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Significance Chromosomal double-strand breaks (DSBs) are cytotoxic forms of DNA damage that must be accurately repaired to maintain genome integrity. The conserved Mre11-Rad50-Xrs2NBS1 complex plays an important role in repair by functioning as a damage sensor and by regulating DNA end processing to ensure repair by the most appropriate mechanism. Yeast Sae2 is known to activate the Mre11 endonuclease to process DNA ends, and previous studies suggest an additional role to dampen checkpoint signaling. Here, we show Sae2 functions independently of the Mre11 nuclease to prevent Rad9 accumulation at DSBs. Excessive Rad9 binding inhibits DNA end processing by the Dna2-Sgs1 and Exo1 nucleases causing sensitivity of Sae2-deficient cells to DNA damaging agents.

Sae2 antagonizes Rad9 accumulation at DNA double-strand breaks to attenuate checkpoint signaling and facilitate end resection