Mitochondrial Genes Cause Nuclear Mischief
DOI: 10.1371/journal.pbio.0020316


Published September 7, 2004

Copyright: © 2004 Public Library of Science. This is an open-access article
distributed under the terms of the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any
medium, provided the original work is properly cited.

While the nucleus of a cell may be its command headquarters, mitochondria
are equally vital-they are the power plants of the cell, and without them
all cellular activity would quickly and irrevocably come to a halt.
Testifying to their origins as once free-living bacteria, mitochondria have
their own DNA, comprising 37 genes in humans on a single circular
chromosome. Whether they invaded their ancestral hosts as parasites or were
captured as subcellular collaborators, they have long since left their
independent ways behind. Their meager complement of genes is far fewer than
is needed to produce these complex organelles; it is clear from analyzing
the nuclear genome that most of the mitochondria's presumed ancestral genes
have been taken into the cell's nucleus, where they are under the strict
control of their host.

The transplanted mitochondrial genes have been faithfully doing their job
under new management since they were first appropriated, probably hundreds
of millions of years ago. However, not all of their DNA descendants have
continued to make themselves so useful. For, in addition to many of the
mitochondria's original genes, the human genome houses over 200
mitochondrial genetic fragments, useless pieces of code whose only remaining
function is to be replicated generation after generation.

Detritus from other sources is even more common within the genome, and most
of it seems to be harmless. But in this issue, Ricchetti and colleagues show
that mitochondrial fragments may not be quite so benign. They have continued
to invade the human genome, even into the present day, and a large
proportion of them take up residence within nuclear genes, possibly
disrupting them and causing human diseases.

Full Text at PLoS Biology
http://www.plosbiology.org/plosonline/?request=get-document&doi=10.1371/journal.pbio.0020316

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