1. Researchers created "mtDNA-mutator mice" with a defective mitochondrial DNA polymerase that lacked exonuclease activity. 2. These mice accumulated somatic mtDNA mutations over time and exhibited premature aging phenotypes such as weight loss, hair loss, bone loss, and heart abnormalities. 3. The median lifespan of mtDNA-mutator mice was 48 weeks compared to over 2 years in normal mice, providing an experimental link between increased somatic mtDNA mutations, mitochondrial dysfunction, and mammalian aging.