ArticleThe Journal of biological chemistry2017
The ATP-dependent chromatin remodeling enzymes CHD6, CHD7, and CHD8 exhibit distinct nucleosome binding and remodeling activities.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 71 citations in OpenAlex.
- [Clinical phenotype and genetic analysis of 7 neonates with CHARGE syndrome caused byZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Article
- Epigenetics in Atrial Fibrillation: Molecular Mechanisms and Therapeutic Avenues.Reviews in cardiovascular medicine · 2026Review
- Molecular Acrobats: How CHD Remodelers Shape the Genetic Playground to License Cell Identity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Genomic Expansion and Adaptation in a Parasitoid WaspInsects · 2026Article
- Molecular interactions of Chd8 in mouse brain highlights a role in chromatin-associated RNA processing.bioRxiv : the preprint server for biology · 2025Article
- Condensation-dependent interactome of a chromatin remodeler underlies tumor suppressor activities.Nature communications · 2025Article
- SINEUP RNA rescues molecular phenotypes associated with CHD8 suppression in autism spectrum disorder model systems.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The proximity-based protein interactome and regulatory logics of the transcription factor p65 NF-κB/RELA.EMBO reports · 2025Article
- Chromatin remodellers as therapeutic targets.Nature reviews. Drug discovery · 2024Review
- Loss-of-function of the Zinc Finger Homeobox 4 (medRxiv : the preprint server for health sciences · 2024Article
- Article
- The complex etiology of autism spectrum disorder due to missense mutations of CHD8.Molecular psychiatry · 2024Article
- Prioritizing susceptibility genes for the prognosis of male-pattern baldness with transcriptome-wide association study.Human genomics · 2024Article
- CHD7 and SOX2 act in a common gene regulatory network during mammalian semicircular canal and cochlear development.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Neurodevelopmental functions of CHD8: new insights and questions.Biochemical Society transactions · 2024Review
- The CHD family chromatin remodeling enzyme, Kismet, promotes both clathrin-mediated and activity-dependent bulk endocytosis.PloS one · 2024Article
- Small molecule modulators of chromatin remodeling: from neurodevelopment to neurodegeneration.Cell & bioscience · 2023Review
- Chromatin remodeler Chd7 regulates photoreceptor development and outer segment length.Experimental eye research · 2023Article
- Identification of transcriptional regulatory variants in pig duodenum, liver, and muscle tissues.GigaScience · 2022Article
- CHD6 promotes broad nucleosome eviction for transcriptional activation in prostate cancer cells.Nucleic acids research · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Proper chromatin regulation is central to genome function and maintenance. The group III chromodomain-helicase-DNA-binding (CHD) family of ATP-dependent chromatin remodeling enzymes, comprising CHD6, CHD7, CHD8, and CHD9, has well-documented roles in transcription regulation, impacting both organism development and disease etiology. These four enzymes are similar in their constituent domains, but they fill surprisingly non-redundant roles in the cell, with deficiencies in individual enzymes leading to dissimilar disease states such as CHARGE syndrome or autism spectrum disorders. The mechanisms explaining their divergent, non-overlapping functions are unclear. In this study, we performed an in-depth biochemical analysis of purified CHD6, CHD7, and CHD8 and discovered distinct differences in chromatin remodeling specificities and activities among them. We report that CHD6 and CHD7 both bind with high affinity to short linker DNA, whereas CHD8 requires longer DNA for binding. As a result, CHD8 slides nucleosomes into positions with more flanking linker DNA than CHD7. Moreover, we found that, although CHD7 and CHD8 slide nucleosomes, CHD6 disrupts nucleosomes in a distinct non-sliding manner. The different activities of these enzymes likely lead to differences in chromatin structure and, thereby, transcriptional control, at the enhancer and promoter loci where these enzymes bind. Overall, our work provides a mechanistic basis for both the non-redundant roles and the diverse mutant disease states of these enzymes
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