RT Journal Article
T1 A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection.
A1 López-Saavedra, Ana
A1 Gómez-Cabello, Daniel
A1 Domínguez-Sánchez, María Salud
A1 Mejías-Navarro, Fernando
A1 Fernández-Ávila, María Jesús
A1 Dinant, Christoffel
A1 Martínez-Macías, María Isabel
A1 Bartek, Jiri
A1 Huertas, Pablo
AB There 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.
YR 2016
FD 2016-08-09
LK http://hdl.handle.net/10668/10347
UL http://hdl.handle.net/10668/10347
LA en
DS RISalud
RD Apr 14, 2025