기초과학 자율운영 중점연구소

생명과학과에서 아래와 같이 세미나를 실시합니다.

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주관: 기초과학연구소(자율운영 중점연구소지원사업)

일시: 2026년 6월 4일 목요일 17:00

장소: 원천관 535호

연사: 이종수 교수(아주대학교 생명과학과)

주제: A newly assigned role of CTCF in homologous recombination repair of DNA double-strand breaks

Multifaceted CTCF facilitates double-strand break (DSB) repair via homologous recombination (HR). Similarly, BRCA1/BARD1 play versatile roles in HR. However, the collaboration between CTCF and BRCA1/BARD1 remains poorly understood. Here, we show how CTCF recruits inactive chromatin proteins, HP1γ, KAP1, histone H3K9 methyltransferases (SUV39H1 and SETDB1), and H3K4 demethylase (KDM5A), to accelerate the localization of BARD1 on DSBs, tethered with its obligate partner BRCA1. CTCF depletion abrogates the enrichment of the inactive chromatin proteins along with H3K9 methylation/H3K4 demethylation at DSBs, thereby impairing rapid BRCA1/BARD1 recruitment. Compromising the expression of one component of the inactive chromatin proteins or deregulating H3K9 methylation or H3K4 demethylation attenuates the early accumulation of the other inactive chromatin proteins along with BRCA1/BARD1 on DSBs. This abrogates the subsequent recruitment of the exonucleases EXO1/DNA2, which is causally linked to defective resection and dysfunctional HR. CTCF constitutes a hierarchical recruitment cascade for HR, in which it promptly recruits the inactive chromatin proteins and subsequent BRCA1/BARD1 at DSBs through cooperation with the inactive chromatin proteins. BRCA1/BARD1 engages extensive resection components, SMARCAD1 and EXO1/DNA2, to promote elongated resection. Overall, our findings identify a critical role of CTCF in conjunction with BRCA1/BARD1 at the licensing point, the resection-step, for HR.