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

Ana López-Saavedra, Daniel Gómez-Cabello, María Salud Domínguez-Sánchez, Fernando Mejías-Navarro, María Jesús Fernández-Ávila, Christoffel Dinant, María Isabel Martínez-Macías, Jiri Bartek and Pablo Huertas ()
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Ana López-Saavedra: Universidad de Sevilla
Daniel Gómez-Cabello: Centro Andaluz de Biología Molecular y Medicina Regenerativa
María Salud Domínguez-Sánchez: Centro Andaluz de Biología Molecular y Medicina Regenerativa
Fernando Mejías-Navarro: Universidad de Sevilla
María Jesús Fernández-Ávila: Centro Andaluz de Biología Molecular y Medicina Regenerativa
Christoffel Dinant: Genome Integrity Unit, Danish Cancer Society Research Centre, Strandboulevarden 49
María Isabel Martínez-Macías: Universidad de Sevilla
Jiri Bartek: Genome Integrity Unit, Danish Cancer Society Research Centre, Strandboulevarden 49
Pablo Huertas: Universidad de Sevilla

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract 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.

Date: 2016
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DOI: 10.1038/ncomms12364

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