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Fig. 7. Loss of Gli3 does not rescue the Fgfr1^-/-;Fgfr2^-/- phenotype. (A-D) E12.5 whole embryos. Development of the telencephalon is severely compromised in the Fgfr1^-/-;Fgfr2^-/-;Gli3^-/- mutant (D) compared with the other genotypes (A-C). t, telencephalon; d, diencephalon. (E-U) RNA in situ hybridization analysis of E12.5 coronal brain sections. In the Fgfr1^-/-;Fgfr2^-/-;Gli3+/- mutant, as in the Fgfr1^-/-;Fgfr2^-/- mutant, Pax6 and Emx2 expression extends to the ventromedial area of the telencephalon at the expense of ventral markers such as Dlx2 (E-M). The remaining expression of Dlx2 in both mutants (L,M) is likely to be hypothalamic rather than telencephalic as it coincides with areas with decreased or absent Foxg1 expression in neighbouring sections (not shown). In the Fgfr1^-/-;Fgfr2^-/-;Gli3^-/- mutant, Foxg1-positive areas express Pax6 but not Dlx2 (N-P). Wnt3a expression in the cortical hem appears normal for all genotypes except Fgfr1^-/-;Fgfr2^-/-;Gli3^-/- (Q-U). Broken lines indicate the Foxg1-positive telencephalic area in an exencephalic mutant (T,U). Scale bar: 0.5 mm in E-U.

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