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. Author manuscript; available in PMC: 2006 Nov 1.
Published in final edited form as: Dev Dyn. 2005 Nov;234(3):633–650. doi: 10.1002/dvdy.20551

Fig. 4.

Fig. 4

The earliest expression of Atoh1 as revealed by different techniques (A, B, D–E) in wildtype and Neurog1 null mice (C) is compared. At E13.5, Atoh1-eGFP shows a profound signal in the vestibular sensory epithelia and in some delaminating cells (arrows in A). However, there is no detectable Atoh1-eGFP signal in the cochlea. In contrast, in situ hybridization (B) and Atoh1-LacZ (E) show Atoh1 expression in the basal turn of E13 and E13.5 animals (B, F). Comparison of Atoh1-LacZ (F) and Atoh1-Cre/Rosa26 (D) shows that more cells are Atoh1 positive in the vestibular sensory epithelia of Atoh1-LacZ animals at an earlier stage (F). In contrast, Atoh1-Cre shows additional expression in delaminating spiral ganglion neurons (Spgl) near the base and vestibular ganglion neurons (Vgl) near the utricle and saccule (D). Of all the techniques employed here, only Atoh1-eGFP shows some of these delaminating cells as well (compare A, D). Atoh1 in situ hybridization in Neurog1 null mutants shows a more apical expression in the E13 cochlea (C). This expression suggests a differential upregulation in the upper middle turn of the cochlea instead of the basal turn as in wildtype littermates (B, C). Note the small size of vestibular sensory epithelia (compare B and C) in Neurog1 mutants. AC, anterior crista; HC, horizontal crista; PC, posterior crista; S, saccule, Spgl, spiral ganglion; U, utricle; Vgl, vestibular ganglion. Bar indicates 100 um.

HHS Vulnerability Disclosure