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

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.

journal_name

Nat Struct Mol Biol

journal_title

Nature structural & molecular biology

authors

Aymard F,Bugler B,Schmidt CK,Guillou E,Caron P,Briois S,Iacovoni JS,Daburon V,Miller KM,Jackson SP,Legube G

doi

10.1038/nsmb.2796

subject

Has Abstract

pub_date

2014-04-01 00:00:00

pages

366-74

issue

4

eissn

1545-9993

issn

1545-9985

pii

nsmb.2796

journal_volume

21

pub_type

杂志文章

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