Steve LaBonne and Mitochondrial genetic codes

Keith Robison robison at lipid.harvard.edu
Mon Aug 28 08:50:36 EST 1995


Erich Schwarz (schwarze.ccomail at starbase1.caltech.edu) wrote:
: HPYockey wrote:

:     My own *opinion*, if anyone cares, is that mitochondria are a bad
: place on which to base arguments about the genetic code, because they do
: not have particularly normal genomes.  In mammals, and possibly many
: organisms, mitochondrial chromosomes are given a sinecure -- with only
: about 15 proteins that they must encode.  They consequently can probably
: tolerate considerably more fluctuation of their genetic code than even
: _Mycoplasma_ (encoding ~800 proteins) could ever do.  

BINGO!  

: At the same time,
: they are probably under considerable pressure to minimize genome size, and
: also probably have somewhat lower fidelity of DNA replication than either
: eubacteria or eukaryotes do.  Finally, they encode their own rRNAs and
: tRNAs, 

Irrevelevant side note: some mitochondria import some of their tRNAs
from the nucleus.

: unlike viruses which must depend entirely on the translational
: machinery of a host cell.  Add this all up over many years, and you've got
: a plausible setting for *late* alteration of mitochondrial codons.

:     If phylogenetic analysis were to show that codon alterations were
: derived characters that arose in the late Precambrian, the argument would
: be over; I leave it to others to describe whether such an analysis is yet
: available, and what it says.

I don't know of the timing, but the phylogeny is quite sound.  rRNA
analysis places the mitochondria in amongst the purple ("gram negative")
bacteria.  Among the purples, mitochondria seem to be the _only_
species with altered genetic codes.  Similarly, all of the other
known deviations from the canonical genetic code are one little
tip of the tree.  Hence, we must conclude that these are late
events, and the best explanation is that a codon fell into disuse
(either through drift in a small genome or codon usage selection),
allowing a switch to another usage (which is what Jukes currently
argues).


Keith Robison
Harvard University
Department of Cellular and Developmental Biology
Department of Genetics / HHMI

robison at mito.harvard.edu 






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