Fig. 5. Ctnnb1^scon mice harbor a functional conditional allele that functions in vivo.

a Small intestinal organoids from WT (Ctnnb1^+/+) and HOM (Vil-CreER^T2; Ctnnb1^scon/scon) mice treated with either 4-OH-tamoxifen (4-OHT) or vehicle for 8 h. Organoids were fixed on Day 4 and stained for β-catenin (gray), phalloidin (green) and DAPI (cyan). Scale bar, 100 μm. Homozygous (Vil-CreER^T2; Ctnnb1^scon/scon) intestines are healthy, with a normal epithelial crypt-villus morphology (b), β-catenin on the cell membrane (b′), and Ki67 marking proliferating cells in the crypts (b″). Heterozygous (Vil-CreER^T2; Ctnnb1^+/scon) intestines show no changes in morphology (c, e), β-catenin (c′, e) or Ki67 (c″, e″) after tamoxifen treatment. In homozygous intestines, tamoxifen treatment leads to the loss of crypts (d), β-catenin staining (d′), and Ki67 staining (d″) on Day 3. On Day 5, the epithelium is completely lost (f–f″). H&E, hematoxylin and eosin. Scale bar, 50 μm. g–j smRNA-FISH of intestinal sections with DAPI (blue), Olfm4 (red), and Wnt3 (white). g, h uninduced intestinal sections of HET (g) and HOM (h) mice; i, j Day 3 after induction with 3 mg tamoxifen per 20 g body weight of HET (i) and HOM (j) mice. Scale bar, 10 μm.