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
article.)
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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