Fig. 7. FGF signalling is required for forebrain patterning during gastrulation and somitogenesis stages. Dorsal (A,D,E,H) or lateral (B,C,F,G,IT) views of whole-mounted control embryos (A-D,I,M,Q), or embryos treated with SU5402 (E-H,J-L,N-P,R-T) during the developmental periods indicated. (A-H) Sister embryos taken from each batch immediately following treatment with either DMSO (A-D) or SU5402 (E-H), and analysed for expression of erm, an FGF-responsive gene, to test the effectiveness of inhibition. Forebrain erm expression is efficiently blocked by SU5402 following treatment from 80% to tailbud stage (A,E), tailbud to 8s (B,F) and 13s to 18s (C,D,G,H). After treatment, remaining embryos were allowed to develop to 24 hpf (I-L) or 30 hpf (M-T). Control embryos express eom in the pallial telencephalon (I). SU5402 treatment from 50% epiboly to tailbud stage eliminates eom expression (J), whereas treatment from 80% epiboly to tailbud results in expansion of eom expression into the subpallial telencephalon (K; compare arrowheads in I and K). SU5402 treatment during somite stages does not alter the eom expression boundary (arrowhead; L). nk2.1b expression in the telencephalon and diencephalon at 30 hpf in a control emrbyo (M). SU5402 treatment from 80% epiboly to tailbud stage (N), or from tailbud to 8s (O), completely blocks expression of nk2.1b in the telencephalon and reduces expression in the ventral thalamus, whereas hypothalamic expression is less affected. Treatment from 13s to 18s results in reduced nk2.1b expression in the telencephalon and ventral thalamus but does not affect hypothalamic expression (P). isl1 expression in the forebrain at 30 hpf in a control embryo (Q). Although isl1 expression in the dorsal diencephalon is expanded, all other sites of expression are reduced or eliminated following SU5402 treatment from 80% epiboly to tailbud (R), or tailbud to 8s (S). There is little effect on isl1 expression following treatment from 13s to 18s (T). fb, forebrain; hb, hindbrain.

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