Fig. 4.

Morphogenetic consequences of Ezrin loss in the adult intestine. (A–C) Altered shape of Ez^−/− epithelial cells. (A and B) β-Catenin staining in colonic epithelia from tamoxifen-treated Ez^lox/lox (control, A) and Vil-Cre-ER^T2;Ez^lox/lox (Ez^−/−, B) mice reveals expanded apical surfaces of control cells as they transition from the crypt to the colonic surface (A) in contrast to the nearly uniformly narrow Ez^−/− cells (B). An asterisk marks the apical surfaces that compose this transition and provides an example of the quantitation shown in C. (A and B) 600× magnification. (C) The number of apical surfaces per transition in control (C) (4.0 ± 0.6) and Ez^−/− (7.6 ± 1.3) mice were determined using two mice of each genotype (P < 0.0001). (D–F) Decreased extrusion of apoptotic cells in Ez^−/− epithelia. Cleaved caspase-3 staining of control (E) and Ez^−/− (F) epithelia reveals a sixfold increase in positive cells at the colonic surface in the absence of Ezrin (control, 0.64% ± 0.25; Ez^−/−, 3.8% ± 0.28; P < 0.01). A minimum of 1,000 epithelial cells per colon were counted using two mice of each genotype. (G and H) SEM across the luminal surface of the colon. Apical defects result in a rough, nonuniform appearance of the Ez^−/− colon (H) compared with the smooth, uniform surface of the control (G). (G and H) 130× magnification. (I and J) SEM across the luminal surface of the small intestinal epithelium from control (I) and Ez^−/− (J) mice. Single-villus units cover the control small intestine, whereas Ez^−/− intestines contain villus structures composed of two or more individual villi fused together. (I and J) 250× magnification.