Artículo
A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection
Autor/es | López Saavedra, Ana
Gómez Cabello, Daniel Domínguez Sánchez, María Salud Mejías Navarro, Fernando Fernández Ávila, María Jesús Martínez Macías, María Isabel Huertas Sánchez, Pablo |
Departamento | Universidad de Sevilla. Departamento de Genética |
Fecha de publicación | 2016 |
Fecha de depósito | 2017-03-17 |
Publicado en |
|
Resumen | 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 ... 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. |
Cita | López Saavedra, A., Gómez Cabello, D., Domínguez Sánchez, M.S., Mejías Navarro, F., Fernández Ávila, M.J., Martínez Macías, M.I. y Huertas Sánchez, P. (2016). A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection. Nature Communications, 7 (12364), 1-14. |
Ficheros | Tamaño | Formato | Ver | Descripción |
---|---|---|---|---|
pub43ncomms12364.pdf | 2.800Mb | [PDF] | Ver/ | |