The article listed below describes (or models the possibilities as to) how mutations arise and accumulate––as a function of gender, age, and cell division. The authors’ model provides a single framework within which to interpret emerging results from evolutionary biology, human genetics, and cancer genetics.
Authors show that the build-up of mutations should track cell divisionsnot only when mutations originate during DNA replication, but also when they arise through non-replicative mechanisms and are repaired efficiently. This insight proposes that previous observations of correlations between mutation and cell division rates actually provide little support to the commonly-held belief that “most germline and somatic mutations arise from replication errors”. Authors further find that only mutations that arise from inefficiently-repaired lesions will accrue according to absolute time. Therefore, without co-variation in life history traits, the phylogenetic “molecular clock” (widely used in evolutionary biology) should not be expected to run at constant rates across multiple distinct species. PLoS_Biol_Germline_vs_Soma~1.pdf