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Fig. 5. BMP- and Wnt-signaling were unaffected by Ndst1 inactivation. (A) Detection of BMP signaling by Smad1-P immunohistochemistry. Smad1-P was observed in E9.5 wild-type nasal mesenchyme (arrow) and branchial arches (arrowhead), but not in Bmp4-mutant embryos. (B) Smad1-P and Smad2-P expressions were not affected in Ndst1-mutant lenses. In both wild-type and mutant embryos, Smad1-P and Smad2-P was expressed at similar levels in the lens. The same section used for Smad1-P staining was also probed with Pax6 and Pax2 antibodies to visualize the lens vesicle. Arrows indicate lens placode; arrowheads indicate lens vesicle. (C) Lack of genetic interaction between Bmp4 and Ndst1. Addition of the Bmp4^LacZ allele did not affect the lens phenotype in Ndst1-mutant eyes (upper panels). Furthermore, Bmp4 expression, as indicated by a knock-in LacZ reporter, was unchanged in the Ndst1 mutant (lower panels). (D) Canonical Wnt signaling indicated by TOPGAL reporter activity was not perturbed by Ndst1 inactivation during lens development. KO/KO, homozygous Ndst1-knockout embryos.

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