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 as LRIK that interacts with Ku, which enhances the ability of the Ku heterodimer to detect the presence of DSBs. Here, we show that depletion of LRIK generates significantly enhanced sensitivity to DSB-inducing agents and reduced DSB repair efficiency. In response to DSBs, LRIK enhances the recruitment of repair factors at DSB sites and facilitates γH2AX signaling. Our results demonstrate that LRIK is necessary for efficient repairing DSBs via nonhomologous end-joining pathway.

尽管我们对长链非编码 RNA (lncRNA) 的功能的理解取得了最新进展，但它们在 DNA 修复途径中的作用和功能仍然知之甚少。通过筛选一组未表征的 lncRNA 以识别那些转录受双链断裂 (DSB) 诱导的 lncRNA，我们确定了一种称为LRIK的新型 lncRNA ，它与 Ku 相互作用，这增强了 Ku 异源二聚体检测存在的能力DSB。在这里，我们表明LRIK 的消耗会显着增强对 DSB 诱导剂的敏感性并降低 DSB 修复效率。作为对 DSB 的响应，LRIK增强了 DSB 位点修复因子的募集并促进了 γH2AX 信号传导。我们的结果表明LRIK 通过非同源末端连接途径有效修复 DSB 是必要的。