BRD4 promotes resection and homology-directed repair of DNA double-strand breaks

John K. Barrows, Baicheng Lin, Colleen E. Quaas, George Fullbright, Elizabeth N. Wallace and David T. Long ()
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John K. Barrows: Medical University of South Carolina
Baicheng Lin: Medical University of South Carolina
Colleen E. Quaas: Medical University of South Carolina
George Fullbright: Medical University of South Carolina
Elizabeth N. Wallace: Medical University of South Carolina
David T. Long: Medical University of South Carolina

Nature Communications, 2022, vol. 13, issue 1, 1-10

Abstract: 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.

Date: 2022
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DOI: 10.1038/s41467-022-30787-6

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