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Silent repair accounts for cell cycle specificity in the signaling of oxidative DNA lesions
Author(s) -
Leroy Christophe,
Mann Carl,
Marsolier MarieClaude
Publication year - 2001
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/20.11.2896
Subject(s) - biology , dna damage , hydrogen peroxide , dna , dna repair , cell cycle , reactive oxygen species , oxidative stress , oxidative phosphorylation , microbiology and biotechnology , base excision repair , biochemistry , cell
Reactive oxygen species are the most important source of DNA lesions in aerobic organisms, but little is known about the activation of the DNA checkpoints in response to oxidative stress. We show that treatment of yeast cells with sublethal concentrations of hydrogen peroxide induces a Mec1‐dependent phosphorylation of Rad53 and a Rad53‐dependent cell cycle delay specifically during S phase. The lack of Rad53 phosphorylation after hydrogen peroxide treatment in the G 1 and G 2 phases is due to the silent repair of oxidative DNA lesions produced at these stages by the base excision repair (BER) pathway. Only the disruption of the BER pathway and the accumulation and/or treatment of DNA intermediates by alternative repair pathways reveal the existence of primary DNA lesions induced at all phases of the cell cycle by hydrogen peroxide. Our data illustrate both the concept of silent repair of DNA damage and the high sensitivity of S‐phase cells to hydrogen peroxide.