Journal
NATURE GENETICS
Volume 40, Issue 4, Pages 392-394Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.95
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Funding
- NATIONAL CANCER INSTITUTE [R01CA102029] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [U01ES011045] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG021905, P01AG001751] Funding Source: NIH RePORTER
- NCI NIH HHS [CA102029] Funding Source: Medline
- NIA NIH HHS [AG01751, AG021905] Funding Source: Medline
- NIEHS NIH HHS [ES11045] Funding Source: Medline
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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. In addition, our results demonstrate that the rate at which mtDNA mutations reach phenotypic expression differs markedly among tissues, which may be an important factor in determining the tolerance of a tissue to random mitochondrial mutagenesis.
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