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Figure 6


Fig. 6. SHH signalling is insufficient to generate ventral precursors in the Fgfr1-/-;Fgfr2-/- mutant. (A) Whole-mount RNA in situ hybridization analysis of E10.5 control and Fgfr1-/-;Fgfr2-/- mutant embryos indicates that Shh remains expressed in the mutant in the ventral mesendoderm underlying the telencephalon (arrowheads). (B,C) RNA in situ hybridization analysis of serial E10 coronal sections through the anterior prosencephalon. In telencephalic areas expressing Foxg1 (B), expression of Gli1, which requires SHH activity, is localised to the ventral areas of the mutant (C, arrows).





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