ArticlePloS one2012
A novel Atoh1 "self-terminating" mouse model reveals the necessity of proper Atoh1 level and duration for hair cell differentiation and viability.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 111 citations in OpenAlex.
- Dicer Deletion in the Ear Can Cut Most Neurons and Their Innervation of Hair Cells to Project to the Ear and the Brainstem.International journal of molecular sciences · 2026Article
- Evolutionary constraints impose multiple checkpoints that block mammalian sensory hair cell regeneration.Frontiers in cell and developmental biology · 2026Review
- Targeted cell interconversions reveal inner hair cell control of organ of Corti cytoarchitecture.Science advances · 2025Article
- Precise genetic control of ATOH1 enhances maturation of regenerated hair cells in the mature mouse utricle.Nature communications · 2024Article
- Harmony in the Molecular Orchestra of Hearing: Developmental Mechanisms from the Ear to the Brain.Annual review of neuroscience · 2024Review
- The proper timing of Atoh1 expression is pivotal for hair cell subtype differentiation and the establishment of inner ear function.Cellular and molecular life sciences : CMLS · 2023Article
- Future Pharmacotherapy for Sensorineural Hearing Loss by Protection and Regeneration of Auditory Hair Cells.Pharmaceutics · 2023Review
- Article
- Critical roles of FGF, RA, and WNT signalling in the development of the human otic placode and subsequent lineages in a dish.Regenerative therapy · 2022Article
- Age-Related Hearing Loss: Sensory and Neural Etiology and Their Interdependence.Frontiers in aging neuroscience · 2022Review
- An Integrated Perspective of Evolution and Development: From Genes to Function to Ear, Lateral Line and Electroreception.Diversity · 2021Article
- POU4F3 pioneer activity enables ATOH1 to drive diverse mechanoreceptor differentiation through a feed-forward epigenetic mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Development in the Mammalian Auditory System Depends on Transcription Factors.International journal of molecular sciences · 2021Review
- Key Signaling Pathways Regulate the Development and Survival of Auditory Hair Cells.Neural plasticity · 2021Review
- Neurog1, Neurod1, and Atoh1 are essential for spiral ganglia, cochlear nuclei, and cochlear hair cell development.Faculty reviews · 2021Review
- Transcription Factor Reprogramming in the Inner Ear: Turning on Cell Fate Switches to Regenerate Sensory Hair Cells.Frontiers in cellular neuroscience · 2021Article
- Combinatorial Atoh1 and Gfi1 induction enhances hair cell regeneration in the adult cochlea.Scientific reports · 2020Article
- Combined Atoh1 and Neurod1 Deletion Reveals Autonomous Growth of Auditory Nerve Fibers.Molecular neurobiology · 2020Article
- Research progress on flat epithelium of the inner ear.Physiological research · 2020Review
- Interaction with ectopic cochlear crista sensory epithelium disrupts basal cochlear sensory epithelium development in Lmx1a mutant mice.Cell and tissue research · 2020Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Atonal homolog1 (Atoh1) is a bHLH transcription factor essential for inner ear hair cell differentiation. Targeted expression of Atoh1 at various stages in development can result in hair cell differentiation in the ear. However, the level and duration of Atoh1 expression required for proper hair cell differentiation and maintenance remain unknown. We generated an Atoh1 conditional knockout (CKO) mouse line using Tg(Atoh1-cre), in which the cre expression is driven by an Atoh1 enhancer element that is regulated by Atoh1 protein to "self-terminate" its expression. The mutant mice show transient, limited expression of Atoh1 in all hair cells in the ear. In the organ of Corti, reduction and delayed deletion of Atoh1 result in progressive loss of almost all the inner hair cells and the majority of the outer hair cells within three weeks after birth. The remaining cells express hair cell marker Myo7a and attract nerve fibers, but do not differentiate normal stereocilia bundles. Some Myo7a-positive cells persist in the cochlea into adult stages in the position of outer hair cells, flanked by a single row of pillar cells and two to three rows of disorganized Deiters cells. Gene expression analyses of Atoh1, Barhl1 and Pou4f3, genes required for survival and maturation of hair cells, reveal earlier and higher expression levels in the inner compared to the outer hair cells. Our data show that Atoh1 is crucial for hair cell mechanotransduction development, viability, and maintenance and also suggest that Atoh1 expression level and duration may play a role in inner vs. outer hair cell development. These genetically engineered Atoh1 CKO mice provide a novel model for establishing critical conditions needed to regenerate viable and functional hair cells with Atoh1 therapy.
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