共 33 条
Escape of Sgs1 from Rad9 inhibition reduces the requirement for Sae2 and functional MRX in DNA end resection
被引:51
作者:

Bonetti, Diego
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Univ Milano Bicocca, Dipartimento Biotecnol & Biosci, Milan, Italy Univ Milano Bicocca, Dipartimento Biotecnol & Biosci, Milan, Italy

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Cassani, Corinne
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Univ Milano Bicocca, Dipartimento Biotecnol & Biosci, Milan, Italy Univ Milano Bicocca, Dipartimento Biotecnol & Biosci, Milan, Italy

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[1] Univ Milano Bicocca, Dipartimento Biotecnol & Biosci, Milan, Italy
关键词:
double-strand break;
Rad9;
resection;
Saccharomyces cerevisiae;
Sgs1;
SINGLE-STRANDED-DNA;
SACCHAROMYCES-CEREVISIAE;
HOMOLOGOUS RECOMBINATION;
DAMAGE RESPONSE;
CHECKPOINT ACTIVATION;
G2/M ARREST;
BREAK ENDS;
CELL-CYCLE;
HELICASE;
REPAIR;
D O I:
10.15252/embr.201439764
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Homologous recombination requires nucleolytic degradation (resection) of DNA double-strand break (DSB) ends. In Saccharomyces cerevisiae, the MRX complex and Sae2 are involved in the onset of DSB resection, whereas extensive resection requires Exo1 and the concerted action of Dna2 and Sgs1. Here, we show that the checkpoint protein Rad9 limits the action of Sgs1/Dna2 in DSB resection by inhibiting Sgs1 binding/persistence at the DSB ends. When inhibition by Rad9 is abolished by the Sgs1-ss mutant variant or by deletion of RAD9, the requirement for Sae2 and functional MRX in DSB resection is reduced. These results provide new insights into how early and long-range resection is coordinated.
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页码:351 / 361
页数:11
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