<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>Chloroplasts and mitochondria originated as bacterial symbionts. The larger, host
cells acquired genetic information from their prokaryotic guests by lateral gene
transfer. The prokaryotically-derived genes of the eukaryotic cell nucleus now
function to encode the great majority of chloroplast and mitochondrial proteins,
as well as many proteins of the nucleus and cytosol. Genes are copied and moved
between cellular compartments with relative ease, and there is no established obstacle
to successful import of any protein precursor from the cytosol. Yet chloroplasts and
mitochondria have not abdicated all genes and gene expression to the nucleus and
to cytosolic translation. What, then, do chloroplast- and mitochondrially-encoded
proteins have in common that confers a selective advantage on the cytoplasmic
location of their genes? The proposal advanced here is that co-location of chloroplast
and mitochondrial genes with their gene products is required for rapid and direct
regulatory coupling. Redox control of gene expression is suggested as the common
feature of those chloroplast and mitochondrial proteins that are encoded <italic>in situ</italic>.
Recent evidence is consistent with this hypothesis, and its underlying assumptions
and predictions are described.</p>
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Comp Funct Genomics. 2003 Feb; 4(1):31-36