Fig. 7. Shh cannot rescue the normal adenohypophysis of fgf3 mutants, but can induce ectopic adenohypophyseal cell specification in an Fgf-dependent manner. All panels show embryos injected with shh mRNA at the 1-cell stage, frontal views on heads. Probes used for in-situ hybridizations are indicated in the lower right corners, ages of embryos, and genotype or further treatment in the upper right corners. (A,C) Wild-type controls; the regular pomc or prl expression domains are indicated by arrows. (B) fgf3 mutant, displaying pomc-positive cells in ectopic positions, whereas the regular region of the adenohypophyseal anlage remains pomc-negative embryo. (D) Moderately affected embryo treated with 12 µM SU54302 from 15-32 hpf, displaying a partial loss of both endogenous and ectopic prl-positive cells. The effect on ectopic prl expression was weaker after SU5402 treatment from 18-22 hpf (data not shown), suggesting that Fgf signaling promoting adenohypophyseal specification in ectopic positions occurs over a longer time period than that by Fgf3 from the infundibular region required for the regular adenohypophysis (compare with Fig. 6E-H).