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. Author manuscript; available in PMC: 2013 Jan 16.
Published in final edited form as: Angiogenesis. 2008 Sep 17;11(4):347–360. doi: 10.1007/s10456-008-9116-2

Fig. 6.

Fig. 6

Wnt5-deficient (ppt) zebrafish display aberrant angiogenesis in vivo. a–b Tg(fli:EGFP) expression (28–30 hpf) as detected by whole mount. An in situ Fli probe shows ordered intersegmental vessel (IS) development in wt-like embryos (a, arrow) as well as proper development of the dorsal aorta (DA), and posterior cardinal vein (PCV) (arrowhead). b Similarly staged ppt mutants display disrupted angiogenesis with defective IS vessel formation (arrow) and reduced DA/PCV expression (arrowhead). c–d Fli-GFP expression in vivo. WT (c) and ppt (d) expression of Fli-GFP. Loss of Wnt5 results in disruption of the Duct of Cuvier/CCV. (e–f) Live in vivo Fli-GFP images of 48 hpf embryos. Irregular vessel formation is seen in ppt relative to WT control. g–h Whole mount staining of WT and ppt embryo head regions. g Robust vasculature can be observed in the anterior and middle cerebral veins within WT embryos. These vessels are diminished and aberrantly patterned within ppt embryos (h)