Temporal failure of vasculogenesis in VE-cadherin null embryos. (A,D) High-magnification images of PECAM-immunolabeled allantoides from normal (A) and VE-cadherin null (D) 8.5-dpc embryos. Note that the extent of vascularization is greatly reduced in the VE-cadherin nulls as compared to controls. Arrows in panel D point to discontinuous PECAM⁺ vessels not apparent in the vascular network of normal allantois explants. (B,E) PECAM-immunolabeled endocardial cells from normal (B) and VE-cadherin null (E) 8.5-dpc embryos. Note the aggregates of PECAM⁺ cells in the hearts of the VE-cadherin nulls as compared to the continuous layer of PECAM⁺ cells that comprise the endocardial tube of the normal heart. (C,F) PECAM-immunolabeled dorsal aortae from normal (C) and VE-cadherin null (F) 8.5-dpc embryos. (G,I) PECAM-immunolabeled 9.5-dpc VE-cadherin wild-type (G) and null (I) embryos. Pronounced abnormalities of the dorsal aortae (da), intersomitic vessels (iv), and cranial vessels (cv) are apparent in the 9.5-dpc VE-cadherin null embryo as compared to the normal 9.5-dpc embryo. (H,J) PECAM-immunolabeled yolk sacs of 9.5-dpc VE-cadherin wild-type (H) and null (J) embryos. The VE-cadherin wild-type yolk sac contains large PECAM⁺ blood vessels and continuous networks of smaller vessels, whereas the yolk sac of the null contains only clusters of PECAM⁺ cells. Panels A through J are confocal images. Bars equal 100 μm.