Journal
EMBO REPORTS
Volume 16, Issue 3, Pages 351-361Publisher
WILEY-BLACKWELL
DOI: 10.15252/embr.201439764
Keywords
double-strand break; Rad9; resection; Saccharomyces cerevisiae; Sgs1
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Funding
- Associazione Italiana per la Ricerca sul Cancro (AIRC) [IG15210]
- Cofinanziamento MIUR/Universita di Milano-Bicocca
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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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