Silent repair accounts for cell cycle specificity in the signaling of oxidative DNA lesions.

摘要: Reactive oxygen species are the most important source of DNA lesions in aerobic organisms, but little is known about activation checkpoints response to oxidative stress. We show that treatment yeast cells with sublethal concentrations hydrogen peroxide induces a Mec1-dependent phosphorylation Rad53 and Rad53-dependent cell cycle delay specifically during S phase. The lack after G1 G2 phases due silent repair produced at these stages by base excision (BER) pathway. Only disruption BER pathway accumulation and/or intermediates alternative pathways reveal existence primary induced all peroxide. Our data illustrate both concept damage high sensitivity S-phase