ArticleDevelopmental biology2013
Atoh1 directs hair cell differentiation and survival in the late embryonic mouse inner ear.
Article in Developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 86 citations in OpenAlex.
- Targeted cell interconversions reveal inner hair cell control of organ of Corti cytoarchitecture.Science advances · 2025Article
- prdm1a drives a fate switch between hair cells of different mechanosensory organs.Nature communications · 2025Article
- Preclinical Models to Study the Molecular Pathophysiology of Meniere's Disease: A Pathway to Gene Therapy.Journal of clinical medicine · 2025Article
- Article
- Single-cell atlas comparison across vertebrates reveals auditory cell evolution and mechanisms for hair cell regeneration.Communications biology · 2024Article
- Harmony in the Molecular Orchestra of Hearing: Developmental Mechanisms from the Ear to the Brain.Annual review of neuroscience · 2024Review
- Sheep as a large animal model for hearing research: comparison to common laboratory animals and humans.Laboratory animal research · 2023Review
- 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
- Dispensable role of Rac1 and Rac3 after cochlear hair cell specification.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Rps14 upregulation promotes inner ear progenitor proliferation and hair cell regeneration in the neonatal mouse cochlea.Cell proliferation · 2023Article
- Depicting pseudotime-lagged causality across single-cell trajectories for accurate gene-regulatory inference.PNAS nexus · 2023Article
- Article
- Gene therapy: an emerging therapy for hair cells regeneration in the cochlea.Frontiers in neuroscience · 2023Review
- Article
- Modelling inner ear development and disease using pluripotent stem cells - a pathway to new therapeutic strategies.Disease models & mechanisms · 2022Review
- BiallelicNeurology. Genetics · 2022Article
- 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
- Molecular Pathways Modulating Sensory Hair Cell Regeneration in Adult Mammalian Cochleae: Progress and Perspectives.International journal of molecular sciences · 2021Review
- Norrie disease protein is essential for cochlear hair cell maturation.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
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Authors and funding
8 authors at 6 institutions in 2 countries.
Funding
Abstract
Atoh1 function is required for the earliest stages of inner ear hair cell development, which begins during the second week of gestation. Atoh1 expression in developing hair cells continues until early postnatal ages, but the function of this late expression is unknown. To test the role of continued Atoh1 expression in hair cell maturation we conditionally deleted the gene in the inner ear at various embryonic and postnatal ages. In the organ of Corti, deletion of Atoh1 at E15.5 led to the death of all hair cells. In contrast, deletion at E16.5 caused death only in apical regions, but abnormalities of stereocilia formation were present throughout the cochlea. In the utricle, deletion at E14.5 or E16.5 did not cause cell death but led to decreased expression of myosin VIIa and failure of stereocilia formation. Furthermore, we show that maintained expression of Barhl1 and Gfi1, two transcription factors implicated in cochlear hair cell survival, depends upon continued Atoh1 expression. However, maintained expression of Pou4f3 and several hair cell-specific markers is independent of Atoh1 expression. These data reveal novel late roles for Atoh1 that are separable from its initial role in hair cell development.
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