The primitive mitochondrion as a fatal parasite

Andrew Gyles acgyles at
Wed Sep 27 17:00:34 EST 2000

The primitive mitochondrion might have been a parasite of primitive
eucaryotic cells that preserved a free-living stage in its life cycle,
gaining its freedom by lysing its host.

Such an association would not have been disastrous for the host species
if it were able to multiply more quickly with the parasite than without
it, and if the parasite did not lyse a cell of its host too frequently.
The great gain in metabolic efficiency conferred by the oxidative
respiration of the primitive mitochondrion would have helped the host
cell to grow more quickly and multiply more quickly, and therefore a
single-celled host species could survive the occasional lysing of some
of its cells.

Nonetheless, the host would gain a further advantage if it could stop
the primitive mitochondrion from lysing the cell of its host. As the
primitive single-celled eucaryotic cell evolved into separate species
each species might have developed its own ways of 'disarming' its
parasite. One way would have been to 'confiscate' those genes of the
parasite that were involved in the lysing of the host and place them in
the nucleus under the control of the host. Another way might have been
for the host cell to interfere in the expression of the genes that
remained functional in the mitochondrion by sending host-derived
control proteins or RNA into the mitochondrion.

The evolution of multi-cellular species could not have proceeded far if
occasionally some of their cells were lysed at random. Such random
lysing would disrupt the organisation upon which multi-cellular species
depend for their success. Therefore we might expect to see in these
organisms a more stringent control of lysing by mitochondria than in
single-celled species.

However, controlled lysing of particular host cells might have been of
great advantage in the evolution of multicellular species. Such an
advantage might have been achieved if the host gained control of the
lysing activity of its mitochondria and applied it in a programmed way
to achieve 'programmed cell death', or apoptosis. And indeed we know
that mitochondria are the focus of many of the drastic processes
involved in apoptosis.

Thus the simple assumption that the primitive mitochondrion was a
parasite that occasionally lysed the cell of its host can explain why
some mitochondrial genes have been transferred to the nucleus in many
species of eucaryotic cell, and why mitochondria are the focus of
apoptotic activity in various multicellular species.

(Note: I have used the terms lysing and lyse in a general sense. I have
used words such as disarming, confiscate, interfere, and so on as a
concise way of expressing the results under natural selection of a few
trillion dice throws on the board of the conditions of existence.)

Andrew Gyles

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