Representative embryonic, larval, and adult phenotypes from selected retroviral insertional alleles. (A) Insertion in the wee1 gene led to an early phenotype of cellular necrosis starting at the gastrulation stage. Images here show a wild-type and mutant embryo at the 12 somite stage. (B) Insertion in the eif3i gene led to a vascular defect in homozygous mutants. The upper panel shows bright field images and the lower panel shows the lack of intersegmental vessels labeled by the flk-gfp transgenic marker in the eif3s3−/− background at 1 day post-fertilization (dpf). (C) An insertion in the snapc1b gene causes embryonic phenotypes including jaw defects and a small liver visible at 5 dpf. Arrows point to the reduced jaw structures in the mutant, dashed lines demarcate the liver. (D) Homozygous rpa1 mutants at 2 dpf have small and necrotic heads, small eyes, and tails curling dorsally. These homozygous phenotypes are weaker but observable at 1 dpf. All homozygotes die at ∼5 dpf. (E) Insertion in a novel gene (zgc:194470) led to the larval phenotype of a larger body at day 12 of development. The mutant is homozygous viable, and the body sizes become the same as that of wild type when reaching the adult stage. One-hundred percent of the homozygous mutants show the larger larval phenotype (N = 200). (F) Slc7a5−/− fish showed no observable embryonic defects, but they are 40% smaller than their wild-type or heterozygous siblings at 4 mo of age. Slc7a5 is a small subunit of the L-type amino acid transporter 1. (G) 6-mo-old adult tg−/− (thyroglobulin) fish showed red swelling under the chins (black arrows), a phenotype reminiscent of human thyroid goiters. Tg−/− fish are fertile and showed no observable embryonic defects.
