The CDK regulates repair of double-strand breaks by homologous recombination during the cell cycle
The CDK regulates repair of double-strand breaks by homologous recombination during the cell cycle
复制标题
DOI：
10.1038/sj.emboj.7600469
复制
发表时间：
2004-12-08
期刊：
影响因子：
11.4
通讯作者：
Kupiec, M
中科院分区：
文献类型：
--
作者：
Aylon, Y;Liefshitz, B;Kupiec, M
DNA双链断裂(DSB)是一种危险的损伤，可导致基因组不稳定和细胞死亡。真核细胞通过非同源末端连接(NHEJ)或同源重组修复DSB。我们研究了酵母细胞(酿酒酵母)在细胞周期的不同阶段通过重组修复单个染色体DSB的能力。我们发现，停滞在细胞周期G(1)期的细胞限制了同源重组，但NHEJ能够修复DSB。此外，我们还证明了重组能力不需要重复染色单体或通过S相，并且在切除步骤中由Clb-CDK活性控制。
DNA double-strand breaks (DSBs) are dangerous lesions that can lead to genomic instability and cell death. Eukaryotic cells repair DSBs either by nonhomologous end-joining (NHEJ) or by homologous recombination. We investigated the ability of yeast cells (Saccharomyces cerevisiae) to repair a single, chromosomal DSB by recombination at different stages of the cell cycle. We show that cells arrested at the G(1) phase of the cell cycle restrict homologous recombination, but are able to repair the DSB by NHEJ. Furthermore, we demonstrate that recombination ability does not require duplicated chromatids or passage through S phase, and is controlled at the resection step by Clb-CDK activity.