questions about mitochondria

Jim Cummins cummins at
Thu Aug 10 02:49:44 EST 2000

In article <3990E304.5B9BBD51 at>, Iuval Clejan
<clejan at> wrote:

> 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? 
Only one of the daughters forms the ovum - the rest are the polar bodies
destined to be discarded. You can certainly amplify mtDNA from the polar
bodies and this has been propsed as a diagnostic tool for mtDNA disorders
in early embryos (Briggs et al. Amplification of DNA sequences in polar
bodies from human oocytes for diagnosis of mitochondrial disease. Lancet
2000; 355: 1520-1521.). I know of no evidence of differential segregation.
> 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?)

The primary oocytes enter a dictyate resting stage during fetal life (I'm
talking mammals here).  Meiosis only resumes around ovulation and in fact
activation of the oocyte (normally by sperm penetration) is the trigger
for the second meiotic division.
> 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.

In mammals the vast majority of maintenance genes have translocated to the
nuclear genome and the only ones left appear to be the minimal set
required for OXPHOS. It's certainly possible that senescence involves
decay in these .In sharp contrast to the over fifty pathogenic mutations
described in mtDNA, only one disease-causing mutation has been identified
in a nuclear gene, that encoding the flavoprotein subunit of complex II
(Bourgeron et al., 1995). This situation will certainly change in the
years to come because there is good, if indirect, evidence that many
generalized syndromes are due to mutations of nDNA-encoded subunits of the
respiratory chain (Di Mauro et al., 1998)

Jim Cummins
Murdoch University
<cummins at>

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