In article <4.2.0.58.19991130124439.00a21ac0 at norm.dpo.uab.edu>,
brookes at uab.edu ("Paul S. Brookes.") wrote:
>> Jim Cummins' comments regarding oocyte mtDNA may be related to another
> hypothesis - namely the reasoning behind inheritance of mtDNA from the
> maternal gamete, and the reason why sperm swim and eggs remain still.
>> It goes something like this...... If both gametes were motile, then both
> would require ATP presumably from mitochondria, and this would carry with
> it an associated level of mtDNA damage. By keeping one gamete stationary
> (the egg), and then sacrificing the mtDNA of the motile one (the sperm),
> the integrity of mtDNA in the progeny is maintained. Of course, this would
> all go to pot if the maternal mtDNA were mutated to begin with, so maybe
> there is some kind of index of mtDNA integrity (such as respiratory
> function/Ca handling) upon which oocytes are selected?
Sperm certainly carry elevated levels of mtDNA damage through exposure to
ROS. However, this can't be the full answer as one gets uniparental
transmission even in protists where there's no anisogamy. I suspect
uniparental transmission came first to avoid genome conflict among
subservient organeleles, and as a consequence eukaryotic systems can
tolerate elevated mtDNA damage in microgametes.
Incidentally maternal transmission means that there's no selection for
male mtDNA "fitness" and consequently some mitochondrial diseases are more
prevalent and more severe in males as compared with females. Some aspects
of male infertility also appear to be related to oxidative damage and
mitochondrial dysfunction - for example the testicular artery is
frequently the first region of the CV system to show atherosclerosis, and
the testis is extremely sensitive to ischaemia (probably one reason for a
scrotum - to reduce oxygen needs).
--
Jim Cummins <cummins at central.murdoch.edu.au.
URL http://numbat.murdoch.edu.au/spermatology/spermhp.html
