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A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection

AutorLópez-Saavedra, Ana ; Gómez-Cabello, Daniel ; Domínguez-Sánchez, María S. ; Mejías-Navarro, Fernando; Fernández-Ávila, María Jesús ; Dinant, Christoffel; Martínez-Macías, María Isabel; Bartek, Jiri; Huertas Sánchez, Pablo
Fecha de publicación2016
EditorNature Publishing Group
CitaciónNature Communications 7: 12364 (2016)
ResumenThere are two major and alternative pathways to repair DNA double-strand breaks: non-homologous end-joining and homologous recombination. Here we identify and characterize novel factors involved in choosing between these pathways; in this study we took advantage of the SeeSaw Reporter, in which the repair of double-strand breaks by homology-independent or -dependent mechanisms is distinguished by the accumulation of green or red fluorescence, respectively. Using a genome-wide human esiRNA (endoribonuclease-prepared siRNA) library, we isolate genes that control the recombination/end-joining ratio. Here we report that two distinct sets of genes are involved in the control of the balance between NHEJ and HR: those that are required to facilitate recombination and those that favour NHEJ. This last category includes CCAR2/DBC1, which we show inhibits recombination by limiting the initiation and the extent of DNA end resection, thereby acting as an antagonist of CtIP.
Versión del editorhttps://doi.org/10.1038/ncomms12364
URIhttp://hdl.handle.net/10261/165148
Identificadoresdoi: 10.1038/ncomms12364
e-issn: 2041-1723
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