Characterization of G1 checkpoint control in the yeast Saccharomyces cerevisiae following exposure to DNA-damaging agents.
Characterization of G1 checkpoint control in the yeast Saccharomyces cerevisiae following exposure to DNA-damaging agents.
复制标题
暴露于 DNA 损伤剂后酿酒酵母 G1 检查点控制的表征。
DOI：
10.1093/genetics/138.2.271
复制
发表时间：
1994
期刊：
影响因子：
3.3
通讯作者：
Friedberg,EC
中科院分区：
文献类型：
--
作者：
Siede,W;Friedberg,AS;Dianova,I;Friedberg,EC
酵母细胞用DNA损伤剂处理后，S相的延迟是一种主动调节的反应，需要功能上的RAD9和RAD24基因。对细胞周期停滞的分析表明，在S期之前，至少存在两个针对受损DNA的检查点：一个在Start(一个由受阻细胞的信息素敏感性表征的G1检查点)和一个在CDC4和CDC7介导的步骤之间的检查点(称为G1/S检查点)。当DNA1-1突变体(影响复制子启动的早期事件)也带有RAD9缺失突变时，在限制性温度下孵育后，它在G1/S中表现出未能阻止。这种未能执行调控的G1/S阻断与集落形成能力的温度敏感性增强有关。为了确定依赖RAD9基因的G1和G1/S细胞周期停滞的信号，我们研究了未切除的光产物持续存在的影响。在核苷酸切除修复缺陷的突变体中，与切除熟练的细胞相比，在低剂量的紫外线照射下观察到S期的停止。然而，这种反应不是RAD9依赖的。我们认为，需要核苷酸切除修复的中间体，如DNA链断裂或单链DNA束，才能激活依赖RAD9的G1和G1/S检查点控制。
The delay of S-phase following treatment of yeast cells with DNA-damaging agents is an actively regulated response that requires functional RAD9 and RAD24 genes. An analysis of cell cycle arrest indicates the existence of (at least) two checkpoints for damaged DNA prior to S-phase; one at START (a G1 checkpoint characterized by pheromone sensitivity of arrested cells) and one between the CDC4- and CDC7-mediated steps (termed the G1/S checkpoint). When a dna1-1 mutant (that affects early events of replicon initiation) also carries a rad9 deletion mutation, it manifests a failure to arrest in G1/S following incubation at the restrictive temperature. This failure to execute regulated G1/S arrest is correlated with enhanced thermosensitivity of colony-forming ability. In an attempt to characterize the signal for RAD9 gene-dependent G1 and G1/S cell cycle arrest, we examined the influence of the continued presence of unexcised photoproducts. In mutants defective in nucleotide excision repair, cessation of S-phase was observed at much lower doses of UV radiation compared to excision-proficient cells. However, this response was not RAD9-dependent. We suggest that an intermediate of nucleotide excision repair, such as DNA strand breaks or single-stranded DNA tracts, is required to activate RAD9-dependent G1 and G1/S checkpoint controls.