title: Sharpening the ends for repair: mechanisms and regulation of DNA resection.
abstract: 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.
authors.affiliation: Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA.
authors.forename: Sharad C
authors.initials: SC
authors.lastname: Paudyal
authors.affiliation: Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA zyou@wustl.edu.
authors.forename: Zhongsheng
authors.initials: Z
authors.lastname: You
mesh_terms: D053903:DNA Breaks, Double-Stranded; D004260:DNA Repair; D004261:DNA Replication; D004277:DNA, Single-Stranded / Q000737:chemistry*; D006570:Heterochromatin / Q000378:metabolism; D016615:Telomere
chemical_list: D004277:DNA, Single-Stranded; D006570:Heterochromatin
keywords: DNA damage response; DNA end resection; Exo1; MRN-CtIP; cancer