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Fig. 6. Ectodermal defects in
Msx2-Cre;β-Catc/c GTs.
(A-H) SEM analysis of wild-type and
Msx2-Cre;β-Catc/c GTs.
Msx2-Cre;β-Catc/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-Catc/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-Catc/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-Catc/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.
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