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Fig. 2 tgfbr3-null mutant embryos do not exhibit angiogenic defects. A, WT (tgfbr3 +/+) and null ∆7 mutant (tgfbr3 ∆7/∆7) embryos, in the fli1:EGFP background, from 48 hpf embryos were immunoflorescently stained for Tgfbr3. Confocal images of these specimen revealed no IVS (intersegmental vessels) migration defects in null embryos. B, Aorta and ISV diameter measurements showed no difference between WT and ∆7 embryos at 48 hpf embryos. Two-tailed Student's t-test was performed, and P values are shown. C, Confocal images of WT and ∆7 adult heart ventricles (V) showed normal distribution of coronary vessels. The identity of these specimens was verified by genotyping as described in Figure 1. D, Using embryos obtained from homozygous crosses of WT (tgfbr3 +/+) or null ∆7 mutant (tgfbr3 ∆7/∆7) fishes, were subjected to knock down experiments with 7 ng of the splicing blocking morpholino (Mo-BG02) or the mismatched control morpholino. Embryos were injected at 1 cell stage and their malformations was analyzed and scored at 48 hpf. Mutant embryos did not show resistance to morpholino effects. E, WT and ∆7 at single cell-stage embryos (in a fli1:EGFP background) were microinjected with 2 ng of Mo-BG02 or control morpholino; subtle vascular defects in the formation of the parachordal lymphatic endothelial cells (LEC) were observed in both WT and ∆7 embryos injected with Mo-BG02, Scale bar: 200 μm