Fig. 6. Embryos lacking BMPRIA in NCCs show defective ventricular myocardium by the 45-50 somite stage. Transverse sections of ventricles from embryos at E11.0 [36-40 somites (A-D)] and E11.5 [45-50 somites (E-H)]. The lower row shows higher magnification images from the sections immediately above. (B,D,F,H) Mutant Wnt1-Cre;Bmpr1a^flox/null embryos; (A,C,E,G) wild-type (control) littermates. (A-D) Histological analysis of ventricular tissue revealed no mutant phenotype at E11.0, with mutant hearts (B,D) having similar degrees of compact myocardium (cm) as control hearts (A,C). (E-H) Control hearts at E11.5 (E,G) have robust compact myocardium as well as trabeculated myocardium occupying much of the ventricular chamber. Mutant hearts (F,H) have reduced compact and trabeculated myocardium, observable prior to global necrosis (inset in F shows the embryo from which heart was taken; embryo appears healthy). (I) Proliferation rates were measured by counting cells stained for anti-phosphohistone H3 (pHH3+) as a percentage of the total at E10.5. A significant reduction (asterisks; P<0.015) was seen in mutant embryos. Scale bars: 250 µm for A,B,E,F; 32 µm for C,D,G,H.