Jim Cummins (cummins at possum.murdoch.edu.au) wrote:
: 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
This may be a wrong extrapolation.
Cellular functions, such as DNA and protein synthesis and cell division,
depends much on the normal functioning of mitochondria.
If mitochondria in a cell carry a heavy mutation load, the cell carrying
these defect mitochondria will not divide as fast as other cells with
normal mitochondria. Thus, inter-cellular selection will eliminate cells
with mutation-damaged mitochondria. In other words, mutation load on
mtDNA may not increase with the number of cell generations.
Xuhua Xia |
Museum of Natural Science | Phone: (504) 388-2841
119 Foster Hall | Fax : (504) 388-3075
Louisiana State University | Email: xuhua at unix1.sncc.lsu.edu
Baton Rouge, LA 70803 |