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首页> 外文期刊>Cellular Signalling >The Caenorhabditis elegans Werner syndrome protein participates in DNA damage checkpoint and DNA repair in response to CPT-induced double-strand breaks
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The Caenorhabditis elegans Werner syndrome protein participates in DNA damage checkpoint and DNA repair in response to CPT-induced double-strand breaks

机译：秀丽隐杆线虫Werner综合征蛋白参与CPT诱导的双链断裂的DNA损伤检查点和DNA修复

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The RecQ helicases play roles in maintenance of genomic stability in species ranging from Escherichia coli to humans and interact with proteins involved in DNA metabolic pathways such as DNA repair, recombination, and replication. Our previous studies found that the Caenorhabditis elegans WRN-1 RecQ protein (a human WRN ortholog) exhibits ATP-dependent 3'-5' helicase activity and that the WRN-1 helicase is stimulated by RPA-1 on a long forked DNA duplex. However, the role of WRN-1 in response to S-phase associated with DSBs is unclear. We found that WRN-1 is involved in the checkpoint response to DSBs after CPT, inducing cell cycle arrest, is recruited to DSBs by RPA-1 and functions upstream of ATL-1 and ATM-1 for CHIC-1 phosphorylation in the S-phase checkpoint. In addition, WRN-1 and RPA-1 recruitments to the DSBs require MRE-11, suggesting that DSB processing controlled by MRE-11 is important for WRN-1 at DSBs. The repair of CPT-induced DSBs is greatly reduced in the absence of WRN-1. These observations suggest that WRN-1 functions downstream of RPA-1 and upstream of CHK-1 in the DSB checkpoint pathway and is also required for the repair of DSB. (C) 2015 Elsevier Inc All rights reserved.
机译：RecQ解旋酶在维持从大肠杆菌到人类的物种的基因组稳定性中发挥作用，并与参与DNA代谢途径（例如DNA修复，重组和复制）的蛋白质相互作用。我们以前的研究发现秀丽隐杆线虫WRN-1 RecQ蛋白（人类WRN直系同源物）表现出ATP依赖的3'-5'解旋酶活性，并且WPA-1解旋酶受RPA-1在长叉状DNA双链体上的刺激。但是，WRN-1在响应与DSB相关的S期中的作用尚不清楚。我们发现，在CPT诱导细胞周期停滞后，RPN-1将WRN-1参与了对DSB的检查点反应，并通过RPA-1募集到DSB，并在ATL-1和ATM-1的上游发挥功能，使SIC中的CHIC-1磷酸化阶段检查点。此外，向DSB征募WRN-1和RPA-1需要MRE-11，这表明MRE-11控制的DSB处理对于DSB的WRN-1很重要。在没有WRN-1的情况下，CPT诱导的DSB的修复大大减少。这些观察结果表明，WRN-1在DSB检查点途径中RPA-1下游和CHK-1上游起作用，也是修复DSB所必需的。 （C）2015 Elsevier Inc保留所有权利。

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