This is beyond interesting. When learned about mitochondrial DNA, and the relative lack of repair mechanisms I wondered why it didn't go wrong more often. I was aware of mitochondrial flux in the sense that each cell had a population of mitochondria that waxed and waned. But I hadn't really thought about selection pressure on that population D'oh!

I suspect that the fragility of mitochondrial DNA and the resultant cellular damage might have led to selection pressure on the organism leading to mitochondrial DNA migration into the nucleus where there is a decent repair mechanism, which would explain the differing number of mtDNA base pairs in different organisms (e.g humans:16,569, drosophila:16,019).

Possibly related: one of the proteins encoded in human mtDNA is Cytochrome C Oxidase (CCO). If you've followed any of Francisco Gonzales-Lima's work, he's shown a connection between reduced amounts of CCO and dysfunction of the CNS. I'd been chasing organic chem (super noob at that), trying to wrap my brain around how CCO might be downregulated. It could simply be a mtDNA issue leading to lower production rates(?) I don't see how selection pressure might do that to a population of mitochondria - but at least I have a different wall to bang my head on. :-)