Expression and Function of Sox21 During Mouse Cochlea Development
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The development of the inner ear is an orchestrated process of morphogenesis with spatiotemporally controlled generations of individual cell types. Recent studies have revealed that the Sox gene family, a family of evolutionarily conserved HMG-type transcriptional factors, is differentially expressed in each cell type of the mammalian inner ear and plays critical roles in cell-fate determination during development. In this study, we examined the expression pattern of Sox21 in the developing and adult murine cochlea. Sox21 was expressed throughout the sensory epithelium in the early otocyst stage but became restricted to supporting cells during adulthood. Interestingly, the expression in adults was restricted to the inner phalangeal, inner border, and Deiters’ cells: all of these cells are in direct contact with hair cells. Evaluations of the auditory brainstem-response revealed that Sox21−/− mice suffered mild hearing impairments, with an increase in hair cells that miss their appropriate planar cell polarity. Taken together with the previously reported critical roles of SoxB1 families in the morphogenesis of inner ear sensory and neuronal cells, our results suggest that Sox21, a counteracting partner of the SoxB1 family, controls fine-tuned cell fate decisions. Also, the characteristic expression pattern may be useful for labelling a particular subset of supporting cells.
KeywordsInner ear Cochlea Development Sox21 Hair cell Supporting cell
We thank Ms. Ayano Mitsui and Dr. T. Nagai for their technical assistance and Dr. Junko Murata (Osaka University) for technical advices. This work was supported by grants from the Ministry of Education, Culture, Sports, Science and Technology (MEXT), the Japan Science and Technology Corporation (JST), and the Funding Program for World-leading Innovative R&D on Science and Technology to H.O., and by a Grant-in-Aid for Scientific Research B (20390444) to K.O., and by a Research on Measures for Intractable Diseases from the Ministry of Health, Labor and Welfare of Japan to M.F., and by a Keio University grant-in-aid for encouragement of young medical scientists to M.F., and by a Keio Gijuku Academic Development Funds to M.F. and by a Grant-in-Aid for Young Scientists B (22791628) to M.F. from MEXT. and by a grant-in-aid from the Global COE Program of MEXT, Japan to Keio University.