Fig 1

she mutants display pericardial edema and loss of blood circulation.

(A) Zebrafish SHE protein diagram. she ci26 and ci30 mutant alleles are predicted to result in a frameshift and premature stop codons. SH2 domain and consensus tyrosine ABL phosphorylation sites are shown. (B-E) In situ hybridization analysis of she expression in wild-type embryos at 24, 48, 72 and 96 hpf stages. Note its expression in the dorsal aorta (arrows), intersegmental vessels, lateral line primordium (arrowhead, B) and neuromasts (arrowheads, C-E). (F-I) In situ hybridization analysis of she expression in she mutants at 24 hpf. Note that she expression is unaffected in she^ci26 embryos while it is strongly reduced in she^ci30 embryos. Homozygous she^ci26 mutant embryos were obtained by an incross of she^ci26-/-; fli1a:she-2A-mCherry; kdrl:GFP parents (which are viable due to fli1a:she-2A-mCherry rescue) and selected for mCherry negative embryos. Wild-type control embryos were obtained by incross of sibling wt; fli1a:she-2A-mCherry parents and selected for mCherry-negative embryos. she^ci30 embryos were obtained by incross of she^ci30+/- parents and genotyped after in situ hybridization. 25% (10 out of 40) embryos showed strong reduction in she expression which correlated with the mutant phenotype. (J-M) Brightfield images of she^ci26 and she^ci30 mutant embryos and their siblings (wild-type and or heterozygous) at 4 dpf. Note the pericardial edema (arrowheads) in the mutant embryos. Embryos were obtained by the incross of heterozygous parents in kdrl:GFP background. 24.9% (265 out of 1064) and 24.2% (80 out of 330) embryos obtained in she^ci26 or she^ci30 incross, respectively, showed this phenotype. A subset of embryos was genotyped to confirm the correlation between the phenotype and genotype.