Miniature apoptosis in mussels (hypothesis)
Mussels have two types of mitochondria and mtDNA: one that is
transmitted from the mother to daughters and sons (the F type), and one
that is transmitted from the father to daughters and sons (the M type).
The female and male embryos receive M mtDNA through the sperm, but
within 24 hours it is eliminated or drastically reduced in female
embryos but is maintained in male embryos (1).
I suggest that M mitochondria have in their outer membrane molecules
that specifically fit a protein that acts as a male-steroid receptor.
When this protein is present in the cytoplasm of the cell in the
absence of male-steroid molecules it binds to the outer membrane of M
mitochondria and permeabilises it, thus destroying the M mitochondria.
I call this action 'miniature apoptosis' because the tiny organelles
are destroyed, but not their host cell. When this protein forms a
complex with a male-steroid molecule its conformation changes, so that
it cannot permeabilise the outer membrane of M mitochondria.
Thus M mitochondria are destroyed in female embryos, whose cells
contain no, or few, male-steroid molecules. But M mitochondria are not
destroyed in male embryos because their cells contain many male-steroid
molecules.
It is possible that F mitochondria have in their outer membrane
molecules that specifically fit a protein that acts as a female-steroid
receptor. When not complexed with a female-steroid molecule this
protein can permeabilise the outer membrane of F mitochondria. When
complexed with a female-steroid molecule the protein cannot
permeabilise the F mitochondrial outer membrane. If the cells of both
female embryos and male embryos contain many female-steroid molecules
the F mitochondria will be maintained in both sexes.
This hypothesis is, I think, given some support by findings in a paper
published last August. In human cells a steroid receptor called TR3,
normally present in the nucleus, translocates to mitochondria in
response to apoptotic stimuli and permeabilises the mitochondrial
membranes, releasing cytochrome c and triggering a series of events
that cause apoptotic cell death. TR3 is called an 'orphan' receptor
because the steroid with which it is assumed to form a specific complex
has not yet been identified (2).
Humans inherit mitochondria and mtDNA only from their mothers. I
suggest that the evolutionary 'ancestor' of TR3 was like the
(hypothetical) female-steroid receptor in mussels that permeabilises
the outer membrane of F mitochondria in the absence of female-steroid
molecules. I suggest that TR3 has evolved in such a way that it can no
longer form a specific complex with a female-steroid molecule, and is
therefore able to permeabilise mitochondria and trigger apoptosis in
all human cells, whether male cells or female cells. It is a
permanent 'orphan'.
1. Sutherland et al, Genetics 148: 341-347 (January, 1998).
2. Li et al, Science 289: 1159-1164 (18 August, 2000); and in the same
issue the perspective by Brenner and Kroemer, pp 1150 and 1151.
(I thank group members who provided information and references on
mitochondrial inheritance.)
Andrew Gyles
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