Journal
NATURE STRUCTURAL & MOLECULAR BIOLOGY
Volume 21, Issue 4, Pages 366-U172Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nsmb.2796
Keywords
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Funding
- Ligue Nationale Contre le Cancer (LNCC)
- Association Contre le Cancer (ARC)
- Fondation pour la Recherche Medicale (FRM)
- Cancer Research UK [C6/A11226]
- European Research Council
- Cancer Research UK
- Wellcome Trust
- Return-to-Europe Federation of European Biochemical Societies fellowship
- University of Cambridge
- ARC
- Agence Nationale pour la Recherche [ANR-09-JCJC-0138]
- Canceropole Grand Sud Ouest (GSO)
- Research Innovation Therapeutic Cancerologie (RITC)
- European Community's Seventh Framework Program (DDResponse)
- Agence Nationale de la Recherche (ANR) [ANR-09-JCJC-0138] Funding Source: Agence Nationale de la Recherche (ANR)
- Cancer Research UK [11224] Funding Source: researchfish
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Although both homologous recombination (HR) and nonhomologous end joining can repair DNA double-strand breaks (DSBs), the mechanisms by which one of these pathways is chosen over the other remain unclear. Here we show that transcriptionally active chromatin is preferentially repaired by HR. Using chromatin immunoprecipitation-sequencing (ChIP-seq) to analyze repair of multiple DSBs induced throughout the human genome, we identify an HR-prone subset of DSBs that recruit the HR protein RAD51, undergo resection and rely on RAD51 for efficient repair. These DSBs are located in actively transcribed genes and are targeted to HR repair via the transcription elongation-associated mark trimethylated histone H3 K36. Concordantly, depletion of SETD2, the main H3 K36 trimethyltransferase, severely impedes HR at such DSBs. Our study thereby demonstrates a primary role in DSB repair of the chromatin context in which a break occurs.
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