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Incomplete and delayed Sox2 deletion defines residual ear neurosensory development and maintenance
Journal article   Open access   Peer reviewed

Incomplete and delayed Sox2 deletion defines residual ear neurosensory development and maintenance

Martina Dvorakova, Israt Jahan, Iva Macova, Tetyana Chumak, Romana Bohuslavova, Josef Syka, Bernd Fritzsch and Gabriela Pavlinkova
Scientific reports, Vol.6(1), pp.38253-38253
12/05/2016
DOI: 10.1038/srep38253
PMCID: PMC5137136
PMID: 27917898
url
https://doi.org/10.1038/srep38253View
Published (Version of record) Open Access

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.
Hair Cells, Auditory - cytology Saccule and Utricle - embryology Hair Cells, Auditory - metabolism Animals SOXB1 Transcription Factors - genetics Neurogenesis - physiology Gene Deletion Mice, Transgenic Mice Saccule and Utricle - cytology SOXB1 Transcription Factors - metabolism

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