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CUT&RUN analysis of H3K36me3 and H4K20me1 in fibroblasts treated with TNFa ± TPCA1

ABSTRACT: Analysis of changes in chromatin modifications H3K36me3 and H4K20me1 in fibroblast cell line GM02036 (Coriell) after treatment with TNFa and/or TPCA1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE277144 | GEO | 2026/03/16

REPOSITORIES: GEO

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CUT&RUN analysis of RelA and MCM2 in fibroblasts treated with TNFA ± TPCA1

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CUT&RUN analysis of H3K27ac and H3K4me1 in fibroblasts treated with TNFa ± deletion of RelA binding site on Chr21.

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BAHCC1 binds H4K20me1 to facilitate the MCM complex loading for DNA replication

Project description:Methylation of histone H4 lysine 20 (H4K20), such as H4K20 mono-methylation (H4K20me1), regulates the biological processes of DNA replication, cell cycle progression, and DNA damage repair1-4. Whereas H4K20me1 is knowingly written by SET85,6 (also known as PR-Set7) and erased by PHF87 (also known as KDM7B), the mechanism underlying H4K20me1-mediated regulation of DNA replication remains murky. Here, we report that a conserved tandem Tudor domain of BAHCC1 (BAHCC1TTD) specifically reads H4K20me1. Our biochemical, structural and cellular analyses demonstrated that the recognition of H4K20me1 by BAHCC1TTD facilitates the BAHCC1 recruitment onto the replication origins, where BAHCC1 interacts and recruits components of Minichromosome Maintenance (MCM) complex, a critical partner machinery of Origin Replication Complex (ORC) for mediating DNA replication8,9. Combined actions of the H4K20me1-reading BAHCC1 and the H4K20me2-reading ORC ensure optimal genomic loading of MCM proteins. Depletion of BAHCC1, or disruption of BAHCC1TTD:H4K20me1 interaction, affected H4K20me1 homeostasis and MCM complex loading, leading to impaired DNA replication and defective cell cycle progression. Together, this study identifies a conserved BAHCC1TTD as an effector linking H4K20me1 to MCM recruitment for efficient DNA replication.

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