Replication-associated repair of Adenine:8-oxoguanine mispairs by MYH

摘要: Cellular DNA is constantly exposed to the risk of oxidation. 8-oxoguanine (8-oxoG) one major lesions generated by oxidation, which primarily corrected base excision repair. When it not repaired prior replication, replicative polymerases yield misinsertion an adenine (A) opposite 8-oxoG on template strand, generating A:8-oxoG mispair [1]. MYH, a mammalian homolog Escherichia coli MutY, glycosylase responsible for initiating repair such excising [2]. Here, using in vivo system, we show that replication enhances mispair. Repair efficiency was lower MYH-deficient murine cells than MYH-proficient cells. Transfection with wild-type MYH expression vector increased repair, indicating significant part this replication-associated depends MYH. Expression mutant PCNA binding motif disrupted did increase efficiency, thus suggesting interaction between and critical MYH-initiated A:8-oxoG.