Paudyal Sharad C, You Zhongsheng
Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA.
Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
Acta Biochim Biophys Sin (Shanghai). 2016 Jul;48(7):647-57. doi: 10.1093/abbs/gmw043. Epub 2016 May 12.
DNA end resection is a key process in the cellular response to DNA double-strand break damage that is essential for genome maintenance and cell survival. Resection involves selective processing of 5' ends of broken DNA to generate ssDNA overhangs, which in turn control both DNA repair and checkpoint signaling. DNA resection is the first step in homologous recombination-mediated repair and a prerequisite for the activation of the ataxia telangiectasia mutated and Rad3-related (ATR)-dependent checkpoint that coordinates repair with cell cycle progression and other cellular processes. Resection occurs in a cell cycle-dependent manner and is regulated by multiple factors to ensure an optimal amount of ssDNA required for proper repair and genome stability. Here, we review the latest findings on the molecular mechanisms and regulation of the DNA end resection process and their implications for cancer formation and treatment.
DNA末端切除是细胞对DNA双链断裂损伤作出反应的关键过程,对基因组维持和细胞存活至关重要。切除涉及对断裂DNA的5'端进行选择性加工,以产生单链DNA突出端,进而控制DNA修复和检查点信号传导。DNA切除是同源重组介导修复的第一步,也是激活共济失调毛细血管扩张症突变和Rad3相关(ATR)依赖性检查点的先决条件,该检查点可协调修复与细胞周期进程及其他细胞过程。切除以细胞周期依赖性方式发生,并受多种因素调节,以确保适当修复和基因组稳定性所需的最佳单链DNA量。在此,我们综述了关于DNA末端切除过程的分子机制和调控及其对癌症形成和治疗影响的最新发现。