ArticlePloS one2012
Expression of Neurog1 instead of Atoh1 can partially rescue organ of Corti cell survival.
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 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Development in the Mammalian Auditory System Depends on Transcription Factors.International journal of molecular sciences · 2021Review
- Near-infrared stimulation of the auditory nerve: A decade of progress toward an optical cochlear implant.Laryngoscope investigative otolaryngology · 2021Review
- Neurog1, Neurod1, and Atoh1 are essential for spiral ganglia, cochlear nuclei, and cochlear hair cell development.Faculty reviews · 2021Review
- Wilhelm His' lasting insights into hindbrain and cranial ganglia development and evolution.Developmental biology · 2018Review
- Multichannel optrodes for photonic stimulation.Neurophotonics · 2018Article
- Pressure in the Cochlea During Infrared Irradiation.IEEE transactions on bio-medical engineering · 2018Article
- UsingDisease models & mechanisms · 2018Review
- Gene, cell, and organ multiplication drives inner ear evolution.Developmental biology · 2017Review
- An Atoh1-S193A Phospho-Mutant Allele Causes Hearing Deficits and Motor Impairment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- The Role of Atonal Factors in Mechanosensory Cell Specification and Function.Molecular neurobiology · 2015Article
- The quest for restoring hearing: Understanding ear development more completely.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Review
- Neurog1 can partially substitute for Atoh1 function in hair cell differentiation and maintenance during organ of Corti development.Development (Cambridge, England) · 2015Article
- Inner ear development: building a spiral ganglion and an organ of Corti out of unspecified ectoderm.Cell and tissue research · 2015Review
- Evolving gene regulatory networks into cellular networks guiding adaptive behavior: an outline how single cells could have evolved into a centralized neurosensory system.Cell and tissue research · 2015Review
- Segregating neural and mechanosensory fates in the developing ear: patterning, signaling, and transcriptional control.Cell and tissue research · 2015Review
- Opportunities and limits of the one gene approach: the ability of Atoh1 to differentiate and maintain hair cells depends on the molecular context.Frontiers in cellular neuroscience · 2015Review
- The role of her4 in inner ear development and its relationship with proneural genes and Notch signalling.PloS one · 2014Article
- Atoh1 directs hair cell differentiation and survival in the late embryonic mouse inner ear.Developmental biology · 2013Article
- The genetics of hair cell development and regeneration.Annual review of neuroscience · 2013Review
- The role of Atonal transcription factors in the development of mechanosensitive cells.Seminars in cell & developmental biology · 2013Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
In the mammalian inner ear neurosensory cell fate depends on three closely related transcription factors, Atoh1 for hair cells and Neurog1 and Neurod1 for neurons. We have previously shown that neuronal cell fate can be altered towards hair cell fate by eliminating Neurod1 mediated repression of Atoh1 expression in neurons. To test whether a similar plasticity is present in hair cell fate commitment, we have generated a knockin (KI) mouse line (Atoh1(KINeurog1)) in which Atoh1 is replaced by Neurog1. Expression of Neurog1 under Atoh1 promoter control alters the cellular gene expression pattern, differentiation and survival of hair cell precursors in both heterozygous (Atoh1(+/KINeurog1)) and homozygous (Atoh1(KINeurog1/KINeurog1)) KI mice. Homozygous KI mice develop patches of organ of Corti precursor cells that express Neurog1, Neurod1, several prosensory genes and neurotrophins. In addition, these patches of cells receive afferent and efferent processes. Some cells among these patches form multiple microvilli but no stereocilia. Importantly, Neurog1 expressing mutants differ from Atoh1 null mutants, as they have intermittent formation of organ of Corti-like patches, opposed to a complete 'flat epithelium' in the absence of Atoh1. In heterozygous KI mice co-expression of Atoh1 and Neurog1 results in change in fate and patterning of some hair cells and supporting cells in addition to the abnormal hair cell polarity in the later stages of development. This differs from haploinsufficiency of Atoh1 (Pax2cre; Atoh1(f/+)), indicating the effect of Neurog1 expression in developing hair cells. Our data suggest that Atoh1(KINeurog1) can provide some degree of functional support for survival of organ of Corti cells. In contrast to the previously demonstrated fate plasticity of neurons to differentiate as hair cells, hair cell precursors can be maintained for a limited time by Neurog1 but do not transdifferentiate as neurons.
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