BRCA1 Accelerates CtIP-Mediated DNA-End Resection

DNA-end resection is a highly regulated and critical step in the response and repair of DNA double-strand breaks. In higher eukaryotes, CtIP regulates resection by integrating cellular signals via its posttranslational modifications and protein-protein interactions, including cell-cycle-controlled interaction with BRCA1. The role of BRCA1 in DNA-end resection is not clear. Here, we develop an assay to study DNA resection in higher eukaryotes at high resolution. We demonstrate that the BRCA1-CtIP interaction, albeit not essential for resection, modulates the speed at which this process takes placeThis work was funded by an R+D+I grant from the Spanish Ministry of Economy and Competitivity (SAF2010-14877). A.C.-G. is funded by a PhD fellowship from the Consejo Nacional de Ciencia y Tecnologı´a (CONACYT). A.L.-S. is the recipient of a predoctoral training fellowship from the Spanish Ministry of Science and Innovation (FPI fellowship)Peer Reviewe