LRIKinteracts with the Ku70-Ku80 heterodimer enhancing the efficiency of NHEJ repair
LRIKinteracts with the Ku70-Ku80 heterodimer enhancing the efficiency of NHEJ repair
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DOI：
10.1038/s41418-020-0581-5
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发表时间：
2020-06-25
影响因子：
12.4
通讯作者：
Chen, Runsheng
中科院分区：
文献类型：
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作者：
Wang, Dan;Zhou, Zheng;Chen, Runsheng
尽管最近我们对长链非编码RNA（lncRNA）功能的理解取得了进展，但它们在DNA修复途径中的作用和功能仍然知之甚少。通过筛选一组未知的lncRNA以鉴定那些由双链断裂（DSB）诱导转录的lncRNA，我们鉴定了一种新的lncRNA，称为LRIK，其与Ku相互作用，其增强Ku异源二聚体检测DSB存在的能力。在这里，我们表明，消耗LRIK产生显着增强的敏感性，DSB诱导剂和降低DSB修复效率。作为对DSB的响应，LRIK增强DSB位点处修复因子的募集并促进γ H2AX信号传导。我们的研究结果表明LRIK是通过非同源末端连接途径有效修复DSB所必需的。
Despite recent advances in our understanding of the function of long noncoding RNAs (lncRNAs), their roles and functions in DNA repair pathways remain poorly understood. By screening a panel of uncharacterized lncRNAs to identify those whose transcription is induced by double-strand breaks (DSBs), we identified a novel lncRNA referred to asLRIKthat interacts with Ku, which enhances the ability of the Ku heterodimer to detect the presence of DSBs. Here, we show that depletion ofLRIKgenerates significantly enhanced sensitivity to DSB-inducing agents and reduced DSB repair efficiency. In response to DSBs,LRIKenhances the recruitment of repair factors at DSB sites and facilitates gamma H2AX signaling. Our results demonstrate thatLRIKis necessary for efficient repairing DSBs via nonhomologous end-joining pathway.