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

Author

Listed:
  • Ana López-Saavedra

    (Universidad de Sevilla
    Centro Andaluz de Biología Molecular y Medicina Regenerativa)

  • 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
    Centro Andaluz de Biología Molecular y Medicina Regenerativa)

  • 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
    Centro Andaluz de Biología Molecular y Medicina Regenerativa
    Present address: Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, UK)

  • Jiri Bartek

    (Genome Integrity Unit, Danish Cancer Society Research Centre, Strandboulevarden 49
    Science for Life Laboratory, Karolinska Institute)

  • Pablo Huertas

    (Universidad de Sevilla
    Centro Andaluz de Biología Molecular y Medicina Regenerativa)

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.

Suggested Citation

  • 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 & Pa, 2016. "A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection," Nature Communications, Nature, vol. 7(1), pages 1-14, November.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12364
    DOI: 10.1038/ncomms12364
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