Re: genetic variation is purely random, right?



"Ron O" rokimoto@xxxxxxx wrote:-

-> Parant A and B live in an environment they are not adapted to. They
are not equiped for their current habitat. Therefore their stresslevels
are skyhigh. Because of this stress the male-parant produces 'hormone
M'. Because of this 'hormone M' the mutation rate in the process in
which his sperm is produced is going up. The offspring of parants A and
B will now be more different from their parants than under normal
circumstances. The genetic variation is adapted to the environment.

This does happen. An example that you can look up is the SOS response
in bacteria. Environmental stress does increase mutation rate. Things
like starvation in bacteria will increase mutation rate, but certain
genes aren't mutated. The mutation rate increases across the genome.
It would likely be the case for metazoans too.

JE:-
Richard De C Studdert (An unpublished Australian researcher) maintained that
stress can pre-select out sperm cells within the genital tract of both the
male and female mouse producing what he termed "transmission ratio
distortion" (TRD). Some of his books are available online:

http://books.idealo.com/160R12C28L83K0-Science-Evolution-General.html


Studdert has always maintained that the data he collected over many years
verifies a significant correlation between significantly distorted Mendelian
common mouse coat color genes and an applied stress acting on either parent.
Studdert experimentally applied contradictory stressors to mouse parents
using Han's Selye's pioneering concept of Eustress (too much of a good
thing) Vs Distress (too much of a bad thing).

http://en.wikipedia.org/wiki/Hans_Selye

Studdert collected the results of gene transmission to the next generation
after he had experimentally applied Eustress or Distress. He maintains that
a distressed mouse (the distress was a light left on over the cage) can TRD
the coat color gene that is _not_ expressed within a distressed heterozygous
parent. In this case significantly more offspring that are homozygous for a
double recessive albino gene are predicted to be transmitted from a
distressed albino hybrid parent, than the Mendelian ratio allows. OTOH
Studdert maintains that TRD can distort gene frequencies the other way if
the conditions of the parent become eustressed (too good). In this case the
expected freq of the albino gene within the next generation will become
significantly less than the predicted Mendelian ratio. Studdert's
transmission ratio distortion (if formally verified) is incredibly important
to evolutionary theory because it actually simulates a futures market in
genes operating in nature. Such a mechanism will significantly speed up
evolution by natural selection. Quite clearly it pays a parent to distort
the genes it may transmitting to the next generation, if it can do so and
relative to any + or - stress that is operating on that parent's expressed
phenotype (which will mostly be the genes that are dominant). As a
hypothetical example, a heterozygous black mouse carrying a recessive albino
allele that finds itself in the snow would greatly benefit its own Darwinian
fitness if it can distort the transmission of the unexpressed white
recessive (no matter what that gene happens to be). This is because the
black gene can be proven not to be adaptive if it is expressed within a
distressed black colored parent (vice-versa if the parent is eustressed).
This being the case, any other gene has to be the better bet than the black
one. Studdert maintained that the immune system remains responsible for TRD.
He argued that sperm cells must carry surface antigens that can indemnify
some of the genes each cell is carrying allowing the immune system to
pre-select out those that are the lowest bet via a parental distress or
eustress indicator.

It is my view that De C Studdert may have been observing meiotic drive
operating on mouse coat color genes. So far, drive has only been verified to
act on alleles that remain very detrimental to the parent's Darwinian
fitness e.g. the t allele in mice. In discussions with Dr Hoelzer within sbe
I stressed that the commonly accepted argument that drive represents gene
centric selection was only conditionally verified. Obviously, it is much
easier to document a negative effect on parental Darwinian fitness than a
positive effect so positive drive may have been overlooked. Just the one
documented case of positive parental fitness drive refutes the gene centric
case because now it can be argued that drive evolved via Darwinian natural
selection operating at just the organism level. If Studdert's work verifies
positive in parental Darwinian fitness drive then it represents the first
documented case of this type so it is important.

As just a private citizen Studdert provided research grants to assist
students at the University Of Newcastle NSW Australia under the
professorship of Dr Tim Roberts. For many years Studdert attempted to
produce a monoclonal antibody for common mouse coat color genes at Robert's
lab by paying his own costs. Unfortunately Studdert became very ill with
Alzheimer's disease and ceased all work about 8-10 years ago. I would advise
anybody who may be interested in his work to contact Professor Tim Roberts
at Newcastle University NSW Australia.

Regards,

John Edser
Independent Researcher

edser@xxxxxxxxxx





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