Fig. 6. Loss of Hh signaling does not result in a general disruption of neural crest development. smu embryos (B,D) and wild-type (WT) siblings (A,C) were probed with crestin to examine migratory neural crest. In smu embryos (B,D), levels of crestin expression are comparable to WT and neural crest do migrate ventrally. However, neural crest cells in smu embryos do not appear to be restricted to the mid-point of the somite (D). In contrast, WT embryos treated with 6 µg/ml cyclopamine beginning at 18 hpf and fixed at 36 hpf show no obvious defects in migration (F) compared with untreated siblings (E). Despite normal patterning and migration, DRG phenotypes in embryos cyclopamine-treated at 18 hpf (G) are similar to the severe disruption of Hh signaling in mutants (Fig. 4).

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