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XB-ART-59146
Nat Commun 2022 May 31;131:3016. doi: 10.1038/s41467-022-30787-6.
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BRD4 promotes resection and homology-directed repair of DNA double-strand breaks.

Barrows JK , Lin B , Quaas CE , Fullbright G , Wallace EN , Long DT .


Abstract
Double-strand breaks (DSBs) are one of the most toxic forms of DNA damage and represent a major source of genomic instability. Members of the bromodomain and extra-terminal (BET) protein family are characterized as epigenetic readers that regulate gene expression. However, evidence suggests that BET proteins also play a more direct role in DNA repair. Here, we establish a cell-free system using Xenopus egg extracts to elucidate the gene expression-independent functions of BET proteins in DSB repair. We identify the BET protein BRD4 as a critical regulator of homologous recombination and describe its role in stimulating DNA processing through interactions with the SWI/SNF chromatin remodeling complex and resection machinery. These results establish BRD4 as a multifunctional regulator of chromatin binding that links transcriptional activity and homology-directed repair.

PubMed ID: 35641523
Article link: Nat Commun
Grant support: [+]

Genes referenced: brd4

References [+] :
Aymard, Transcriptionally active chromatin recruits homologous recombination at DNA double-strand breaks. 2014, Pubmed