ArticleCommunications biology2021
The chromatin remodelling factor Chd7 protects auditory neurons and sensory hair cells from stress-induced degeneration.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Disrupted Vestibular Nuclei Neuron Development in a Chick Model for Congenital Vestibular Disorders.Developmental neurobiology · 2026Article
- Mutation of CHD7 impairs the output of neuroepithelium transition that is reversed by the inhibition of EZH2.Molecular psychiatry · 2025Article
- AAV-mediated Gene Cocktails Enhance Supporting Cell Reprogramming and Hair Cell Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Advance and Application of Single-cell Transcriptomics in Auditory Research.Neuroscience bulletin · 2024Review
- Whole-exome sequencing reveals genetic variants that may play a role in neurocytomas.Journal of neuro-oncology · 2024Article
- ATM-dependent phosphorylation of CHD7 regulates morphogenesis-coupled DSB stress response in fetal radiation exposure.Molecular biology of the cell · 2023Article
- The spectrum of cochlear malformations in CHARGE syndrome and insights into the role of the CHD7 gene during embryogenesis of the inner ear.Neuroradiology · 2023Review
- Review
- Chromatin remodeler Chd7 regulates photoreceptor development and outer segment length.Experimental eye research · 2023Article
- CHD7 regulates otic lineage specification and hair cell differentiation in human inner ear organoids.Nature communications · 2022Article
- Characterization of Two MouseInternational journal of molecular sciences · 2022Article
- Eyes on CHARGE syndrome: Roles of CHD7 in ocular development.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Neurons and sensory cells are particularly vulnerable to oxidative stress due to their high oxygen demand during stimulus perception and transmission. The mechanisms that protect them from stress-induced death and degeneration remain elusive. Here we show that embryonic deletion of the chromodomain helicase DNA-binding protein 7 (CHD7) in auditory neurons or hair cells leads to sensorineural hearing loss due to postnatal degeneration of both cell types. Mechanistically, we demonstrate that CHD7 controls the expression of major stress pathway components. In its absence, hair cells are hypersensitive, dying rapidly after brief exposure to stress inducers, suggesting that sound at the onset of hearing triggers their degeneration. In humans, CHD7 haploinsufficiency causes CHARGE syndrome, a disorder affecting multiple organs including the ear. Our findings suggest that CHD7 mutations cause developmentally silent phenotypes that predispose cells to postnatal degeneration due to a failure of protective mechanisms.
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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.