DNA damage checkpoint and recombinational repair differentially affect the replication stress tolerance of Smc6 mutants.

ABSTRACT: DNA damage checkpoint and recombinational repair are both important for cell survival of replication stress. Because these two processes influence each other, isolation of their respective contributions is challenging. Research in budding yeast shows that removal of the DNA helicase Mph1 improves survival of cells with defective Smc5/6 complex under replication stress. mph1 is known to reduce the levels of recombination intermediates in smc6 mutants. Here, we show that mph1 also hyperactivates the Mec1 checkpoint. We dissect the effects of recombination regulation and checkpoint hyperactivation by altering the checkpoint circuitry to enhance checkpoint signaling without reducing recombination intermediate levels. We show that these approaches, similar to mph1, lead to better survival of sm

SUBMITTER: Chen YH 

PROVIDER: S-EPMC3727935 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature