ArticleJCI insight2018
CHD7 represses the retinoic acid synthesis enzyme ALDH1A3 during inner ear development.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026Review
- Synergistic SHH activation and BMP inhibition remodel progenitor niche for enhanced hair cell generation.Science China. Life sciences · 2026Article
- Thymus Ontogeny and Development.Advances in experimental medicine and biology · 2025Review
- The pathogenic role of retinoid nuclear receptor signaling in cancer and metabolic syndromes.The Journal of experimental medicine · 2024Review
- Role of miRNA-mRNA Interactome in Pathophysiology of Arrhythmogenic Cardiomyopathy.Biomedicines · 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
- Primary and secondary defects of the thymus.Immunological reviews · 2024Review
- Review
- CHD7 regulates otic lineage specification and hair cell differentiation in human inner ear organoids.Nature communications · 2022Article
- Partial CHARGE syndrome with bilateral retinochoroidal colobomas associated with 7q11.23 duplication syndrome: case report.BMC ophthalmology · 2022Article
- Chromatin remodeler CHD7 is critical for cochlear morphogenesis and neurosensory patterning.Developmental biology · 2021Article
- Advances and challenges in adeno-associated viral inner-ear gene therapy for sensorineural hearing loss.Molecular therapy. Methods & clinical development · 2021Review
- Inborn errors of thymic stromal cell development and function.Seminars in immunopathology · 2021Review
- Chromatin Imbalance as the Vertex Between Fetal Valproate Syndrome and Chromatinopathies.Frontiers in cell and developmental biology · 2021Review
- CHD7 promotes neural progenitor differentiation in embryonic stem cells via altered chromatin accessibility and nascent gene expression.Scientific reports · 2020Article
- Practical aspects of inner ear gene delivery for research and clinical applications.Hearing research · 2020Review
- Epigenetics in neuronal regeneration.Seminars in cell & developmental biology · 2020Review
- Molecular Insights Into the Causes of Human Thymic Hypoplasia With Animal Models.Frontiers in immunology · 2020Review
- Transcriptome Profiling of Primary Skin Fibroblasts Reveal Distinct Molecular Features BetweenGenes · 2019Article
- Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
CHD7, an ATP-dependent chromatin remodeler, is disrupted in CHARGE syndrome, an autosomal dominant disorder characterized by variably penetrant abnormalities in craniofacial, cardiac, and nervous system tissues. The inner ear is uniquely sensitive to CHD7 levels and is the most commonly affected organ in individuals with CHARGE. Interestingly, upregulation or downregulation of retinoic acid (RA) signaling during embryogenesis also leads to developmental defects similar to those in CHARGE syndrome, suggesting that CHD7 and RA may have common target genes or signaling pathways. Here, we tested three separate potential mechanisms for CHD7 and RA interaction: (a) direct binding of CHD7 with RA receptors, (b) regulation of CHD7 levels by RA, and (c) CHD7 binding and regulation of RA-related genes. We show that CHD7 directly regulates expression of Aldh1a3, the gene encoding the RA synthetic enzyme ALDH1A3 and that loss of Aldh1a3 partially rescues Chd7 mutant mouse inner ear defects. Together, these studies indicate that ALDH1A3 acts with CHD7 in a common genetic pathway to regulate inner ear development, providing insights into how CHD7 and RA regulate gene expression and morphogenesis in the developing embryo.
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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.