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Persistence of separate mitochondrial genome

Andrew Gyles acgyles at my-deja.com
Sat Sep 16 00:25:54 EST 2000

Mark Dowton, Holger Hufpfer, Ram Samudrala and David Mathog,

Thank you for your insightful responses to my original message. Is it
all right if I respond to them in the one message, as I have further

Ram, your insight seems particularly appropriate to the
most 'primitive' mitochondrion  yet discovered, in the flagellate
Reclinomonas americana, which has an mtDNA genome of 69 kilobases, with
62 protein-coding genes. And it may also be appropriate to the
mitochondria of plants, which have a large genome size ranging from 200
to 2500 kilobases; these genomes seem to have been elaborated from the
primitive one.

On the other side, as Saccone et al remarked, are the metazoa
(multicellular animals), in which the size of the mtDNA genome is about
14-17 kilobases. It seems appropriate to ask, Why has the 'primitive'
genome been reduced in the metazoa?

David Mathog, your remarks about the effect of mutations on an
organelle with only a single copy of its genome, and the possible
better repairing of mutated sequences in nuclear genes than in
mitochondrial genes, strike a chord with me. I have suggested that
mitochondria have multiple copies of their genome so that they can
eliminate substitution mutations by detecting the physical distortion
they cause in the double-stranded mtDNA, and then either destroying the
entire copy of the double-stranded circular genome or ejecting it from
the organelle. This is speculative, of course.

(The fact that mitochondria have multiple copies of their genome is not
widely appreciated, because it does not seem to be emphasised in
teaching. The best indication I have found of the number of copies of
mtDNA in the mitochondria of humans is about 10. Your point about
recombination is pertinent: the copies in the mitochondrion are
identical, so the benefits of recombination cannot be gained.)

Mark Dowton and Holger Hupfer, thank you for your reference to Race et
al in Trends in Genetics; I hope to be able to access this tomorrow,
and also a review by Caccone et al in Gene (1999), 238 (1), 195-209.
Your remarks about the situation in plants are illuminating. It seems
reasonable to conclude that their mitochondria and chloroplasts cope
very well with the threat of damage to their DNA by oxygen free
radicals: they do not have to send their genes to the relative safety
of the nucleus. And so we have to find another reason why many of the
mitochondrial genes of multicellular animals have gone from the
mitochondrion to the nucleus.

There is one other aspect of mitochondrial activity that we might be
able to explain in connection with the reduced mtDNA genome in
multicellular animals. In mammals (perhaps in all the metazoa, I am not
sure) they play a part in the programmed killing of cells: apoptosis.

Please excuse my ignorance of the fine details of chloroplasts and
mitochondria in vascular plants. May I ask whether the number of copies
of the genome in chloroplasts is about the same as the number in
mitochondria? Is it possible to quote a fairly typical number, or is
there wide variation from species to species?

Andrew Gyles

In article <8pourc$ndr$1 at mercury.hgmp.mrc.ac.uk>,
  Mark Dowton <mdowton at uow.edu.au> wrote:
> HI Andrew,
> There's an interesting article published recently on this topic in TIG
> [Trends in Genetics(1999): 15, 364 - Why have organelles retained
> genomes?].  It's based on an hypothesis of John F. Allen that there's
> selective advantage for the proteins most susceptible to free radical
> attack to be synthesized close to where damage is sustained frome
> radicals.  Of course, for this to work, you have to keep all the
> machinery to make these proteins.  It makes sense to me, but perhaps
> Saccone knew of some flaws in this argument that aren't apparent to
> I'd be interested to hear if that was the case.
> Cheers, Mark

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