Abstract: All artificially induced haploid fish embryos show extensive lethality and a cluster of developmental defects known as haploid syndrome, in which oedema, expansion of pericardial cavity and distemperedness of blood circulation are the most common characteristics, and its molecular mechanisms remain incompletely understood. In order to study the causes of abnormal development of the circulatory system in haploid fish embryos, the etv2 (Ets variant 2, also known as ER71 or Etsrp), a master regulatory gene for embryonic vasculogenesis, was cloned in goldfish (Carassius auratus) and its expression patterns in gynogenetic haploid and inbred diploid embryos were compared. The full-length cDNA of goldfish etv2 contained 1531 nucleotides with a 1116 bp open reading frame (ORF) that encodes a protein of 371 amino acids. Amino acid sequence alignment showed that the structure of goldfish ETV2 protein consisted an ETS DNA binding domain at the C-terminal, which was conservatively shared with the ETS transcription factor family. The amino acid sequence of this domain has more than 60% homology with other vertebrates ETV2 proteins. In adult goldfish, the etv2 transcripts were expressed in liver, heart, muscle, kidney, testis, brain and spleen, but not in ovary and mature egg. Real-time quantitative PCR (qRT-PCR) showed that etv2 expression started at bud stage, increased as somitogenesis progression, reached a peak at the 20-somite stage and then gradually decreased in later stages of embryogenesis. Whole mount in situ hybridization analysis showed that embryonic etv2 expression was restricted to the lateral plate mesoderm, hemangioblasts, angioblasts and vascular endothelial cells. At the 14-somite stage and the 20-somite stage, the expression of etv2 in gynogenetic haploid embryos was reduced or lost in certain parts of trunk and tail, especially in the midline, and its transcription level was significantly lower than that of inbred diploids. These results indicated that the number of angioblasts in gynogenetic haploid embryos decreased and failed to migrate towards the midline, which may be an important reason for the abnormal vasculogenesis of gynogenetic haploid.