Phenotypic characterization of mutants after early cardiomyocyte-restricted Gata4 deletion. (A) Survival of mutant embryos after myocyte-restricted deletion of Gata4. Numbers indicate total number of embryos genotyped at each gestational age. Expected Mendelian incidence was 25%. (B and C) Unstained whole-mount control and G4^NK embryos at E10.5, showing pericardial effusion (white arrows) of the mutant embryo. (D–I) Control and mutant hearts, viewed from the left lateral (D–F) and right anterior oblique (G–I) positions. In control (G) and in 6 of 21 mutant (H) embryos systematically examined, the RV and OFT (arrows) connected normally to the right lateral aspect of the LV. In the remaining 15 of 21 mutant embryos, the RV was very hypoplastic or not apparent, and the OFT connected to the rostral aspect of the LV (I). The groove at the atrioventricular junction (arrowhead) was preserved in mutant embryos. (J–P). H&GE-stained transverse sections at the level of the atrioventricular canal (J and K) and the OFT (N–P). (L and M) Higher-magnification views of boxed regions in J and K, respectively. Mutant embryos had severe myocardial hypoplasia with reduced trabeculation. Arrowheads indicate the endocardial cushions, which were small and markedly hypocellular in mutant embryos (K and O) compared with those of controls (J and N). In some mutant embryos, the RV and OFT were thin walled but normally positioned (O), while in other mutant embryos the RV was not apparent, and the OFT arose in an abnormal position from the ventricular chamber (P). Embryos in D–P had 31–32 somites. Original magnification, ×20 (B and C), ×60 (D–I). Scale bars: 100 μm (J–P).