More errata:
In (5) I did not mean that urea is produced in mitochondria, but that
mitochondrial enzymes are part of the urea cycle.
Looking at the cross species ploidy data more carefully, I realized that
the primates and rodents that did not have significant tetraploidy, did
have binucleated hepatocytes (each nucleus diploid) at levels
approximately the same as all studied rodents, insects, and primates.
Since I am postulating that the important thing is to increase gene copy
(more specifically nuclear genes involved in mitochondrial maintenance),
these animals are no exception. What is different about them is that
they are not as responsive to reinitiating cytokinesis of binucleates as
rats, mice and humans. Restated, higher ploidy in the initially diploid
liver is a two step process, the first step is binucleation, the second
is cytokinesis of binucleates (after they go through S-phase). Only the
first step is essential for doubling gene copy, making the cell
tetraploid. Higher ploidies probably do not give much more advantage as
far as mitochondrial maintenance, but happen because cells need to be
replaced.
I am also not sure if the uricotelic organisms use glutamine synthetase
and other mitochondrial enzymes in their mitochondria to get rid of
ammonia.
