and their mates) is
> presumably far from linkage equilibrium because selection for
> epistatic gene fitnesses has moved the population away from linkage
> equilibrium. This population then gives birth to a much larger population
> of infertile immature ticks. This immature population is presumably
> much closer to linkage equilibrium due to the processes of recombination
> and fertilization. Then nature takes its course and selection takes its
> toll (even though you choose to call it "sub selection" for some reason),
> and we end up with something much like our original population -
> small again, but back far from linkage equilibrium. This second
> generation population might, by stretching the terminology, be said to
> have "inherited" epistatic information from its parents.
>
> However, ISTM (and this is the point I would appreciate comment upon)
> that this kind of "inheritance" is not really inheritance at all. The
> "epistatic information" was created by selection acting on the population
> of infertile ticks. It was not "inherited" in the sense needed in order
> for NS to act cumulatively. (As "proof" of this, notice that even ticks
> whose parents did not have the "epistatic information" may have it after
> recombination, fertilization, and selection.) So, even with John's
> eccentric choice of sexual maturity as the starting point in the life-cycle,
> the epistatic information is mostly not heritable - and therefore we are not
> doing violence to the truth by ignoring it in our models of evolution.
>
> Comments?

I don't really favour this analysis:

The idea that this information is created again in each generation
has merit - but the information *does* come from somewhere - even if
some of it arises from environmental factors and self-organisation
processes acting under physical law.

If the information in organisms is preserved across extended periods -
and across generations - I think it's fair enough to describe it as
being inherited - *even* if a selective process generates it in each
generation - and even if some of it comes from environmental sources.

The form of the selective process involved is itself likely to be
at least partly controlled by the organism's genes.

However, what it might be reasonable to claim is that the magnitude of
such information might well be less than it at-first appears - since the
self-organisation processes responsible for its generation might be doing
something like acting as a PRNG - and generating a lot of complex-looking
data from very little initial information.

My understanding is that genes that are selected together
tend to migrate to adjacent locations on chromosomes - so
that genes that depend on each other are less likely to be
split during meiosis - and so a reduced level of selection
is needed to keep them together.

The main result of all this is slightly bigger effective genes.
--
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Relevant Pages

  • Epistasis and Linkage - was: Ernst Mayr: Where Are We (1976)
    ... >> the process of recombination undoes any linkage disequilibrium created ... > immatures) determine the probability that two alleles at two different ... > selection and not selection because they are only dependently and not ... have "inherited" epistatic information from its parents. ...
    (sci.bio.evolution)
  • Re: Understanding and Testing TDF (Total Darwinian FItness)
    ... > which only about 1.something survive to fertile adulthood then intense ... You seem to be saying that highly fecund species have intense ... selective pressure on immatures, ... > intense level of survival sub selection but then pass the one definitive ...
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  • Re: Reproductive excess model
    ... >>> independent of the reproductive excess. ... >> It is impossible to separate the fitness of alleles from ... > and Haldane) treats all selection as "survival selection". ... > acts by killing off unfit immatures. ...
    (sci.bio.evolution)
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