The checkpoint protein Rad24 of Saccharomyces cerevisiae is involved in processing double-strand break ends and in recombination partner choice
The checkpoint protein Rad24 of Saccharomyces cerevisiae is involved in processing double-strand break ends and in recombination partner choice
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DOI：
10.1128/mcb.23.18.6585-6596.2003
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发表时间：
2003-09-01
影响因子：
5.3
通讯作者：
Kupiec, M
中科院分区：
文献类型：
--
作者：
Aylon, Y;Kupiec, M
在染色体损伤时，细胞激活检查点反应，包括细胞周期停滞和DNA修复的刺激。检查点蛋白Rad 24是单个可修复双链断裂（DSB）存活的关键。然而，rad 24细胞的低存活率并不是因为它们不能阻止细胞周期进程。在rad 24突变体中，断裂末端的处理被延迟和延长，导致DSB修复的延长动力学和细胞死亡。rad 24突变体的有限切除也通过依赖于相互作用的同源供体序列的长度的机制影响重组伴侣的选择。出乎意料的是，具有DSB的rad 24细胞最终在细胞周期的G（2）/M期积聚并死亡。这种停滞依赖于纺锤体检查点蛋白Mad 2。
Upon chromosomal damage, cells activate a checkpoint response that includes cell cycle arrest and a stimulation of DNA repair. The checkpoint protein Rad24 is key to the survival of a single, repairable double-strand break (DSB). However, the low survival of rad24 cells is not due to their inability to arrest cell cycle progression. In rad24 mutants, processing of the broken ends is delayed and protracted, resulting in extended kinetics of DSB repair and in cell death. The limited resection of rad24 mutants also affects recombination partner choice by a mechanism dependent on the length of the interacting homologous donor sequences. Unexpectedly, rad24 cells with a DSB eventually accumulate and die at the G(2)/M phase of the cell cycle. This arrest depends on the spindle checkpoint protein Mad2.