ArticlePloS one2010
Neurod1 suppresses hair cell differentiation in ear ganglia and regulates hair cell subtype development in the cochlea.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
89 citing papers in PubMed, 123 citations in OpenAlex.
- Conditional Deletion of Isl1 Disrupts Cochlear Sensory and Neuronal Development, Leading to Hearing Loss.Molecular neurobiology · 2026Article
- Regulatory Networks Driving the Specification, Differentiation, and Diversification of Neurons in the Mouse Inner Ear.Journal of the Association for Research in Otolaryngology : JARO · 2026Review
- Multifaceted roles of sonic hedgehog signaling in mammalian inner ear development.Developmental biology · 2025Review
- Article
- NEUROD1: transcriptional and epigenetic regulator of human and mouse neuronal and endocrine cell lineage programs.Frontiers in cell and developmental biology · 2024Review
- Early Steps towards Hearing: Placodes and Sensory Development.International journal of molecular sciences · 2023Review
- ISL1 is necessary for auditory neuron development and contributes toward tonotopic organization.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Neurosensory development of the four brainstem-projecting sensory systems and their integration in the telencephalon.Frontiers in neural circuits · 2022Article
- Early Deletion ofFrontiers in cell and developmental biology · 2022Article
- Age-Related Hearing Loss: Sensory and Neural Etiology and Their Interdependence.Frontiers in aging neuroscience · 2022Review
- Development and evolution of the vestibular apparatuses of the inner ear.Journal of anatomy · 2021Review
- Targeted deletion of Atoh8 results in severe hearing loss in mice.Genesis (New York, N.Y. : 2000) · 2021Article
- Development in the Mammalian Auditory System Depends on Transcription Factors.International journal of molecular sciences · 2021Review
- Smoothened overexpression causes trochlear motoneurons to reroute and innervate ipsilateral eyes.Cell and tissue research · 2021Article
- Embryology, Malformations, and Rare Diseases of the Cochlea.Laryngo- rhino- otologie · 2021Article
- Neurog1, Neurod1, and Atoh1 are essential for spiral ganglia, cochlear nuclei, and cochlear hair cell development.Faculty reviews · 2021Review
- Effects of Neurod1 Expression on Mouse and Human Schwannoma Cells.The Laryngoscope · 2021Article
- Molecular Aspects of the Development and Function of Auditory Neurons.International journal of molecular sciences · 2020Review
- Combined Atoh1 and Neurod1 Deletion Reveals Autonomous Growth of Auditory Nerve Fibers.Molecular neurobiology · 2020Article
- Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAt least five bHLH genes regulate cell fate determination and differentiation of sensory neurons, hair cells and supporting cells in the mammalian inner ear. Cross-regulation of Atoh1 and Neurog1 results in hair cell changes in Neurog1 null mice although the nature and mechanism of the cross-regulation has not yet been determined. Neurod1, regulated by both Neurog1 and Atoh1, could be the mediator of this cross-regulation. METHODOLOGY/PRINCIPAL
findingsWe used Tg(Pax2-Cre) to conditionally delete Neurod1 in the inner ear. Our data demonstrate for the first time that the absence of Neurod1 results in formation of hair cells within the inner ear sensory ganglia. Three cell types, neural crest derived Schwann cells and mesenchyme derived fibroblasts (neither expresses Neurod1) and inner ear derived neurons (which express Neurod1) constitute inner ear ganglia. The most parsimonious explanation is that Neurod1 suppresses the alternative fate of sensory neurons to develop as hair cells. In the absence of Neurod1, Atoh1 is expressed and differentiates cells within the ganglion into hair cells. We followed up on this effect in ganglia by demonstrating that Neurod1 also regulates differentiation of subtypes of hair cells in the organ of Corti. We show that in Neurod1 conditional null mice there is a premature expression of several genes in the apex of the developing cochlea and outer hair cells are transformed into inner hair cells. CONCLUSIONS/SIGNIFICANCE: Our data suggest that the long noted cross-regulation of Atoh1 expression by Neurog1 might actually be mediated in large part by Neurod1. We suggest that Neurod1 is regulated by both Neurog1 and Atoh1 and provides a negative feedback for either gene. Through this and other feedback, Neurod1 suppresses alternate fates of neurons to differentiate as hair cells and regulates hair cell subtypes.
Indexed as
Identifiers
What OpenQuestion holds
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.