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. 2016 Dec 5;6:38253. doi: 10.1038/srep38253

Figure 2. Isl1-cre mediated Sox2 loss disrupts neuron formation and results in massive neuronal degeneration by activation of Caspase3.

Figure 2

(a,b) Immunofluorescence staining of neurofilament in the Sox2 CKO shows similar formation of vestibular neurons at E11.5 compared to controls. (a’,b’) At E13.5, fibers are aberrantly projecting toward the utricle (or combined utricle and anterior and horizontal canal cristae) and posterior canal cristae of the Sox2 CKO. (a”,b”,a”’,b”’) Fibers to the posterior canal crista start to retract in the absence of target HCs starting at E14.5 in the mutant. (b”’) Only a few radial fibers are formed near the base of the E15.5 Sox2 CKO cochlea. (c, c’,d,d’) Immunofluorescence of activated Caspase3 reveals positive staining restricted mainly in the VG in the E11.5 Sox2 CKO comparable to the control littermates. (c”,c”’,d”,d”’) However, Caspase3 mediated cell death is massively progressed to IVG, SVG, and SG at E15.5 compared to no caspase positive cells in the control littermates. Scale bars: 100 μm. AC, anterior canal crista; CD, cochlear duct; FN, facial nerve; HS, Hoechst nuclear stain; IGSB, intraganglionic spiral bundle; IVG, inferior vestibular ganglion; IN, intermediate nerve; HC, horizontal canal crista; PC, posterior canal crista; S, saccule; SG, spiral ganglion; SVG, superior vestibular ganglion; U, utricle; VG, vestibular ganglia.