questions about mitochondria

Jim Cummins cummins at central.murdoch.edu.au
Sun Sep 10 01:33:11 EST 2000

In article <39B8580F.B3B92DB7 at mindspring.com>, Iuval Clejan
<clejan at mindspring.com> wrote:

> Thanks for all the replies and pointers to the Alberts' book.
> From Alberts': "In most vertebrates oocyte maturation is arrested at metaphase
> of meiosis II and the secondary oocyte completes meiosis II only after
> fertilization."
> Does this mean that the oocyte divides into an egg with a sperm and a polar
> body, after the sperm enters it? Metaphase is before actual division, so this
> seems to be the case. But it doesn't sound right.
No.  Sperm entry triggers oocyte activation: calcium oscillations and
release of cortical granule proteases that harden the zona pellucida
against further sperm entry, plus completion of meiosis and release of the
oocyte's second polar body.  The haploid sperm nucleus decondenses. In
most species (except Murid rodents as far as we know) the sperm centrosome
in the neck region acts as a mirotubule organising centre: MTs radiate
throughout the egg cytoplasm and eventually locate and reel in the female
haploid pronucleus. The two pronulei are brought together, nuclear
membranes break down and the two haploid sets of chromosomes pair up on
the first mitotic spndle.
> Refined hypothesis A: During telophase I and/or II of meiosis, "good"
> mitochondria stay in the oocyte and "bad" mitochondria end up in the polar
> body. This mechanism is responsible for resetting of the ageing clock in most
> vertebrates. Any ideas on what it would take to test this hypothesis?
There's no evidence to support or refute this.  The homoplasmy of the
oocyte's mitochondria is almost certainly established by a rigorous
numerical filter during the formation of the promordial germ cells in
early embryonic life, and  clonal expansion of mitochondria from this
restricted pool - some think the effective founder size could be a single
mitochondrion.  This MAY be reinforced by selection against oocytes
containing dysfunctional mitochondria during fetal and adult life, but the
evidence for this is weak and circumstantial.
> Hypothesis B: "Bad" mitochondria only occur at cellular senescence, or in non
> dividing cells. Since eggs don't experience cellular senescence, there is no
> need to reset the clock. How to test this one?
The vast majority of eggs are never released - in humans numbers peak at 7
million in mid-gestation  but of these only a few hundred are ever
released. Eggs DO undergo senescence - there's a vast literature on the
problems of the aged oocyte both in vivo and in vitro.

Jim Cummins
Murdoch University
<cummins at central.murdoch.edu.au>

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