RAD9-DEPENDENT-G(1) ARREST DEFINES A 2ND CHECKPOINT FOR DAMAGED DNA IN THE CELL-CYCLE OF SACCHAROMYCES-CEREVISIAE

被引:183
作者
SIEDE, W [1 ]
FRIEDBERG, AS [1 ]
FRIEDBERG, EC [1 ]
机构
[1] UNIV TEXAS,SW MED CTR LAB,DEPT PATHOL,MOLEC PATHOL,DALLAS,TX 75235
关键词
UV RADIATION; DNA REPAIR;
D O I
10.1073/pnas.90.17.7985
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:7985 / 7989
页数:5
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