<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>Angiogenesis is a fundamental vertebrate developmental process that requires signalling by the secreted protein vascular endothelial growth factor-A (<italic>VEGF-A</italic>). <italic>VEGF-A</italic> functions in the development of embryonic structures, during tissue remodelling and for the growth of tumour-induced vasculature. The study of the role of <italic>VEGF-A</italic> during normal development has been significantly complicated by the dominant, haplo-insufficient nature of <italic>VEGF-A</italic>-targeted mutations in mice. We have used morpholino-based targeted gene knock-down technology to generate a zebrafish <italic>VEGF-A</italic> morphant loss of function model. Zebrafish <italic>VEGF-A</italic> morphant embryos develop with an enlarged pericardium and with major blood vessel deficiencies. Morphological assessment at 2 days of development indicates a nearly complete absence of both axial and intersegmental vasculature, with no or reduced numbers of circulating red blood cells. Molecular analysis using the endothelial markers <italic>fli-1</italic> and <italic>flk-1</italic> at 1 day of development demonstrates a fundamental distinction between <italic>VEGF-A</italic> requirements for axial and intersegmental vascular structure specification. <italic>VEGF-A</italic> is not required for the initial establishment of axial vasculature patterning, whereas all development of intersegmental vasculature is dependent on <italic>VEGF-A</italic> signalling. The zebrafish thus serves as a quality model for the study of conserved vertebrate angiogenesis processes during embryonic development.</p>
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Yeast. 2000; 17(4):294-301