Medaka mutants of organogenesis : an animal model for human diseases

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We have screened for mutants defective in organogenesis in the medaka, Oryzias latipes. Males were mutagenized with ethylnitrosourea (ENU), and we identified mutants that were defective in the development of blood cells and various organs, including heart, blood vessels, ear, and fins. In addition, larvae were stained with alizarin red, and we isolated bone mutants. Finally we established 53 mutations affecting organogenesis, and some mutants exhibited a unique phenotype that has not been described in zebrafish. After establishing selected 20 mutant clones, we have started the positional cloning and characterization of mutants, and several candidate genes are available. For characterization, GFP transgenic lines specific for bone and blood vessel have been established, and then were mated with mutant clones to analyze their defects. A hypochromic anemia mutant, whiteout (who), that shows an elongated morphology of blood cells and little hemoglobin activity, was caused by a mutation in the gene for □-aminolevulinic acid dehydratase (ALAD). Another mutant, unextended fin (ufi), which shows the defect of fin extension resulting a shrunken and short fin, was caused by a mutation in the gene for hoxb8, displaying non-canonical wnt pathway defects. Medaka mutants possibly represent models for the human diseases.