Siede W, Friedberg A S, Friedberg E C
Department of Pathology, University of Texas Southwestern Medical Center, Dallas 75235-9072.
Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):7985-9. doi: 10.1073/pnas.90.17.7985.
Exposure of the yeast Saccharomyces cerevisiae to ultraviolet (UV) light, the UV-mimetic chemical 4-nitroquinoline-1-oxide (4NQO), or gamma radiation after release from G1 arrest induced by alpha factor results in delayed resumption of the cell cycle. As is the case with G2 arrest following ionizing radiation damage [Weinert, T. A. & Hartwell, L. H. (1988) Science 241, 317-322], the normal execution of DNA damage-induced G1 arrest depends on a functional yeast RAD9 gene. We suggest that the RAD9 gene product may interact with cellular components common to the G1/S and G2/M transition points in the cell cycle of this yeast. These observations define a checkpoint in the eukaryotic cell cycle that may facilitate the repair of lesions that are otherwise processed to lethal and/or mutagenic damage during DNA replication. This checkpoint apparently operates after the mating pheromone-induced G1 arrest point but prior to replicative DNA synthesis, S phase-associated maximal induction of histone H2A mRNA, and bud emergence.
酿酒酵母在从α因子诱导的G1期阻滞释放后，暴露于紫外线（UV）、模拟紫外线的化学物质4-硝基喹啉-1-氧化物（4NQO）或γ辐射下，会导致细胞周期恢复延迟。与电离辐射损伤后G2期阻滞的情况一样[韦纳特，T. A. & 哈特韦尔，L. H.（1988年）《科学》241卷，317 - 322页]，DNA损伤诱导的G1期阻滞的正常执行依赖于功能性的酵母RAD9基因。我们认为RAD9基因产物可能与该酵母细胞周期中G1/S和G2/M转换点共有的细胞成分相互作用。这些观察结果定义了真核细胞周期中的一个检查点，该检查点可能有助于修复那些在DNA复制过程中否则会被处理成致死性和/或致突变性损伤的损伤。这个检查点显然在交配信息素诱导的G1期阻滞点之后、复制性DNA合成之前、与S期相关的组蛋白H2A mRNA最大诱导以及芽出现之前起作用。
Zotero 插件