Iuval Clejan wrote:
> What about the mitochondria of clones? Has anyone looked at frequency
> of mutations of mtDNA in clones?
The only studies I know of on the mtDNA of cloned animals are rather
preliminary -- they are investigations of the relative contributions
of donor and host cell to the animals' mtDNA. Evans et al, Nature
Genetics 23:90 and Hiendleder et al, Mol Reprod Dev 54:24. It will
certainly be very interesting to see what is found in this regard.
> Is there a resetting of the clock
> mechanism operative for mtDNA damage, just like there is for telomere
> length?
There is sure to be, because this is a virtually inevitable result of
the rapid cell division during embryogenesis. Cells with ramdomly lower
levels of mtDNA damage will typically divide more rapidly because they
have better ATP synthesis capacity, and their descendents will form the
bulk of the organism. This is probably accentuated by the fact that
mitochondria can't divide very fast unless they are genetically intact.
> In "traditional " reproduction, is there a selection of less
> damaged mitochondria within an individual egg when the zygote starts
> dividing (can't see a way for this to happen), or just selection of
> eggs with more undamaged mtDNA during meiosis?
There's the intercellular competition described above; there's also a
lot of selection at ovulation (many eggs begin to mature but only one
gets out of the ovary each month), though we don't know how this is
driven; finally there is a very clever trick known as the mtDNA
bottleneck, whereby the egg cells are prevented from containing small
but non-zero levels of mutant mtDNA (which is the worst case, since it
could escape the selection process at ovulation but still be damaging
later).
Aubrey de Grey
