Fig. 3. Schematic representation of the morphogenesis, the phenotypes, and the transcriptional regulatory mechanisms for FoxG1 expression of during mouse inner ear development.
(A) Morphogenesis of the mouse inner ear during early development. The labyrinth develops from a simple otic vesicle. Between embryonic day 10.5 (E10.5) and E13.5, the major structure of the inner ear develops its shape, whereas cell specification and differentiation continue for a longer time. OV, otic vesicle; ES, endolymphatic sac; ED, endolymphatic duct; ASC, anterior semicircular canal; PSC, posterior semicircular canal; LSC, lateral semicircular canal; SM, saccular macula; OC, organ of Corti; SC, semicircular canal. (B) Schematic representation of the phenotypes that result in gene knockout. In FoxG1-/-, a reduction in the size of the cochlear duct is shown. Lack of Pax2 leads to complete loss of the cochlear duct. Additionally, a reduction of the cochlear duct and abnormal morphology of the semicircular canal was observed in Gata3 knockout mice. (C) Cis-regulation of FoxG1 expression during otic vesicle development. Binding of SIX3 in the promoter region results in transcriptional activation of FoxG1, whereas the mir-9/124 represses FoxG1 expression by binding to 3'-UTR of FoxG1. The otic vesicle-specific expression of FoxG1 is regulated by SOXE (SOX8/9/10) via E2 enhancer.
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