Post-replicative lesion processing limits DNA damage-induced mutagenesis.

ABSTRACT: DNA lesions are a threat to genome stability. To cope with them during DNA replication, cells have evolved lesion bypass mechanisms: Translesion Synthesis (TLS), which allows the cell to insert a nucleotide directly opposite the lesion, with the risk of introducing a mutation, and error-free damage avoidance (DA), which uses homologous recombination to retrieve the genetic information from the sister chromatid. In this study, we investigate the timing of lesion bypass in yeast and its implications for the accuracy of the process. Our findings reveal that DNA polymerase η can bypass common, UV-induced cyclobutane pyrimidine dimers at the fork, immediately after encountering the blocking lesion. In contrast, TLS at (6-4) photoproducts and bulky G-AAF adducts, mediated by Rev1 and Pol ζ, take

SUBMITTER: Maslowska KH 

PROVIDER: S-EPMC11925729 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature