Disruption of the nuclear COX5 gene delays senescence, increase longevity between 7- and 15-fold (in 30 tested isolates) and the onset of senescence is not associated by accumulation of senescence-specific mtDNA molecules. COX5 deletion results in exclusive use of the alternative respiratory pathway and a decrease in production of reactive oxygen species and the prevention of the accumulation of several senescence-specific mitochondrial DNA molecules [10759557].
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