Fig. 1.

Fig. 1. foxd1 expression is reduced in rx3^−/− mutant optic vesicles and lost in rx3^−/− upon combined abrogation of Shh and Fgf. (A-U) Frontal sections at the level of the forming telencephalon, optic vesicles and hypothalamus, with dorsal upwards; genotype, stage and/or treatment are indicated in the top right corner and the genes analysed are indicated in the bottom left corner. (A-D) Expression of rx3 (A) and nkx2.1 (B) in 4 ss wild-type/rx3^−/− embryos (indistinguishable at this stage with a representative embryo shown) and emx3 in 10 ss wild-type (C) and rx3^−/− (D) embryos, highlighting the prospective telencephalic (t), hypothalamic (hy) and eye-forming (ov) domains. (E-H,J-M) Expression of foxg1 (E-H) and foxd1 (J-M) in 4 ss (E,G,J,L) and 10 ss (F,H,K,M) embryos. (I) Double in situ hybridisation of foxd1 or foxg1 and nkx2.1 (red) to show the relationship between optic vesicles and the hypothalamus. (N-U) 10 ss stage embryos showing expression of foxg1 (N-Q) or foxd1 (R-U) in embryos treated with DMSO (N,P,R,T) or cyclopamine+SU5402 (O,Q,S,U). (V) Schematic representation of the conditions in R-U. Thirty to 50 embryos were treated and processed together per experiment and marker. rx3^−/− embryos were recovered at the expected mendelian proportions and the phenotypes observed were fully penetrant. Scale bars: 100 µm. Dashed lines indicate the contour of the optic vesicles. dhy, dorsal hypothalamus; hy, hypothalamus; ov, optic vesicles; t, telencephalon.