Fig. 1

Loss of Ets1 function exacerbates vascular defects in etv2−/−embryos. (A-H′) Confocal images of Tg(kdrl:GFP) expression in wt, ets1−/−, etv2−/−and ets1−/−; etv2−/−embryos at 34 hpf and 60 hpf using 4× and 10× objectives. ets1−/−embryos display normal vascular patterning (B-B′, F-F′), similar to wild type embryos (A-A′,E-E′). ISVs begin to emerge in etv2−/−embryos at ~34 hpf (C′) but are absent in ets1−/−; etv2−/− double mutant embryos (D′). At 60 hpf, ets1−/−; etv2−/−embryos have fewer ISVs and less recovery in axial vasculature than etv2−/− embryos (G-H′). (I–J) Quantitative analysis of total number of ISVs and ISV height at 60 hpf. Note the reduction in number of ISVs (I) and full sprouts (J) in ets1−/−; etv2−/−compared to etv2−/−embryos. ∗P ​< ​0.05, ∗∗P ​< ​0.01; n.s – not significant. Horizontal bars within violin plots represent median. Arrowheads indicate mis-patterned and stunted ISVs.