Fig. 8.

The effect of Atoh1 null mutation (B, D, G) on the pattern of innervation of the posterior crista is compared with a wildtype (A, C, F) and a npn1-^sema3a- mutant (E) as revealed with lipophilic tracers (A–F) and acetylated tubulin immunocytochemistry (G). The initial growth toward the posterior crista is unaffected in E11.5 embryos (A, B). However, afferent fibers continue to branch outside the sensory epithelium in both Atoh1 null and npn1-^sema3a- mutant embryos (D, E) whereas fibers have entered and branch inside the sensory epithelium in wildtype littermates (C). By E13.5 afferents have entered the epithelium and branched to reach the Bdnf positive undifferentiated hair cells of the Atoh1 null mutant. This branching is more profuse in wildtype animals and the fibers have split into two areas, each supplying the Bdnf positive hair cells of the hemichristae (F). These data suggest that Atoh1 absence interferes with homing of afferent fibers near the target sensory epithelium. Bar indicates 100 μm.