Journal article
Incomplete and delayed Sox2 deletion defines residual ear neurosensory development and maintenance
Scientific reports, Vol.6(1), pp.38253-38253
12/05/2016
DOI: 10.1038/srep38253
PMCID: PMC5137136
PMID: 27917898
Abstract
The role of Sox2 in neurosensory development is not yet fully understood. Using mice with conditional Islet1-cre mediated deletion of Sox2, we explored the function of Sox2 in neurosensory development in a model with limited cell type diversification, the inner ear. In Sox2 conditional mutants, neurons initially appear to form normally, whereas late- differentiating neurons of the cochlear apex never form. Variable numbers of hair cells differentiate in the utricle, saccule, and cochlear base but sensory epithelium formation is completely absent in the apex and all three cristae of the semicircular canal ampullae. Hair cells differentiate only in sensory epithelia known or proposed to have a lineage relationship of neurons and hair cells. All initially formed neurons lacking hair cell targets die by apoptosis days after they project toward non-existing epithelia. Therefore, late neuronal development depends directly on Sox2 for differentiation and on the survival of hair cells, possibly derived from common neurosensory precursors.
Details
- Title: Subtitle
- Incomplete and delayed Sox2 deletion defines residual ear neurosensory development and maintenance
- Creators
- Martina Dvorakova - Faculty of Science, Charles University, Prague, CzechiaIsrat Jahan - Department of Biology, University of Iowa, Iowa City, IA, USAIva Macova - Faculty of Science, Charles University, Prague, CzechiaTetyana Chumak - Institute of Experimental Medicine CAS, Prague, CzechiaRomana Bohuslavova - Institute of Biotechnology CAS, Prague, CzechiaJosef Syka - Institute of Experimental Medicine CAS, Prague, CzechiaBernd Fritzsch - Department of Biology, University of Iowa, Iowa City, IA, USAGabriela Pavlinkova - Institute of Biotechnology CAS, Prague, Czechia
- Resource Type
- Journal article
- Publication Details
- Scientific reports, Vol.6(1), pp.38253-38253
- DOI
- 10.1038/srep38253
- PMID
- 27917898
- PMCID
- PMC5137136
- NLM abbreviation
- Sci Rep
- ISSN
- 2045-2322
- eISSN
- 2045-2322
- Publisher
- England
- Grant note
- R03 DC013655 / NIDCD NIH HHS P30 DC010362 / NIDCD NIH HHS
- Language
- English
- Date published
- 12/05/2016
- Academic Unit
- Iowa Neuroscience Institute; Biology; Craniofacial Anomalies Research Center
- Record Identifier
- 9984070864902771
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