ArticleNature structural & molecular biology2024
ISWI catalyzes nucleosome sliding in condensed nucleosome arrays.
Article in Nature structural & molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Single-molecule imaging reveals DNA shape read-out by the INO80 chromatin remodeler.Nature communications · 2026Article
- Principles and mechanisms of plant acclimation to heat stress.Nature reviews. Molecular cell biology · 2026Review
- Insights from single-molecule force spectroscopy into chromatin topology.Biophysical reviews · 2026Review
- Nucleosome Linker Length and Distribution as Major Players in Epigenetic Regulation: Insights from Cryo-Electron Microscopy and Modeling of Retina Cell Maturation.DNA and cell biology · 2025Review
- ATP-dependent remodeling of chromatin condensates reveals distinct mesoscale outcomes.Science (New York, N.Y.) · 2025Article
- Dynamics of nucleosomes and chromatin fibers revealed by single-molecule measurements.BMB reports · 2025Review
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11 authors at 8 institutions in 4 countries.
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Abstract
How chromatin enzymes work in condensed chromatin and how they maintain diffusional mobility inside remains unexplored. Here we investigated these challenges using the Drosophila ISWI remodeling ATPase, which slides nucleosomes along DNA. Folding of chromatin fibers did not affect sliding in vitro. Catalytic rates were also comparable in- and outside of chromatin condensates. ISWI cross-links and thereby stiffens condensates, except when ATP hydrolysis is possible. Active hydrolysis is also required for ISWI's mobility in condensates. Energy from ATP hydrolysis therefore fuels ISWI's diffusion through chromatin and prevents ISWI from cross-linking chromatin. Molecular dynamics simulations of a 'monkey-bar' model in which ISWI grabs onto neighboring nucleosomes, then withdraws from one before rebinding another in an ATP hydrolysis-dependent manner, qualitatively agree with our data. We speculate that monkey-bar mechanisms could be shared with other chromatin factors and that changes in chromatin dynamics caused by mutations in remodelers could contribute to pathologies.
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Registered trials
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