ArticleNature communications2025
H3K56 acetylation regulates chromatin maturation following DNA replication.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Identifying critical lysines in mammalian histone H3 with high-throughput CRISPR prime editing.Nature genetics · 2026Article
- Newly synthesized histones: passive or active players in the regulation of epigenetic inheritance?Nucleic acids research · 2026Review
- Chromatin architecture sets origin licensing capacity.Research square · 2026Article
- Chromatin architecture sets origin licensing capacity.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic maintenance of PRC2-repressed chromatin requires RTT109 but not H3K56 acetylation.bioRxiv : the preprint server for biology · 2026Article
- Nucleosome spacing across cell types, diseases, and ages.Nucleic acids research · 2026Review
- Stabilization of the MAPK-Epigenetic Signaling Axis Underlies the Protective Effect of Thyme Oil Against Cadmium Stress in Root Meristem Cells ofInternational journal of molecular sciences · 2025Article
- The eukaryotic replisome intrinsically generates asymmetric daughter chromatin fibers.bioRxiv : the preprint server for biology · 2025Article
- Piezo1 Activation Improves NSCLC Liver Metastasis Immunotherapy by Overriding Matrix Stiffness-Mediated Bimodal PD-L1/CXCL10 Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Class IIa HDACs Are Important Signal Transducers with Unclear Enzymatic Activities.Biomolecules · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Following DNA replication, the newly reassembled chromatin is disorganized and must mature to its steady state to maintain both genome and epigenome integrity. However, the regulatory mechanisms governing this critical process remain poorly understood. Here, we show that histone H3K56 acetylation (H3K56ac), a mark on newly-synthesized H3, facilitates the remodeling of disorganized nucleosomes in nascent chromatin, and its removal at the subsequent G2/M phase of the cell cycle marks the completion of chromatin maturation. In vitro, H3K56ac enhances the activity of ISWI chromatin remodelers, including yeast ISW1 and its human equivalent SNF2h. In vivo, a deficiency of H3K56ac in nascent chromatin results in the formation of closely packed di-nucleosomes and/or tetra-nucleosomes. In contrast, abnormally high H3K56ac levels disrupt chromatin maturation, leading to genome instability. These findings establish a central role of H3K56ac in chromatin maturation and reveal a mechanism regulating this critical aspect of chromosome replication.
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