Analysis of CPD Ultraviolet Lesion Bypass in Chicken DT40 Cells: Polymerase η and PCNA Ubiquitylation Play Identical Roles

摘要: Translesion synthesis (TLS) provides a mechanism of copying damaged templates during DNA replication. This potentially mutagenic process may operate either at the replication fork or post-replicative gaps. We used example T-T cyclobutane pyrimidine dimer (CPD) bypass to determine influence polymerase recruitment via PCNA ubiquitylation versus REV1 protein on efficiency and outcome TLS. Using mutant chicken DT40 cell lines we show that, this numerically most important UV lesion, defects in η similarly result long-term failure lesion with persistent strand gaps opposite elevation mutations amongst successful TLS events. Our data suggest that promotes CPD mainly by recruiting η, resulting majority lesions bypassed an error-free manner. In contrast, find ζ is responsible for CPD-dependent mutations, but has no essential function completion bypass. These findings point hierarchy access different polymerases suggesting temporal order their recruitment. The similarity REV3 phenotypes confirms involvement largely determined its REV1. demonstrate success accuracy