Maintenance of genome sequence integrity in long-and short-lived rodent species

DNA mutations in somatic cells have been implicated in the causation of aging, with longer-lived species having a higher capacity to maintain genome sequence integrity than shorter-lived species. In an attempt to directly test this hypothesis, we used single-cell whole-genome sequencing to analyze spontaneous and bleomycin-induced somatic mutations in lung fibroblasts of four rodent species with distinct maximum life spans, including mouse, guinea pig, blind mole-rat, and naked mole-rat, as well as humans. As predicted, the mutagen-induced mutation frequencies inversely correlated with species-specific maximum life span, with the greatest difference observed between the mouse and all other species. These results suggest that long-lived species are capable of processing DNA damage in a more accurate way than short-lived species.

Automated summary

Long-lived species demonstrate a higher capacity for accurate DNA damage repair, which may help slow down the aging process. The mutagen-induced mutation frequencies are inversely correlated with the maximum life span of different species, with the most significant difference observed between mice and other species.