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Mitochondria perform critical functions, including respiration, ATP
production, small molecule metabolism, anti-oxidation, and they are
involved in a number of human diseases. While the mitochondrial genome
contains a small number of protein-coding genes, the vast majority of
mitochondrial proteins are encoded by nuclear genes. In fission yeast,
Schizosaccharomyces pombe, we screened 457 deletion (del) mutants
deficient in nuclear-encoded mitochondrial proteins, searching for those
that fail to form colonies in culture medium containing low glucose
(0.03–0.1%; low-glucose sensitive, lgs), but that proliferate in regular
2–3% glucose medium. Sixty-five (14%) of the 457 deletion mutants
displayed the lgs phenotype. Thirty-three of them are defective either in
dehydrogenases, subunits of respiratory complexes, the TCA cycle, or in
one of the 9 steps of the CoQ10 biosynthetic pathway. The remaining 32 lgs
mutants do not seem to be directly related to respiration. Fifteen are
implicated in translation, and 6 encode transporters. The remaining 11
function in anti-oxidation, amino acid synthesis, repair of DNA damage,
microtubule cytoskeleton, intracellular mitochondrial distribution, or
unknown functions. These 32 diverse lgs genes collectively maintain
mitochondrial functions under low (1/20~1/60x normal) glucose
concentrations. Interestingly, 30 of them have homologs associated with
human diseases.
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