"Donald Forsdyke"  wrote in message
news:cav347$tlr$1{at}darwin.ediacara.org...
> jimmenegay{at}sbcglobal.net (Jim Menegay) wrote in message
news:...
> > "Donald Forsdyke" 
wrote in message
news:...
> > > The article "Polymorphism for hybrid male sterility in
Drosophila"
should
> > > not be lightly dismissed. It is part of a growing literature on
Haldane's
> > > rule that casts doubt on the idea that speciation has a genic origin.
> > > Naveira and Maside (1998) even go so far as to suggest that
"hybrid
male
> > > sterility results from the ...[introduction] of a minimum number of
randomly
> > > dispersed factors" that include "factors" in
non-coding DNA. They
suggest
> > > that "a new paradigm is emerging, which will force us
... to revise
many
> > > conclusions of past studies."
> > >
> > > For more on this see my new JTB paper:
> > > http://post.queensu.ca/~forsdyke/speciat2.htm
> >
> > Dr. Forsdyke,
> > Thank you for calling my attention to this literature, and my
> > compliments on a very nice web site.  You have me convinced that
> > GC is a plausible mechanism for producing hybrid infertility.
> >
> > However, one thing puzzles me, and I would appreciate a
> > clarification or a pointer to a clarification.  Pre-zygotic
> > isolation can readily be explained as an adaptation at the
> > individual level to the prior existence of post-zygotic
> > isolation.  But it is difficult to see post-zygotic isolation
> > as an adaptation, and also difficult to see how, in the face
> > of hybrid infertility, the incipient species can arise as
> > a distinctive subpopulation of homozygotes.  That strikes
> > me as the central problem of speciation.  Various theories
> > of speciation solve this problem in various ad-hoc ways.
> >
> > The puzzle is whether your theory solves this problem in a
> > better, less ad-hoc, way than its competitors.  In my quick
> > perusal of your literature I see some hints that you believe
> > that it does - particularly in your mention of (incipient?)
> > species-level selection and in the mention of thresholds
> > of GC difference for inhibiting recombination.  But I didn't
> > follow the logic of how these help in solving the problem.
> >
> > The question is whether you see your theory as having a
> > better solution to what I called the "central problem of
> > speciation", or whether you are simply correcting the
> > misunderstandings of critics who have claimed that it is a
> > worse solution, or that it is empirically refuted.
>
>          You find it "difficult to see post-zygotic isolation as an
> adaptation" and cannot see "how, in the face of hybrid infertility,
> the incipient species can arise as a distinctive subpopulation of
> homozygotes."
>
>         You will agree that adaptations are ultimately to maximize the
> number and fertility of offspring. If a horse is eaten by a tiger it
> is phenotypically selected against and produces less offspring. If a
> horse that is potentially a member of an incipient species crosses
> with a member of the main species it is "reprotypically" selected
> against and produces less offspring (i.e. the hybrids are sterile).

Yes, but I was asking whether the hybrid sterility is itself an
adaptation - for some entity.

>         If a horse that is potentially a member of an incipient
> species crosses with another member of the same incipient species then
> there is no reprotypic counterselection (i.e. hybrid sterility). The
> offspring are abundant and fertile. As Romanes noted in 1886, finding
> a reprotypically compatible mate is likely to be a rare event, but
> then, speciation itself is a rare event. For more on this see section
> 7 of my new JTB paper (URL above).

Allow me to put this into my own words, which you may then
critique:

The sterility of the mule (and the inviability of her brother)
cannot be seen as adaptive for the mule individual.  Nor can
her sterility be seen as adaptive for her parents - an individual
horse and ass.  However, the hybrid insterility CAN be seen
as an adaptation of the horse SPECIES (or the ass species, or
both).  The small loss of fitness that this entails for the
mule's individual parents can be described as a kind of "tough
love" that the species imposes on its members.  This is
(incipient) species-level selection.

The eventual appearance of pre-zygotic modes of isolation can
be explained by ordinary individual-level selection.  The
individuals avoid some of the costs of the species's injunction
against crossing, without contravening it.

If this summarizes your position correctly, then I must say
that I am predisposed to be receptive.  I have argued in this
group that species-level selection exists, that it acts on
traits defined thru frequency-dependent feedback loops at
the individual level, and that it may operate counter to
the "interests" of individual species members.

However, I still don't see - and this was my main question -
whether your non-genic GC model is superior to a more
conventional polygenic model in explaining how the incipient
species arises as an entity with its own interests that can
run counter to the short-term interests of its members.
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