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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).
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