Fig. 7.

Phenotypic comparison of radil-b single and of rasip1/radil-b double mutants suggests partially overlapping functions during vascular morphogenesis. (A) Immunofluorescence analysis of ZO-1 and VE-cadherin distribution in Tg(kdrl:EGFP)^s843 at 32 hpf. The graph shows the percentage of DLAVs exhibiting a clear ring at 32 hpf. Number of embryos and junctions analyzed at 32 hpf: WT (5, 15), rasip1^ubs28 (3, 11), radil-b^sa20161 (3, 6) and double mutant (2, 3). (B) Live images at 48 hpf using Tg(ve-cad:ve-cadVENUS); Tg(fliep:gal4ff)^ubs3; (UAS:mRFP) reporter lines. Scale bars: 20 µm. (C) Quantification of blood flow defects in ISVs at 48, 72 and 120 hpf in rasip1^ubs28, radil-b^sa20161 and in double mutants. radil-b^sa20161 mutants show only transient defects in blood flow at 48 hpf. rasip1^ubs28; radil-b^sa20161 double mutants show a strongly enhanced phenotype. Number of embryos and ISVs analyzed at 48, 72 and 120 hpf, respectively: WT (4, 44; 5, 71; 6, 87), rasip1^ubs28 (12, 176; 8, 119; 10, 118), radil-b^sa20161 (9, 105; 8, 78; 5, 41) and double mutant (5, 56; 10, 102; 6, 55). Analyzed by unpaired two-tailed Mann–Whitney test (A,C) (NS, no significance; *P<0.1, **P<0.01, ***P<0.001, ****P<0.0001); error bars indicate s.d.