Silent repair accounts for cell cycle specificity in the signaling of oxidative DNA lesions.
EMBO J
; 20(11): 2896-906, 2001 Jun 01.
Article
en En
| MEDLINE
| ID: mdl-11387222
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 G1 and G2 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.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteínas Quinasas
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Saccharomyces cerevisiae
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Daño del ADN
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Ciclo Celular
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Proteínas Serina-Treonina Quinasas
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Estrés Oxidativo
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Proteínas de Ciclo Celular
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Proteínas de Saccharomyces cerevisiae
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Reparación del ADN
Idioma:
En
Revista:
EMBO J
Año:
2001
Tipo del documento:
Article
País de afiliación:
Francia
Pais de publicación:
Reino Unido