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Brief Communication
Nature Genetics 40, 392–394 (1 April 2008) | doi:10.1038/ng.95
DNA deletions and clonal mutations drive premature aging in mitochondrial mutator mice
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Abstract
Mitochondrial DNA (mtDNA) mutations are thought to have a causal role in many age-related pathologies. Here we identify mtDNA deletions as a driving force behind the premature aging phenotype of mitochondrial mutator mice, and provide evidence for a homology-directed DNA repair mechanism in mitochondria that is directly linked to the formation of mtDNA deletions.
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