ZFIN Image: Rodriguez et al., 2008, Fig. 3

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Figure Caption

Fig. 3 Dep1a-MO induced blood circulation defects, but vasculogenesis appeared normal. O-dianisidine staining of hemoglobin was done on wild type (A) and Dep1a-MO1 (B) injected embryos at 48 hpf. The arrow indicates hemorrhages at the aortic bifurcation and the asterisk blood accumulation around the posterior cardinal vein. Fli1a::egfp1 transgenic zebrafish embryos were injected with Dep1a-MO1 (D) or Dep1a-MO2 (E) at the 1-cell stage and the vasculature was visualized at 30 hpf. A non-injected fli1a::gfp1 embryo served as a control (C). Microangiography was done by injection of rhodamine-conjugated dextran into the heart of embryos. Circulation of the dye was visualized using a fluorescence microscope. Non-injected control (F), Dep1a-MO1 injected (G) and Dep1a-MO2-injected embryos (H) all at 48 hpf are depicted here. (J–K) Magnifications of the area where circulation is blocked (arrow).

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Acknowledgments

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Reprinted from Developmental Biology, 324(1), Rodriguez, F., Vacaru, A., Overvoorde, J., and den Hertog, J., The receptor protein-tyrosine phosphatase, Dep1, acts in arterial/venous cell fate decisions in zebrafish development, 122-130, Copyright (2008) with permission from Elsevier. Full text @ Dev. Biol.