作者: A. G. Paulovich , Leland H. Hartwell , C. D. Armour
DOI: 10.1093/GENETICS/150.1.75
关键词: Biology 、 G2-M DNA damage checkpoint 、 Saccharomyces cerevisiae 、 DNA damage 、 DNA repair 、 Sister chromatid exchange 、 Mutagenesis 、 Mutation 、 Gene 、 Genetics
摘要: In wild-type Saccharomyces cerevisiae, a checkpoint slows the rate of progression an ongoing S phase in response to exposure DNA-alkylating agent. Mutations that eliminate regulation also confer sensitivity alkylating agents, leading us suggest that, by regulating rate, cells are either better able repair or replicate damaged DNA. this study, we determine effects mutations impair on ability excision repair-defective irreparably UV-damaged We assay survival after UV irradiation, as well genetic consequences replicating template, namely mutation and sister chromatid exchange induction. find RAD9, RAD17, RAD24, MEC3 required for UV-induced (although not spontaneous) mutagenesis, RAD9 RAD17 (but REV3, MEC3) maximal induction replication-dependent exchange. Therefore, genes only control cell cycle damage, but play role accommodating DNA damage during replication.