Morpholino knockdown of nr2f1b causes defects in vascular development. a In uninjected control embryos, the arota (da) and posterior cardinal vein (pcv) have formed by 30 hpf and intersegmental vessels (isv) have reached the DLAV at the dorsal aspect of the embryo. At the same stage ISVs are stalled mid-somite in nr2f1bi1e2 (b), nr2f1be1i1 (e) and nr2f1bATG (f) morphants. Overexpression of nr2f1b has no obvious defect in vasculature (d), but rescues the defect of ISV stalling (solid arrowhead) as shown in (c). g Quantification of percentage of completed ISV shows a 40 % increase compare to nr2f1b morphants (*** refers to p < 0.0001 by an unpaired student's t-test. Scale bars are 50 μm for (a-f). h and i Imaging of endothelial nuclei in green and vessels in red at 30 hpf in wild-type control and nr2f1b MO-treated embryos using Tg(fli1a:nEGFP)
ci5 double transgenic line. nr2f1b morphants showed reduced ISV nuclei numbers (i). j Quantification of ISV nuclei number in nr2f1b morphants (n = 18) compared to wild-type control (n = 16). ***P < 0.001, Student t test.