DNA resection in eukaryotes: deciding how to fix the break.

DNA resection in eukaryotes: deciding how to fix the break.
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DOI:
10.1038/nsmb.1710
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发表时间:
2010-01
影响因子:
16.8
通讯作者:
--
中科院分区:
生物学1区
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--
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DNA双链断裂通过不同的机制修复,包括同源重组和非同源末端连接。DNA末端切除是DNA重组的第一步,也是决定DSB修复方式选择的关键步骤。切除是一个进化上保守的过程,产生单链DNA,与检查点激活有关,对生存至关重要。如果不能调节和执行这一过程,就会导致有缺陷的重组,并可能导致人类疾病。在这里,我回顾了最近的研究结果切除真核生物的机制,从酵母到脊椎动物,提供的监管策略,控制它的见解,并强调其损害和放松管制的后果。
DNA double-strand breaks are repaired by different mechanisms, including homologous recombination and nonhomologous end-joining. DNA-end resection, the first step in recombination, is a key step that contributes to the choice of DSB repair. Resection, an evolutionarily conserved process that generates single-stranded DNA, is linked to checkpoint activation and is critical for survival. Failure to regulate and execute this process results in defective recombination and can contribute to human disease. Here, I review recent findings on the mechanisms of resection in eukaryotes, from yeast to vertebrates, provide insights into the regulatory strategies that control it, and highlight the consequences of both its impairment and its deregulation.
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