ZFIN ID: ZDB-FIG-070314-18
Leslie et al., 2007 - Endothelial signalling by the Notch ligand Delta-like 4 restricts angiogenesis. Development (Cambridge, England)   134(5):839-844 Full text @ Development
ADDITIONAL FIGURES
PHENOTYPE:
Fish:
Condition:
Knockdown Reagents:
Observed In:
Stage Range: Prim-15 to Protruding-mouth

Fig. 3 Effects of Dll4 knockdown on endothelial cell behaviour. (A) Schematic depiction of ISV and DLAV formation and the concomitant changes in endothelial cell morphology. (B,C) Leading cell of an ISV sprout at 30 hpf in a living uninjected embryo (B) or in a living embryo injected with 10 ng MO[Dll4] (C). (D,E) DLAV and dorsal ISVs at 2.5 dpf in a living uninjected embryo (D) or in a living embryo injected with 10 ng MO[Dll4] (E). (F-I) Similar region at 2.5 dpf of living embryos treated with 100 μm DAPT (G,I) or control embryos treated with DMSO (F,H). Treatment with DMSO or DAPT began at either 33 hpf (F,G) or at 48 hpf (H,I) and continued through the course of the experiment. Higher magnifications of D-I are shown in D'-I'. (J) DLAV and ISVs of a 3-dpf embryo injected with 7 ng of a morpholino targeted against Notch1b. (K,L) ISV sprouts at 30 hpf of a normal sibling (K) and a hsp70:Gal4;UAS:NICD embryo (L). Embryos in K and L were given a heat shock at 24 hpf. S, somite. Scale bar: 50 μm in B-I; 17 μm in D'-I'; 40 μm in J; 70 μm in K,L.

Gene Expression Details No data available
Antibody Labeling Details No data available
Phenotype Details
Fish Conditions Stage Phenotype
kca3Tg; kca4Tg heat shock Prim-15 blood vessel endothelial cell migration disrupted, abnormal
Prim-15 intersegmental vessel decreased length, abnormal
y1Tg + MO2-notch1b standard conditions Prim-15 blood vessel morphogenesis disrupted, abnormal
Protruding-mouth intersegmental vessel morphology, abnormal
Protruding-mouth regulation of blood vessel endothelial cell migration disrupted, abnormal
y1Tg + MO3-dll4 standard conditions Prim-15 intersegmental vessel morphology, abnormal
Prim-15 regulation of blood vessel endothelial cell migration disrupted, abnormal
Acknowledgments:
ZFIN wishes to thank the journal Development (Cambridge, England) for permission to reproduce figures from this article. Please note that this material may be protected by copyright. Full text @ Development