Fig. 1.

Establishing a system to trace the fate of wild-type and β-catenin-deficient acinar cells. Control (Ctnnb1^lox/+; R26R^EYFP/+; ElaCreERT) and acinar-specific β-catenin knockout (ABKO: Ctnnb1^Δ/lox; R26R^EYFP/+; ElaCreERT) mice received tamoxifen at 2 months of age and were analyzed 10 days later by immunofluorescence on frozen sections. (A,B) EYFP (green) is widely expressed in amylase+ acinar cells (red), indicating successful recombination. Scale bar: 100 μm. (C) Overall EYFP labeling of acinar cells does not differ between genotypes, 10 days post-tamoxifen (n=2 mice per genotype; P=0.48). (D–G) In controls, β-catenin localizes normally to the cell membrane of EYFP+ acinar cells, whereas, in ABKO pancreata, EYFP marks cells that have lost β-catenin expression. (H–K) E-cadherin exhibits identical membrane localization in EYFP+ acinar cells of control and ABKO mice, suggesting that loss of β-catenin does not perturb cell-cell adhesion. (L–O) Expression and apical localization of amylase is identical in control and β-catenin-deficient cells, indicating that loss of β-catenin does not affect acinar polarity or differentiation state.