I propose that the gene coding for the receptor in the mitochondrial
membrane is located in the nucleus. I propose that its sequence is
similar to that of the gene coding for the receptor in the
mitochondrial membrane for TR3.
In their perspective on apoptosis, Brenner and Kroemer wrote: 'What is
the mitochondrial receptor for TR3?', so it is not yet known. I gave
the reference in my hypothesis 'Miniature apoptosis in mussels' posted
I propose that the gene coding for the receptor for the male-steroid
molecule is located in the nucleus, and has a sequence similar to that
of the gene coding for TR3.
In article <8tt088$fk4$1 at mercury.hgmp.mrc.ac.uk>,
Dmitri Sherbakov <sherb at srv01.lin.irk.ru> wrote:
>> What gene do you propose as the candidate for coding the receptor?
> everything coded in mit genome, where place is quite restricted, is
> located inside mitochondrion or in inner membrane. On the other hand,
> dont think it is likely according to your hypothesis, that the
> is coded in nucleus.
>> Dmitri Sherbakov
>> On 2 Nov 2000, Andrew Gyles wrote:
>> > The evolving mitochondrion as a killer of male embryos
> > In any species of animal in which mitochondria are inherited only
> > the mother a conflict exists between the selfish interest of the
> > and the interest of the species.
> > The selfish interest of the mitochondrion and its mtDNA is to be
> > transmitted by every mature individual of the species to the next
> > generation. But in the case of uniparental maternal inheritance of
> > mtDNA half of the individuals, the males, do not transmit their
> > to the next generation. And in the more complex animals the mothers
> > expend much energy and time in bearing each offspring.
> > In this situation if a mitochondrion in a male embryo could think,
> > could detect the sex of the embryo, it would realise that the best
> > chance of ensuring the transmission of its mtDNA to the next
> > would be to kill the embryo. It has zero chance of being
> > the next generation if it is in a male embryo. If it kills the male
> > embryo the mother will soon have another chance to conceive, and
> > is a 50 per cent chance that her next offspring will be a female,
> > will transmit the same mtDNA to the next generation in the fullness
> > time. This is true because the mtDNA in the mitochondrion in the
> > embryo is identical to the mtDNA in the mother.
> > Of course mitochondria cannot think, but natural selection acting on
> > random mutations of mtDNA (like throws of dice on the board of the
> > conditions of existence) could produce the same effect. The mtDNA
> > animal species in which inheritance of mtDNA is uniparental and
> > maternal will evolve so that the mitochondria can detect the sex of
> > embryo and, if it be male, kill it. The killing mechanism would, I
> > suggest, have been similar to the "miniature apoptosis" that
> > male-line (M type) mitochondria in female embryos in mussels. (I
> > about this hypothetical miniature apoptosis in mussels in another
> > article.)
> > In the present case the maternally inherited (F type) mitochondria
> > would be destroyed, leaving the cell with no mitochondria. The
> > would die.
> > The result of this evolution would be that most of the offspring
> > in each generation would be female. But this would not be good for
> > species as a whole. In the long run natural selection would favour
> > those populations of individuals in which the mtDNA genes coding for
> > proteins that detected and killed male embryos had
> > by the nucleus of the cell and brought under the control of the
> > nucleus. I suggest that this is the reason why humans, for example,
> > have only 13 protein-coding genes left in the mtDNA, all of them
> > for respiratory enzymes. The mitochondria have been disarmed.
> > In my hypothesis on miniature apoptosis in mussels I suggested that
> > female-line (M type) mitochondria might have receptors in their
> > membrane for a protein that was a receptor for the female-steroid
> > molecule, and that in the abscence of the female-steroid molecule
> > protein fitted specifically into the receptor in the outer membrane
> > permeabilised it, thus destroying the mitochondrion. Such a
> > might help the species by causing the death of any mussel embryo,
> > whether male of female, that did not quickly produce a typical
> > female-steroid molecules.
> > How could a mechanism like this in the ancestors of species that
> > inherit all of their mtDNA maternally be modified by evolution to
> > about the destruction of male embryos by miniature apoptosis? I
> > that the protein that was a receptor for the female-steroid molecule
> > would have to evolve so that when it formed a specific complex with
> > male-steroid molecule it fitted specifically into the receptor in
> > outer membrane of the mitochondrion and permeabilised the membrane.
> > Andrew Gyles
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