Proliferation of arterial ECs is decreased in DT embryos. (A) BrdU incorporation studies show 16% of ECs per aortic cross-section of DT embryo are proliferating, compared with 28% in WT embryos (P < .01). Number of ECs per aortic cross-section is increased in DT embryos. (B) In WT embryos there are on average 8.5 ECs per aortic cross-section, in DT embryos there are 11.5 ECs, representing a 35% increase (P < .01). Apoptosis of arterial ECs is increased in DT embryos. (C) In WT embryos, on average, 2.6% of arterial ECs are apoptotic, in DT embryos, on average, that frequency is 4.7%, representing a 80% increase in arterial endothelial apoptosis frequency (P < .01). Endothelial cell migration is delayed in DT embryos. Wholemount PECAM1 immunostaining of E8.5 and E9.5 WT and DT embryos. (D) WT embryo at E8.5. (E) DT embryo at E8.5 showing a delay in the migration of ECs from the DA to form the intersomitic blood vessels, relative to control embryo (D). (F) WT embryo at E8.5. (G) DT embryo at E9.5 showing a continued delay in the migration of ECs from the DA to form the intersomitic blood vessels, relative to control embryo (F). Angiogenic sprouting is reduced in DT embryos (H) Cephalic region of WT embryo at E9.5. (I) DT embryo at E9.5 showing a lowered number of new blood vessel sprouts in cephalic region, relative to control embryo.