The vascular endothelial growth factor (VEGF) and its high-affinity binding receptors, the tyrosine kinases Flt-1 and Flk-1, are thought to be important for the development of embryonic vasculature. Here we report that Flt-1 is essential for the organization of embryonic vasculature, but is not essential for endothelial cell differentiation. Mouse embryos homozygous for a targeted mutation in the flt-1 locus, flt-1lcz, formed endothelial cells in both embryonic and extra-embryonic regions, but assembled these cells into abnormal vascular channels and died in utero at mid-somite stages. At earlier stages, the blood islands of flt-1lcz homozygotes were abnormal, with angioblasts in the interior as well as on the periphery. We suggest that the Flt-1 signalling pathway may regulate normal endothelial cell-cell or cell-matrix interactions during vascular development.
Pubmed ID: 7596436 RIS Download
Mesh terms: Animals | Base Sequence | Cell Differentiation | DNA Primers | Embryo, Mammalian | Endothelial Growth Factors | Endothelium, Vascular | Heterozygote | Homozygote | Humans | Lymphokines | Mice | Molecular Sequence Data | Mutagenesis | Proto-Oncogene Proteins | Receptor Protein-Tyrosine Kinases | Stem Cells | Vascular Endothelial Growth Factor A | Vascular Endothelial Growth Factor Receptor-1 | Vascular Endothelial Growth Factors
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