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

0469273 - BTÚ 2017 RIV GB eng J - Článek v odborném periodiku
Dvořáková, Martina - Jahan, I. - Mácová, Iva - Chumak, Tetyana - Bohuslavová, Romana - Syka, Josef - Fritzsch, B. - Pavlínková, Gabriela
Incomplete and delayed Sox2 deletion defines residual ear neurosensory development and maintenance.
Scientific Reports. Roč. 6, Dec 5 (2016), č. článku 38253. ISSN 2045-2322. E-ISSN 2045-2322
Grant CEP: GA ČR(CZ) GA13-07996S; GA MŠMT(CZ) ED1.1.00/02.0109
Výzkumný záměr: CEZ:AV0Z50520701
Institucionální podpora: RVO:86652036 ; RVO:68378041
Klíčová slova: inner ear * neurons * hair cells
Kód oboru RIV: EB - Genetika a molekulární biologie; FH - Neurologie, neurochirurgie, neurovědy (UEM-P)
Impakt faktor: 4.259, rok: 2016

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.
Trvalý link: http://hdl.handle.net/11104/0267071