Figure 1. Induced Fgfr1op deletion disrupts intestinal crypts.

(A) In situ hybridization of small intestinal tissues with a probe for Fgfr1op mRNA. Tissues are counterstained with anti-Epcam to visualize the intestinal epithelium. The image is representative of 6 mice examined. Scale bar 50 μm.

(B) Representative confocal images of FGFR1OP expression in the crypt and villus. Sections were counterstained with anti-α-tubulin. Red arrows, FGFR1OP expression in the apical side of epithelial cells in crypts and villi; white arrows, FGFR1OP staining in the microtubule-organizing center in dividing cells. Images are representative of 6 mice examined. Scale bar 10 μm.

(C-E) Schematic of the experimental time course: Cre was induced by intraperitoneal (i.p.) injection of TAM for 5 consecutive days prior to analysis on days 6, 9, and 12 post Cre induction (C). Weight loss (n=10 mice, mean±SD, Multiple Mann-Whitney test with Holm-Šídák correction; ****P<0.0001, **P<0.01) (D) and survival (E) upon TAM-induced Fgfr1op deletion [Log-rank (Mantel-Cox) test]; data is representative of two independent experiments.

(F-G) H&E images of small intestine on days 6, 9, and 12 post Cre induction (F). Images are representative of 3 independent experiments; Scale bar 100 μm. Crypt numbers in duodenum, jejunum, and ileum (n=4–9 mice per genotype and time point; mean±SD, one-way ANOVA with Tukey’s correction; *P<0.05, **P<0.01, ****P<0.0001) (G). Due to the disappearance of well-oriented crypts as part of the Fgfr1op^cKO phenotype, all crypts in the vision field were counted regardless of their appearance and size in both, Fgfr1op^cKO and control mice.