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-9, RADl 7, and RAD24 Are Required for S Phase Regulation in Saccharomyces cerevisiae in Response to DNA Damage

We have previously shown that a checkpoint dependent on MECl and RAD53 slows the rate of S phase progression in Saccharomyces cereuisiae in response to alkylation damage. Whereas wild-type cells exhibit a slow S phase in response to damage, mal-1 and rad53 mutants replicate rapidly in the presence or absence of DNA damage. In this report, we show that other genes (RAD9, RADl 7, RAD24) involved in the DNA damage checkpoint pathway also play a role in regulating S phase in response to DNA damage. Furthermore, RAD9, RAD1 7, and RAD24 fall into two groups with respect to both sensitivity to alkylation and regulation of S phase. We also demonstrate that the more dramatic defect in S phase regulation in the mecl-l and rad53 mutants is epistatic to a less severe defect seen in rad9A, radl 7A, and rad24A. Furthermore, the triple rad9A radl 7 A rad24A mutant also has a less severe defect than mcl-1 or rad53 mutants. Finally, we demonstrate the specificity of this phenotype by showing that the DNA repair and/or checkpoint mutants mgtlA, magla, apnlA, rev3A, radl8A, radl6A, dud-A100, sad4-1, tellA, rad26A, rad5lA, rad52-1, rad54A, radl4A, radlA, p0130-46, p0130-52, mad3A, pdslA/esp2A, pmlA, mlhlA, and m h 2 A are all proficient at S phase regulation, even though some of these mutations confer sensitivity to alkylation.