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Fig. 5. BMPRIA mutant embryos show cardiac outflow tract defects. (A-D) Dissections at E9.5 show mutant embryos (B,D) to have shortened outflow tract and future ventricular tissue (rv and lv indicate future right and left ventricle, respectively; broken lines indicate limit of the future right ventricle). These defects continue through E10.5 (E-H) and E11.5 (I-L) with reduced contributions of NCCs to outflow tract tissue clearly visible by E10.5 (H; black arrows highlight extent of NCC migration into outflow tract). (M-P) Frontal sections of E11.0 Wnt1-Cre;Bmpr1a^flox/null; R26R embryos (NCCs stained blue) show no occlusion of the outflow tract lumen (N) or aortic arch arteries (P, black arrowheads) but do reveal a reduction in endocardial cushion (ec) size compared with wild type (M). (Q,R) Tie2-lacZ transgene expression marks endothelial cells, highlighting the lack of outflow tract septation in mutants at E12.0: red arrowhead indicates aorta, blue arrowhead indicates pulmonary artery, purple arrowhead indicates persistent (unseptated) truncus arteriosus. (S,T) Injection of ink into E11.5 ventricles shows dispersion through aortic sac to peripheral vasculature in both control and mutant embryos. Note the hypoplastic arch arteries evident in mutants (T; iii, third aortic arch artery; iv, fourth aortic arch artery). (U,V) Frontal section through a necrotic Wnt1-Cre;Bmpr1a^flox/null embryo at E12 still reveals a blood filled, but unoccluded outflow tract. White arrows indicate lumenal edge. All paired images are shown at identical magnification.

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