ArticleNature2016
Structure and regulation of the chromatin remodeller ISWI.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 95 citations in OpenAlex.
- Combinatorial histone modifications direct ATP-dependent chromatin remodeling by NURF to promoter-proximal nucleosomes.Nucleic acids research · 2026Article
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- A competitive regulatory mechanism of the Chd1 remodeler is integral to distorting nucleosomal DNA.Nature structural & molecular biology · 2025Article
- Article
- Regulation of DNA translocation of chromatin remodeler enzyme Chd1 by exit DNA unwrapping.Life metabolism · 2025Article
- Phosphorylation regulates the chromatin remodeler SMARCAD1 in nucleosome binding, ATP hydrolysis, and histone exchange.The Journal of biological chemistry · 2024Article
- How does CHD4 slide nucleosomes?Biochemical Society transactions · 2024Review
- Molecular and structural basis of the chromatin remodeling activity by Arabidopsis DDM1.Nature communications · 2024Article
- Cryo-EM structure and functional analysis of the chromatin remodeler RSF.Acta crystallographica. Section F, Structural biology communications · 2024Article
- Energy-driven genome regulation by ATP-dependent chromatin remodellers.Nature reviews. Molecular cell biology · 2024Review
- Structure of the ISW1a complex bound to the dinucleosome.Nature structural & molecular biology · 2024Article
- Novel biological insights revealed from the investigation of multiscale genome architecture.Computational and structural biotechnology journal · 2023Review
- The role of auxiliary domains in modulating CHD4 activity suggests mechanistic commonality between enzyme families.Nature communications · 2022Article
- Eight (histone H4 genes) is too much: A CRISPR/Cas9 strategy to replace highly duplicated genes with a single modified version for mutational analysis.The Plant cell · 2022Article
- Systematic histone H4 replacement in Arabidopsis thaliana reveals a role for H4R17 in regulating flowering time.The Plant cell · 2022Article
- Article
- The Regulatory Roles of Intrinsically Disordered Linker in VRN1-DNA Phase Separation.International journal of molecular sciences · 2022Article
- Mechanism of Rad26-assisted rescue of stalled RNA polymerase II in transcription-coupled repair.Nature communications · 2021Article
- The emerging role of ISWI chromatin remodeling complexes in cancer.Journal of experimental & clinical cancer research : CR · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ISWI is a member of the SWI2/SNF2 family of chromatin remodellers, which also includes Snf2, Chd1, and Ino80. ISWI is the catalytic subunit of several chromatin remodelling complexes, which mobilize nucleosomes along genomic DNA, promoting replication progression, transcription repression, heterochromatin formation, and many other nuclear processes. The ATPase motor of ISWI is an autonomous remodelling machine, whereas its carboxy (C)-terminal HAND-SAND-SLIDE (HSS) domain functions in binding extranucleosomal linker DNA. The activity of the catalytic core of ISWI is inhibited by the regulatory AutoN and NegC domains, which are in turn antagonized by the H4 tail and extranucleosomal DNA, respectively, to ensure the appropriate chromatin landscape in cells. How AutoN and NegC inhibit ISWI and regulate its nucleosome-centring activity remains elusive. Here we report the crystal structures of ISWI from the thermophilic yeast Myceliophthora thermophila and its complex with a histone H4 peptide. Our data show the amino (N)-terminal AutoN domain contains two inhibitory elements, which collectively bind the second RecA-like domain (core2), holding the enzyme in an inactive conformation. The H4 peptide binds to the core2 domain coincident with one of the AutoN-binding sites, explaining the ISWI activation by H4. The H4-binding surface is conserved in Snf2 and functions beyond AutoN regulation. The C-terminal NegC domain is involved in binding to the core2 domain and functions as an allosteric element for ISWI to respond to the extranucleosomal DNA length.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.