Fig. 5. Effect of FGF2 treatment and electroporation of activated and dominant negative cdx variants on Hoxb9 expression. Dorsal views of stage 15 embryos hybridized with Hoxb9 following treatment with FGF2 and/or electroporation of Xcad constructs. D,E,F shows higher magnification of A,B,C, respectively. (A,D) An embryo treated overnight with FGF2 as a control of the effect of FGF. (B,E) Electroporation of an activated form of Xcad (XcadVP16) unilaterally in the left side of the neural tube induces an anterior expansion of Hoxb9 expression (bracket in B and arrowheads in E). (C,F) An embryo electroporated with a dominant negative form of Xcad (XcadEnR) unilaterally on the left side of the neural tube and cultured for overnight in the presence of FGF2 shows that the FGF mediated induction of Hoxb9 is reduced. Note that the anterior boundary of Hoxb9 expression on the right side (non-electroporated side) is just posterior to the otic vesicle (OV) because of the FGF treatment. The bracket in C and white arrowheads in F mark the zone where the ectopic expression of Hoxb9 caused by FGF treatment is down-regulated by electroporation of the XcadEnR construct.