Cited by 670DNA Repair MechanismsGenomics and Chromatin DynamicsCRISPR and Genetic Engineering

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Transcriptionally active chromatin recruits homologous recombination at DNA double-strand breaks

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Aymard, François, Bugler, Beatrix, Schmidt, Christine K, Guillou, Emmanuelle, Caron, Pierre, Briois, Sébastien, Iacovoni, Jason S, Daburon, Virginie, Miller, Kyle M, Jackson, Stephen P, Legube, Gaëlle·2014·Nature Structural & Molecular Biology

DOI 10.1038/nsmb.2796PMC PMC4300393

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Abstract

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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Authors: Aymard, F., Bugler, B., Schmidt, C. K., Guillou, E., Caron, P., Briois, S., Iacovoni, J. S., Daburon, V., Miller, K. M., Jackson, S. P., & Legube, G.
Affiliations: Centre National de la Recherche Scientifique (FR)
University of Cambridge (GB)
Inserm (FR)
Corresponding author: Legube, Gaëlle
ORCID: Schmidt, Christine K
Guillou, Emmanuelle
Caron, Pierre
Daburon, Virginie
Miller, Kyle M
Jackson, Stephen P
Legube, Gaëlle
Venue: Nature Structural & Molecular Biology
Publisher: Springer Science and Business Media LLC
Published: 2014-03-23
Volume: 21
Issue: 4
Pages: 366-374
ISSN: 1545-9985 (ISSN-L)
1545-9993
DOI: 10.1038/nsmb.2796
PMC: PMC4300393
OpenAlex: W2097027640
Cited by: 668
References: 52
Citations by year: 2026: 33 · 2025: 51 · 2024: 50 · 2023: 47 · 2022: 65 · 2021: 79 · 2020: 69 · 2019: 53 · 2018: 47 · 2017: 62 · 2016: 52 · 2015: 40 · 2014: 18
FWCI: 23.52
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Structural & Molecular Biology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
HAL (submittedVersion)
Research Explorer (The University of Manchester) (submittedVersion, other-oa)
Funders: Wellcome Trust (086861, 092096)
European Molecular Biology Laboratory
Broad Institute
Cancer Research UK (C6/A11226, 11224, A11224)
Agence Nationale de la Recherche (ANR-09-JCJC-0138)
National Cancer Institute (F31CA260794)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › CRISPR and Genetic Engineering
Keywords: DNA double-strand breaks, homologous recombination, non-homologous end joining, RAD51, SETD2, transcriptionally active chromatin, DNA resection, transcription elongation, chromatin context
MeSH terms: Cell Line, Chromatin, DNA Repair, DNA-Binding Proteins, Histones, Humans, Neoplasm Proteins, Transcription, Genetic, Rad51 Recombinase, DNA Breaks, Double-Stranded, Homologous Recombination, DNA End-Joining Repair

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Transcriptionally active chromatin recruits homologous recombination at DNA double-strand breaks

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