ArticleNature communications2026
Histone Acetylation Differentially Modulates CTCF-CTCF Loops and Intra-TAD Interactions.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Cohesin residence time gates 3D genome response to histone hyperacetylation.bioRxiv : the preprint server for biology · 2026Article
- Whole-genome 3D architectural screen reveals modulators of brain DNA structure.bioRxiv : the preprint server for biology · 2026Article
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10 authors.
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Abstract
The cohesin complex structures the interphase genome of human cells by extruding loops and organizing topologically associating domains (TADs), yet how chromatin state regulates cohesin-chromatin interactions remains unclear. Here, we show that histone hyperacetylation induced by trichostatin A (TSA) selectively disrupts short-range intra-TAD interactions while largely preserving CTCF-anchored loops. These distinct responses define two functional cohesin populations: a TSA-sensitive pool associated with dynamic loop extrusion, and a TSA-resistant pool at CTCF sites maintained by topological entrapment. Using a semi-in vitro system with TEV-cleavable RAD21, we demonstrate that hyperacetylation increases the sensitivity of CTCF-anchored loops to cohesin ring cleavage, supporting a topological basis for their stability. We further identify a TSA-sensitive cohesin fraction at CTCF sites, suggesting transient, non-encircling intermediates. Together, our results reveal that cohesin exists in distinct biochemical states that differentially regulate chromatin loop stability and responsiveness to epigenomic perturbation.
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