ArticleDevelopment (Cambridge, England)2024
Deletion of the Ebf1, a mouse deafness gene, causes a dramatic increase in hair cells and support cells of the organ of Corti.
Article in Development (Cambridge, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- EBF1 regulates sensory establishment in the cochlea by positioning the medial boundary of the prosensory domain and restricting proliferation of the sensory progenitor population.Development (Cambridge, England) · 2026Article
- Anxiety-like behavior in deaf Ebf1 conditional knockout mice.Hearing research · 2026Article
- Kölliker's Organ Functions as a Developmental Hub in Mouse Cochlea Regulating Spiral Limbus and Tectorial Membrane Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Long-rangeProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Molecular Characterization of Subdomain Specification of Cochlear Duct Based on Foxg1 and Gata3.International journal of molecular sciences · 2024Article
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Authors and funding
8 authors.
Funding
Abstract
Following up on our previous observation that early B cell factor (EBF) sites are enriched in open chromatin of the developing sensory epithelium of the mouse cochlea, we investigated the effect of deletion of Ebf1 on inner ear development. We used a Cre driver to delete Ebf1 at the otocyst stage before development of the cochlea. We examined the cochlea at postnatal day (P) 1 and found that the sensory epithelium had doubled in size but the length of the cochlear duct was unaffected. We also found that deletion of Ebf1 led to ectopic sensory patches in the Kölliker's organ. Innervation of the developing organ of Corti was disrupted with no obvious spiral bundles. The ectopic patches were also innervated. All the extra hair cells (HCs) within the sensory epithelium and Kölliker's organ contained mechanoelectrical transduction channels, as indicated by rapid uptake of FM1-43. The excessive numbers of HCs were still present in the adult Ebf1 conditional knockout (cKO) animal. The animals had significantly elevated auditory brainstem response thresholds, suggesting that this gene is essential for hearing development.
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