López-Saavedra, AnaGómez-Cabello, DanielDomínguez-Sánchez, María SaludMejías-Navarro, FernandoFernández-Ávila, María JesúsDinant, ChristoffelMartínez-Macías, María IsabelBartek, JiriHuertas, Pablo2023-01-252023-01-252016-08-09http://hdl.handle.net/10668/10347There 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.enAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/Adaptor Proteins, Signal TransducingCarrier ProteinsCell Line, TumorChromatinDNA DamageDNA End-Joining RepairEndodeoxyribonucleasesGene Regulatory NetworksGenome, HumanHumansModels, BiologicalNuclear ProteinsProtein BindingRecombinational DNA Repairresearch article27503537open access10.1038/ncomms123642041-1723PMC4980490https://www.nature.com/articles/ncomms12364.pdfhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4980490/pdf