ArticleNucleic acids research2026
CTCF primes repressive chromatin for rapid BRCA1/BARD1 recruitment to drive homologous recombination repair of DNA double-strand breaks.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Multifaceted CTCF facilitates double-strand break (DSB) repair via homologous recombination (HR), and BRCA1/BARD1 play key roles in HR. However, whether and how CTCF cooperates with BRCA1/BARD1 for HR remain poorly understood. Here, we show CTCF recruits repressive chromatin proteins, HP1γ, KAP1, SUV39H1, SETDB1, and KDM5A, thereby enabling rapid accumulation of BRCA1/BARD1 at DSBs. CTCF depletion abrogates the enrichment of these repressive chromatin proteins, accompanied by loss of H3K9 methylation/H3K4 demethylation at DSBs, resulting in defective rapid BRCA1/BARD1 recruitment. Deprivation of one component of the repressive chromatin proteins or deregulating H3K9 methylation/H3K4 demethylation compromises the immediate accumulation of the other repressive chromatin proteins as well as BRCA1/BARD1 on DSBs. Consequently, recruitment of the exonucleases EXO1/DNA2 is abrogated, which is causally linked to defective DNA end resection and dysfunctional HR. Collectively, our findings suggest that CTCF establishes a hierarchical recruitment cascade in HR, by coordinating the repressive chromatin assembly and BRCA1/BARD1 recruitment at DSBs, facilitating the exonucleases EXO1/DNA2-mediated extensive DNA resection. Finally, we identify a critical role of CTCF in coupling BRCA1/BARD1 with the HR licensing point, the DNA end resection step, for HR.
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