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First published online 26 October 2005
doi: 10.1242/dev.02087
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1 Department of Biochemistry and Biophysics and Cardiovascular Research
Institute, Programs in Developmental Biology, Genetics, and Human Genetics,
University of California San Francisco, 1550 Fourth street, San Francisco, CA
94143, USA
2 Department of Molecular, Cellular, and Developmental Biology, University of
California Los Angeles, Los Angeles, CA 90095, USA
Author for correspondence (e-mail:
didier_stainier{at}biochem.ucsf.edu)
Accepted 14 September 2005
Tube and lumen formation are essential steps in forming a functional vasculature. Despite their significance, our understanding of these processes remains limited, especially at the cellular and molecular levels. In this study, we analyze mechanisms of angioblast coalescence in the zebrafish embryonic midline and subsequent vascular tube formation. To facilitate these studies, we generated a transgenic line where EGFP expression is controlled by the zebrafish flk1 promoter. We find that angioblasts migrate as individual cells to form a vascular cord at the midline. This transient structure is stabilized by endothelial cell-cell junctions, and subsequently undergoes lumen formation to form a fully patent vessel. Downregulating the VEGF signaling pathway, while affecting the number of angioblasts, does not appear to affect their migratory behavior. Our studies also indicate that the endoderm, a tissue previously implicated in vascular development, provides a substratum for endothelial cell migration and is involved in regulating the timing of this process, but that it is not essential for the direction of migration. In addition, the endothelial cells in endodermless embryos form properly lumenized vessels, contrary to what has been previously reported in Xenopus and avian embryos. These studies provide the tools and a cellular framework for the investigation of mutations affecting vasculogenesis in zebrafish.
Key words: Endothelial cell, Migration, Endoderm, VEGF, Angioblast, Zebrafish
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