ArticlePLoS biology2024
Chromatin remodeller Chd7 is developmentally regulated in the neural crest by tissue-specific transcription factors.
Article in PLoS 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.
- Craniofacial development: genetics, signaling pathways, teratogenic mechanisms, and clinal significance.Molecular biomedicine · 2026Review
- Multi-omic analyses identify molecular targets of Chd7 that contribute to CHARGE syndrome model phenotypes.Disease models & mechanisms · 2026Article
- CHD7 regulates cardiac neural crest cell differentiation through SOX5-mediated self-activation.iScience · 2025Article
- Analysis of the clinical features of neurocristopathy-related hearing loss and how these relate to outcomes after cochlear implantation.Scientific reports · 2025Article
- Development of the semicircular canals and otolithic organs of the vertebrate inner ear.Current topics in developmental biology · 2025Review
- SMPD3 expression is spatially regulated in the developing embryo by SOXE factors.Developmental biology · 2024Article
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Authors and funding
15 authors.
Funding
Abstract
Neurocristopathies such as CHARGE syndrome result from aberrant neural crest development. A large proportion of CHARGE cases are attributed to pathogenic variants in the gene encoding CHD7, chromodomain helicase DNA binding protein 7, which remodels chromatin. While the role for CHD7 in neural crest development is well documented, how this factor is specifically up-regulated in neural crest cells is not understood. Here, we use epigenomic profiling of chick and human neural crest to identify a cohort of enhancers regulating Chd7 expression in neural crest cells and other tissues. We functionally validate upstream transcription factor binding at candidate enhancers, revealing novel epistatic relationships between neural crest master regulators and Chd7, showing tissue-specific regulation of a globally acting chromatin remodeller. Furthermore, we find conserved enhancer features in human embryonic epigenomic data and validate the activity of the human equivalent CHD7 enhancers in the chick embryo. Our findings embed Chd7 in the neural crest gene regulatory network and offer potentially clinically relevant elements for interpreting CHARGE syndrome cases without causative allocation.
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Registered trials
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