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Significance A large number of nucleotides is continuously damaged in every cell. Damaged nucleotides stall replicative DNA polymerases on template strands. Resulting replication blockage is released by two alternative pathways, error-free template switching (TS) and error-prone translesion DNA synthesis (TLS). TLS plays a major role in converting DNA damage to mutations, and thus, the relative usage of TLS over TS determines the frequency of mutagenesis. The relative usage is controlled by post-translational modification of proliferating cell nuclear antigen (PCNA), which physically interacts with DNA synthesis enzymes, inSaccharomyces cerevisiae. Environmental DNA damage induces ubiquitylation of PCNA and promotes TLS. We here show that SUMOylation of PCNA ensures the release of replication blockage by error-free TS pathways and prevents mutagenesis during the physiological cell cycle.

SUMOylation of PCNA by PIAS1 and PIAS4 promotes template switch in the chicken and human B cell lines