The evolving mitochondrion as a killer of male embryos
sherb at srv01.lin.irk.ru
Thu Nov 2 19:12:26 EST 2000
What gene do you propose as the candidate for coding the receptor? AFAIK
everything coded in mit genome, where place is quite restricted, is
located inside mitochondrion or in inner membrane. On the other hand, I
dont think it is likely according to your hypothesis, that the receptor
is coded in nucleus.
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 from
> the mother a conflict exists between the selfish interest of the mtDNA
> 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 mtDNA
> 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, and
> could detect the sex of the embryo, it would realise that the best
> chance of ensuring the transmission of its mtDNA to the next generation
> would be to kill the embryo. It has zero chance of being transmitted to
> 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 there
> is a 50 per cent chance that her next offspring will be a female, which
> will transmit the same mtDNA to the next generation in the fullness of
> time. This is true because the mtDNA in the mitochondrion in the male
> 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 in an
> animal species in which inheritance of mtDNA is uniparental and
> maternal will evolve so that the mitochondria can detect the sex of an
> embryo and, if it be male, kill it. The killing mechanism would, I
> suggest, have been similar to the "miniature apoptosis" that destroys
> male-line (M type) mitochondria in female embryos in mussels. (I wrote
> about this hypothetical miniature apoptosis in mussels in another
> In the present case the maternally inherited (F type) mitochondria
> would be destroyed, leaving the cell with no mitochondria. The embryo
> would die.
> The result of this evolution would be that most of the offspring born
> in each generation would be female. But this would not be good for the
> 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 been "consficated"
> 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 coding
> 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 outer
> membrane for a protein that was a receptor for the female-steroid
> molecule, and that in the abscence of the female-steroid molecule this
> protein fitted specifically into the receptor in the outer membrane and
> permeabilised it, thus destroying the mitochondrion. Such a mechanism
> might help the species by causing the death of any mussel embryo,
> whether male of female, that did not quickly produce a typical level of
> 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 bring
> about the destruction of male embryos by miniature apoptosis? I think
> 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 a
> male-steroid molecule it fitted specifically into the receptor in the
> outer membrane of the mitochondrion and permeabilised the membrane.
> Andrew Gyles
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> Before you buy.
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