In article <3apegiINNakc at newsman.csu.murdoch.edu.au>, cummins at possum.murdoch.edu.au (Jim Cummins) writes:
|> According to Hurst (Proc R Soc B 128: 135-140, 1992) uniparental
|> inheritance of mitochondrial DNA has evolved as a means of avoiding
|> potentially lethal intragenomic conflict. Another possibility is the
|> limitation of mtDNA mutations.
|> In human females, there's an estimated 24 cell divisions between zygote
|> and egg, whereas for males the number of precursor cell divisions is
|> around 36 for sperm produced at puberty, increasing at a constant rate
|> of 23 per year.
|> Thus the sperm produced by a 45-year old man have been through c. 770
|> cell divisions, with a concomitant increase in the rate of mutations.
|> This undoubtedly underlies the well-known disproportionate
|> contributions of male parents to mutations (first pointed out by
|> Haldane: Ann Eugen 13: 262-271, 1947).
|> As the mitochondrial DNA mutates c 10x faster than nuclear DNA, the
|> effect is likely to be even more disproportionate. As the average
|> nuclear DNA mutation causes about 2% reduction in fitness, it seems
|> that the effects of any paternal mitochondrial DNA inheritance would be
|> rapid and lethal. Of course, this argument can't apply to those
|> organisms (eg Sequoia) where paternal inheritance of mtDNA is the rule.
|> However, in these cases there may be different patterns of mitotic
|> proliferation leading up to meiosis. Anyone know?
There is a school of thought that mutation rate is a function of time,
not number of cell divisions (under this model the major cause of mutations
are mutagens and DNA repair, rather than DNA replication). I believe this
is suggested by the rate constancy between species with different generation
times (each generation including a roughly equal number of cell divisions).
I don't know whether an exception is made for mitochondrial DNA or not; or
how they explain the reported male/female discrepancy, although I'm pretty
sure they do have some sort of explanation.