Population size interacts with reproductive longevity to shape the germline mutation rate DOI Creative Commons
Luke Zhu, Annabel C. Beichman, Kelley Harris

et al.

Proceedings of the National Academy of Sciences, Journal Year: 2025, Volume and Issue: 122(21)

Published: May 20, 2025

Mutation rates vary across the tree of life by many orders magnitude, with fewer mutations occurring each generation in species that reproduce quickly and maintain large effective population sizes. A compelling explanation is sizes facilitate selection against weakly deleterious “mutator alleles” such as variants modulate cell division or interfere molecular efficacy DNA repair. However, while fidelity a single largely determines microorganisms’ mutation rates, relationship rate to determinants damage repair more complex multicellular long times. Since generations leave time for accrue generation, we posit likely amplifies fitness consequences any agent defect creates extra spermatogonia oocytes. This leads counterintuitive prediction highest germline per are also most mechanisms avoiding repairing their reproductive cells. Consistent this, show cells inversely correlated time; contrast, number occur during prepuberty development trends upward increases. Our results parallel recent findings longest-lived have lowest adult somatic tissues, potentially due keep lifetime load below harmful threshold.

Language: Английский

Population size interacts with reproductive longevity to shape the germline mutation rate DOI Creative Commons
Luke Zhu, Annabel C. Beichman, Kelley Harris

et al.

Proceedings of the National Academy of Sciences, Journal Year: 2025, Volume and Issue: 122(21)

Published: May 20, 2025

Mutation rates vary across the tree of life by many orders magnitude, with fewer mutations occurring each generation in species that reproduce quickly and maintain large effective population sizes. A compelling explanation is sizes facilitate selection against weakly deleterious “mutator alleles” such as variants modulate cell division or interfere molecular efficacy DNA repair. However, while fidelity a single largely determines microorganisms’ mutation rates, relationship rate to determinants damage repair more complex multicellular long times. Since generations leave time for accrue generation, we posit likely amplifies fitness consequences any agent defect creates extra spermatogonia oocytes. This leads counterintuitive prediction highest germline per are also most mechanisms avoiding repairing their reproductive cells. Consistent this, show cells inversely correlated time; contrast, number occur during prepuberty development trends upward increases. Our results parallel recent findings longest-lived have lowest adult somatic tissues, potentially due keep lifetime load below harmful threshold.

Language: Английский

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