Transcriptionally active chromatin recruits homologous recombination at DNA double-strand breaks - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue Nature Structural and Molecular Biology Année : 2014

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

Résumé

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.

Dates et versions

Identifiants

Citer

François Aymard, Béatrix Bugler, Christine Schmidt, Emmanuelle Guillou, Pierre Caron, et al.. Transcriptionally active chromatin recruits homologous recombination at DNA double-strand breaks. Nature Structural and Molecular Biology, 2014, 21 (4), pp.366-374. ⟨10.1038/nsmb.2796⟩. ⟨hal-03477002⟩
14 Consultations
0 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More