期刊
NATURE COMMUNICATIONS
卷 7, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms12364
关键词
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资金
- Spanish Ministry of Economy and Competitivity [SAF2010-14877]
- ERC
- Spanish Ministry of Education
- Juan de la Cierva Postdoctoral Grant
- EMBO short-term fellowship
- Danish National Research Foundation [DNRF125]
- Danish Council for Independent Research [DFF-1331-00262]
- Novo Nordisk Foundation [NNF16584]
- Lundbeck Foundation [R93-2011-8990] Funding Source: researchfish
- Novo Nordisk Fonden [NNF12OC0002290, NNF15OC0016584] Funding Source: researchfish
- The Danish Cancer Society [R124-A7785] Funding Source: researchfish
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/endjoining 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.
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