GATAD2B containing NuRD complex drives R-loop dependent chromatin boundary formation at double strand breaks

2024 · doi:10.1101/2024.02.19.581003
preprint OA: gold CC-BY-4.0
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This paper investigates how chromatin architecture around DNA double-strand breaks is regulated, focusing on the GATAD2B-containing NuRD complex and its association with DSBs. Using a combination of mechanistic experiments, the authors report that GATAD2B-NuRD recruitment to DSBs depends on transcription and R-loops, and that it promotes histone deacetylation and chromatin condensation to form a temporal boundary between open and closed chromatin. They find that this boundary is required for proper termination of DNA end resection, and that loss of the complex causes chromatin hyper-relaxation, extended end resection, and homologous recombination repair failure. The paper does not discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

Double-strand breaks (DSBs) are the most lethal form of DNA damage. Transcriptional activity at DSBs, as well as transcriptional repression around DSBs, are both required for efficient DNA repair. The chromatin landscape defines and coordinates these two opposing events. However, the regulation of the open and condensed chromatin architecture is still unclear. In this study, we show that the GATAD2B-NuRD complex associates with DSBs in a transcription- and R-loop-dependent manner, to promote histone deacetylation and chromatin condensation, creating a temporal boundary between open and closed chromatin. This boundary is necessary for correct DNA end resection termination. The lack of the GATAD2B-NuRD complex leads to chromatin hyper-relaxation and extended DNA end resection, resulting in HR repair failure. Our results suggest that the GATAD2B-NuRD complex is a key coordinator of the dynamic interplay between transcription and chromatin landscape and underscore its biological significance in the RNA-dependent DNA damage response.
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Abstract Double-strand breaks (DSBs) are the most lethal form of DNA damage. Transcriptional activity at DSBs, as well as transcriptional repression around DSBs, are both required for efficient DNA repair. The chromatin landscape defines and coordinates these two opposing events. However, the regulation of the open and condensed chromatin architecture is still unclear. In this study, we show that the GATAD2B-NuRD complex associates with DSBs in a transcription- and R-loop-dependent manner, to promote histone deacetylation and chromatin condensation, creating a temporal boundary between open and closed chromatin. This boundary is necessary for correct DNA end resection termination. The lack of the GATAD2B-NuRD complex leads to chromatin hyper-relaxation and extended DNA end resection, resulting in HR repair failure. Our results suggest that the GATAD2B-NuRD complex is a key coordinator of the dynamic interplay between transcription and chromatin landscape and underscore its biological significance in the RNA-dependent DNA damage response. Competing Interest Statement The authors have declared no competing interest.

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License: CC-BY-4.0