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首页> 外文期刊>Cell cycle >Give me a break, but not in mitosis: the mitotic DNA damage response marks DNA double-strand breaks with early signaling events.
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Give me a break, but not in mitosis: the mitotic DNA damage response marks DNA double-strand breaks with early signaling events.

机译：给我休息，但不要破坏有丝分裂：有丝分裂的DNA损伤反应标志着DNA双链断裂，并伴有早期信号事件。

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: DNA double-strand breaks (DSBs) are extremely cytotoxic with a single unrepaired DSB being sufficient to induce cell death. A complex signalling cascade, termed the DNA damage response (DDR), is in place to deal with such DNA lesions and maintain genome stability. Recent work by us and others has found that the signalling cascade activated by DSBs in mitosis is truncated, displaying apical, but not downstream, components of the DDR. The E3 Ubiquitin ligases RNF8, RNF168 and BRCA1, along with the DDR mediator 53BP1, are not recruited to DSB sites in mitosis, and activation of downstream checkpoint kinases is also impaired. Here, we show that RNF8 and RNF168 are recruited to DNA damage foci in late mitosis, presumably to prime sites for 53BP1 recruitment in early G1. Interestingly, we show that, although RNF8, RNF168 and 53BP1 are excluded from DSB sites during most of mitosis, they associate with mitotic structures such as the kinetochore, suggesting roles for these DDR factors during mitotic cell division. We discuss these and other recent findings and suggest how these novel data collectively contribute to our understanding of mitosis and how cells deal with DNA damage during this crucial cell cycle stage.
机译：DNA双链断裂（DSB）具有极强的细胞毒性，单个未修复的DSB足以诱导细胞死亡。已经建立了一个复杂的信号级联，称为DNA损伤响应（DDR），以处理此类DNA损伤并维持基因组稳定性。我们和其他人最近的工作发现，由有丝分裂中的DSB激活的信号级联被截断，显示DDR的顶端但不下游。 E3泛素连接酶RNF8，RNF168和BRCA1以及DDR介体53BP1未被募集到有丝分裂的DSB位点，并且下游检查点激酶的激活也受到损害。在这里，我们显示RNF8和RNF168被募集到有丝分裂晚期的DNA损伤灶，大概是G1早期募集到53BP1的主要位点。有趣的是，我们显示，尽管在大多数有丝分裂期间RNF8，RNF168和53BP1被排除在DSB位点之外，但它们与有丝分裂结构（如动粒）相关联，暗示了这些DDR因子在有丝分裂细胞分裂过程中的作用。我们讨论了这些以及其他最近的发现，并提出了这些新颖的数据如何共同有助于我们对有丝分裂的理解以及在这个关键的细胞周期阶段细胞如何处理DNA损伤。

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