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Fig. 3. In vivo confirmation that Barx1 enables attenuation of Wnt signaling in prospective stomach epithelium. (A,B) lacZ staining in Barx1^-/-;TOPGAL^Tg (B) and control Barx1^+/-;TOPGAL^Tg (A) mouse fetal stomach at E16.5, when endogenous Wnt signaling is virtually abolished and there is no esophageal activity (dashed lines) in control embryos but strong signals remain in Barx1 mutants. (C,D) Histochemical confirmation of persistent ß-gal activity in rostral Barx1^-/-;TOPGAL^Tg stomach endoderm (D, arrowheads) in relation to negligible signal in corresponding Barx1^+/-;TOPGAL^Tg tissue (C). (E,F) Further confirmation by lacZ in situ hybridization of mRNA persistence in rostral E16.5 Barx1^-/-;TOPGAL stomach endoderm (F), which contrasts with the absence of expression in control E16.5 Barx1^+/+;TOPGAL tissue (E). (G-I) Persistent Wnt signaling is further revealed by nuclear localization of ß-catenin in the emerging squamous epithelium of Barx1^-/- (G, boxed area shown at higher magnification in H) but not control (I) foregut. (J,K) Similarly, ß-gal activity persists in E18.5 Barx1^-/-;Axin2^lacZ fetal stomach (K) compared with Barx1^+/-;Axin2^lacZ controls (J). Dashed and solid lines in A and J demarcate normal esophagus (Es) and duodenum (Du), respectively. St, stomach; fore, forestomach; hind, hind-stomach (the blurred boundaries between fore- and hindstomach are represented by dotted lines). Scale bars: 75 µm in C; 60 µm in D; 75 µm in E,F.

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