Fig. 6. Ectodermal defects in Msx2-Cre;β-Cat^c/c GTs. (A-H) SEM analysis of wild-type and Msx2-Cre;β-Cat^c/c GTs. Msx2-Cre;β-Cat^c/c GTs show absence of an urethral seam (arrowheads, A) at E12.5 (B), an ectopic opening in proximal GT at E13.5 (arrowheads, D), and a distal bifurcation at E14.5 (arrowhead, F). (I-P) Tissue lineage analysis revealed an ectodermal rupture in Msx2-cre;β-Cat^c/c GTs. The development of the ectodermal surface epithelium marked by Msx2-Cre;R26R was examined by X-Gal staining. β-Gal-positive ectodermal cells (blue) cover the entire GT surface throughout early development (I,K,M,O). By contrast, the mutant surface epithelium breaks down at the midline (arrowheads, J) and the disruption continues to expand (L,N). At E16.5, the ventral side of the GT is completely devoid of β-Gal-positive ectodermal epithelium (P). (Q,R) Shh in situ hybridization showing that Shh-expressing UE is covered by ventral ectoderm in wild-type GT (arrowheads, Q), but is exposed and expanded on the GT surface in Msx2-Cre;β-Cat^c/c GTs at E12.5 (arrowheads, R). The planes of section are indicated in I,J. (S,T) H&E staining showing an ectopic opening in the proximal region of Msx2-Cre;β-Cat^c/c GTs (T). (U,V) X-Gal staining showing that exposed epithelium in the mutant GT is Msx2-Cre negative. (W,X) Shh in situ hybridization showing that the exposed epithelium (arrowheads, X) expresses Shh. The planes of section in S-X are indicated in K and L. Scale bars: 100 µm in Q-X.