RN ase L facilitates the repair of DNA double‐strand breaks through the nonhomologous end‐joining pathway

• Published in: FEBS letters 2019-06, Vol.593 (11), p.1190-1200
• Main Authors: Zhong, Yiran, Pan, Bingxin, Zhu, Jie, Fu, Hanjiang, Zheng, Xiaofei
• Format: Article
• Language: English
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1002/1873-3468.13426

RNA molecules have been found to play important roles in DNA double‐strand break ( DSB ) repair, but the exact underlying mechanism remains unclear. Here, we aimed to clarify the function of RN ase L, an important ribonuclease in the immune system of vertebrates, in DSB repair. Knockdown of RN ase L reduces cell survival after induction of DSB s by ionizing radiation or camptothecin and causes a significant decrease in DSB repair, as evidenced by an increase in the extent of phosphorylation of histone H2 AX on Ser139 (γH2 AX ) and γH2 AX nuclear foci formation. Thus, our findings indicate that RN ase L interacts with the core factors involved in DNA end joining, such as XRCC 4 and Lig4, and facilitates DSB repair through the nonhomologous end‐joining pathway.