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Artificial Induction of Sox21 Regulates Sensory Cell Formation in the Embryonic Chicken Inner Ear

During embryonic development, hair cells and support cells in the sensory epithelia of the inner ear derive from progenitors that express Sox2, a member of the SoxB1 family of transcription factors. Sox2 is essential for sensory specification, but high levels of Sox2 expression appear to inhibit hai...

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Autores principales: Freeman, Stephen D., Daudet, Nicolas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468625/
https://www.ncbi.nlm.nih.gov/pubmed/23071561
http://dx.doi.org/10.1371/journal.pone.0046387
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author Freeman, Stephen D.
Daudet, Nicolas
author_facet Freeman, Stephen D.
Daudet, Nicolas
author_sort Freeman, Stephen D.
collection PubMed
description During embryonic development, hair cells and support cells in the sensory epithelia of the inner ear derive from progenitors that express Sox2, a member of the SoxB1 family of transcription factors. Sox2 is essential for sensory specification, but high levels of Sox2 expression appear to inhibit hair cell differentiation, suggesting that factors regulating Sox2 activity could be critical for both processes. Antagonistic interactions between SoxB1 and SoxB2 factors are known to regulate cell differentiation in neural tissue, which led us to investigate the potential roles of the SoxB2 member Sox21 during chicken inner ear development. Sox21 is normally expressed by sensory progenitors within vestibular and auditory regions of the early embryonic chicken inner ear. At later stages, Sox21 is differentially expressed in the vestibular and auditory organs. Sox21 is restricted to the support cell layer of the auditory epithelium, while it is enriched in the hair cell layer of the vestibular organs. To test Sox21 function, we used two temporally distinct gain-of-function approaches. Sustained over-expression of Sox21 from early developmental stages prevented prosensory specification, and abolished the formation of both hair cells and support cells. However, later induction of Sox21 expression at the time of hair cell formation in organotypic cultures of vestibular epithelia inhibited endogenous Sox2 expression and Notch activity, and biased progenitor cells towards a hair cell fate. Interestingly, Sox21 did not promote hair cell differentiation in the immature auditory epithelium, which fits with the expression of endogenous Sox21 within mature support cells in this tissue. These results suggest that interactions among endogenous SoxB family transcription factors may regulate sensory cell formation in the inner ear, but in a context-dependent manner.
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spelling pubmed-34686252012-10-15 Artificial Induction of Sox21 Regulates Sensory Cell Formation in the Embryonic Chicken Inner Ear Freeman, Stephen D. Daudet, Nicolas PLoS One Research Article During embryonic development, hair cells and support cells in the sensory epithelia of the inner ear derive from progenitors that express Sox2, a member of the SoxB1 family of transcription factors. Sox2 is essential for sensory specification, but high levels of Sox2 expression appear to inhibit hair cell differentiation, suggesting that factors regulating Sox2 activity could be critical for both processes. Antagonistic interactions between SoxB1 and SoxB2 factors are known to regulate cell differentiation in neural tissue, which led us to investigate the potential roles of the SoxB2 member Sox21 during chicken inner ear development. Sox21 is normally expressed by sensory progenitors within vestibular and auditory regions of the early embryonic chicken inner ear. At later stages, Sox21 is differentially expressed in the vestibular and auditory organs. Sox21 is restricted to the support cell layer of the auditory epithelium, while it is enriched in the hair cell layer of the vestibular organs. To test Sox21 function, we used two temporally distinct gain-of-function approaches. Sustained over-expression of Sox21 from early developmental stages prevented prosensory specification, and abolished the formation of both hair cells and support cells. However, later induction of Sox21 expression at the time of hair cell formation in organotypic cultures of vestibular epithelia inhibited endogenous Sox2 expression and Notch activity, and biased progenitor cells towards a hair cell fate. Interestingly, Sox21 did not promote hair cell differentiation in the immature auditory epithelium, which fits with the expression of endogenous Sox21 within mature support cells in this tissue. These results suggest that interactions among endogenous SoxB family transcription factors may regulate sensory cell formation in the inner ear, but in a context-dependent manner. Public Library of Science 2012-10-10 /pmc/articles/PMC3468625/ /pubmed/23071561 http://dx.doi.org/10.1371/journal.pone.0046387 Text en © 2012 Freeman, Daudet http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Freeman, Stephen D.
Daudet, Nicolas
Artificial Induction of Sox21 Regulates Sensory Cell Formation in the Embryonic Chicken Inner Ear
title Artificial Induction of Sox21 Regulates Sensory Cell Formation in the Embryonic Chicken Inner Ear
title_full Artificial Induction of Sox21 Regulates Sensory Cell Formation in the Embryonic Chicken Inner Ear
title_fullStr Artificial Induction of Sox21 Regulates Sensory Cell Formation in the Embryonic Chicken Inner Ear
title_full_unstemmed Artificial Induction of Sox21 Regulates Sensory Cell Formation in the Embryonic Chicken Inner Ear
title_short Artificial Induction of Sox21 Regulates Sensory Cell Formation in the Embryonic Chicken Inner Ear
title_sort artificial induction of sox21 regulates sensory cell formation in the embryonic chicken inner ear
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468625/
https://www.ncbi.nlm.nih.gov/pubmed/23071561
http://dx.doi.org/10.1371/journal.pone.0046387
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