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?
Jim "I refuse to have a signature" Cummins
School of Veterinary Studies
Murdoch University
Western Australia 6150 Tel +61-9-360 2668 Fax +61-9-310 4144
E-mail cummins at possum.murdoch.edu.au
