questions about mitochondria

Iuval Clejan clejan at
Tue Aug 8 23:50:13 EST 2000

I hope some kind soul answers these questions from a physicist who is
pretty ignorant of biology (not just Aubrey):

1. Can there be a mechanism of segregation of "bad" mitochondria into 3
of the four oocytes that form from one oogonium, and good mitochondria
into the viable oocyte? Why is everyone insisting that there is a
selection mechanism operating prior to meiosis? Sorry Aubrey but I have
not found support for this in the references you provided (maybe I
didn't understand). Maybe something similar occurs in replicating
oocytes to what occurs in replicating yeast with ERCs (what is the
biochemical reason for the asymmetry in that case?)

2. Actually I don't understand oogenesis. My understanding is that
mitosis occurs a few times in the embryo and that the cells are then
called oogonia. After the first meiotic division the cells are called
primary oocytes (diploid?). And after the second meiotic division (which
occurs during sexual maturity) the cells are called secondary oocytes.
Is this correct? Some people have told me that meiosis is not complete
until ovulation (how so?) I also read in a texbook that Drosophila
produces 15 "nurse cells" for every real egg. Does this mean there are 4
instead of two meiotic divisions for Drosophila? Or maybe the first two
are mitotic.

3. What proteins that are involved in mitochondrial welfare are coded
for by the nucleus? Anything for repair of mtDNA? Replication of mtDNA/
transcription of mtDNA? Why is tellomerase anti-apopototic? Is it
possible that senescent cells stop expressing some of the genes
necessary for mitochondrial welfare? I am thinking that one of the main
differences between mitos and aerobic bacteria is that mitos are
symbiotic with the nucleus, whereas bacteria are rugged individualists.
So what if mitos are mutating at a high rate, so are bacteria, as long
as they keep reproducing they will survive. One thing that might keep
them from reproducing is a nuclear clock (e.g. tellomere shortening
followed by activation of P53 followed by apoptotic signals) This
scenario would favor mitos in post mitotic cells, if other mechanisms
didn't come into play.

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