Fig. 5. Defects in endocardial cushion and valve formation in Foxp1^–/– hearts. H+E staining of embryonic sections of wild-type (A,C) and Foxp1^–/– (B,D) were performed to characterize defects in endocardial cushion and valve development at E14.5. By E14.5, endocardial cushion mesenchyme in wild-type heart valves has already begun to regress to form the mature pulmonary (A) and atrial-ventricular heart valves (C). In Foxp1^–/– hearts, the cushion mesenchyme has not regressed as far and the cushions appear as large bulges (B,D, arrows). At E11.5, TUNEL assays reveal decreased levels of apoptosis in the outflow tract endocardial cushion mesenchyme in Foxp1^–/– hearts (E) relative to wild type (F). At E11.5, cell proliferation as determined by phospho-histone H3 immunostaining is unchanged in Foxp1 outflow tract cushions (G,H). Nfatc1 expression (J,L, arrowheads) in Foxp1^–/– hearts persists in the endocardial cushion mesenchyme in both pulmonary (J) and mitral cushions (L) compared with wild-type pulmonary (I) and mitral (K) cushions at E14.5. Quantification of both TUNEL-positive cells (M) and phosphohistone H3-positive cells (N) for data shown in E-H. E,G and F,H are adjacent histological sections. Scale bars: 400 µm in A-D; 200 µm in E-L.