Genetically controlled mtDNA deletions prevent ROS damage by arresting oxidative phosphorylation.

ABSTRACT: Deletion of mitochondrial DNA in eukaryotes is currently attributed to rare accidental events associated with mitochondrial replication or repair of double-strand breaks. We report the discovery that yeast cells arrest harmful intramitochondrial superoxide production by shutting down respiration through genetically controlled deletion of mitochondrial oxidative phosphorylation genes. We show that this process critically involves the antioxidant enzyme superoxide dismutase 2 and two-way mitochondrial-nuclear communication through Rtg2 and Rtg3. While mitochondrial DNA homeostasis is rapidly restored after cessation of a short-term superoxide stress, long-term stress causes maladaptive persistence of the deletion process, leading to complete annihilation of the cellular pool of intact mitoch

SUBMITTER: Stenberg S 

PROVIDER: S-EPMC9427111 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature