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We therefore suggest that the zebrafish VEGF receptor comprises seven Ig-like domains.The ligand binding function of the Flt1 and Flk1 recep-tors resides within the first four Ig-like domains[20¨C24].In both identified mutant flk1 alleles,premature stop codons presumably lead to a truncated protein compris-ing the first four or five Ig-like domains,respectively.Therefore,a truncated Flk1 receptor might retain some VEGF binding activity in mutant embryos.However,the morpholino knockdown of flk1 phenocopies the chemi-cally induced mutations.In addition,flk1 transcripts are almost absent in flk1 mutant embryos,probably due to nonsense-mediated mRNA decay.These findings strongly suggest that flk1t20257 and flk1t21588 represent null mutations.The loss of flk1 in zebrafish does not disturb vasculo-genesis and hematopoiesis but specifically disrupts an-giogenic sprouting of blood vessels from preexisting vessels.This phenotype differs from the results of gene targeting experiments for both Fl

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