ArticleFrontiers in molecular neuroscience2017
The Repression of Atoh1 by Neurogenin1 during Inner Ear Development.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Characteristics and Cell Lineage Tracing of Neurod1-Cre and Neurod1-iCreER Mice Targeting Cochlear Neurons.Neuroscience bulletin · 2026Article
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- Transcriptional Regulation ofMolecular and cellular biology · 2023Article
- Viral Status Predicts the Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma.The Journal of investigative dermatology · 2022Article
- Homodimeric and Heterodimeric Interactions among Vertebrate Basic Helix-Loop-Helix Transcription Factors.International journal of molecular sciences · 2021Review
- Differential regulation of mammalian and avian ATOH1 by E2F1 and its implication for hair cell regeneration in the inner ear.Scientific reports · 2021Article
- HIC1 Represses Atoh1 Transcription and Hair Cell Differentiation in the Cochlea.Stem cell reports · 2021Article
- Open chromatin dynamics in prosensory cells of the embryonic mouse cochlea.Scientific reports · 2019Article
- Approaches for the study of epigenetic modifications in the inner ear and related tissues.Hearing research · 2019Review
- DNA methylation dynamics during embryonic development and postnatal maturation of the mouse auditory sensory epithelium.Scientific reports · 2018Article
- Intracellular Regulome Variability Along the Organ of Corti: Evidence, Approaches, Challenges, and Perspective.Frontiers in genetics · 2018Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atonal homolog 1 (Atoh1) and Neurogenin1 (Neurog1) are basic Helix-Loop-Helix (bHLH) transcription factors crucial for the generation of hair cells (HCs) and neurons in the inner ear. Both genes are induced early in development, but the expression of Atoh1 is counteracted by Neurog1. As a result, HC development is prevented during neurogenesis. This work aimed at understanding the molecular basis of this interaction. Atoh1 regulation depends on a 3'Atoh1-enhancer that is the site for Atoh1 autoregulation. Reporter assays on chick embryos and P19 cells show that Neurog1 hampers the autoactivation of Atoh1, the effect being cell autonomous and independent on Notch activity. Assay for Transposase-Accessible Chromatin with high throughput sequencing (ATAC-Seq) analysis shows that the region B of the 3'Atoh1-enhancer is accessible during development and sufficient for both activation and repression. Neurog1 requires the regions flanking the class A E-box to show its repressor effect, however, it does not require binding to DNA for Atoh1 repression. This depends on the dimerization domains Helix-1 and Helix-2 and the reduction of Atoh1 protein levels. The results point towards the acceleration of Atoh1 mRNA degradation as the potential mechanism for the reduction of Atoh1 levels. Such a mechanism dissociates the prevention of Atoh1 expression in neurosensory progenitors from the unfolding of the neurogenic program.
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