Transport defects as the physiological basis for eye color mutants of Drosophila melanogaster.
Kynurenine-H3 transport and conversion to 3-hydroxykynurenine were studied in organ culture using the Malpighian tubules and developing eyes from wild type and the eye color mutants w, st, ltd, ca, and cn of Drosophila melanogaster. Malpighian tubules from wild type have the ability to concentrate kynurenine and convert it to 3-hydroxykynurenine. The tubules from w, st, ltd, and ca are deficient in the ability to transport kynurenine, as are the eyes of the mutants w, st, and ltd. This defect in kynurenine transport provides a physiological explanation for the phenotypic properties of the mutants. The relationship of these measurements to previous observations on these eye color mutants is discussed and the transport defect hypothesis is consistently supported. We have concluded that several of the eye color mutants in Drosophila are transport mutants.
D000818:Animals; D004331:Drosophila melanogaster / Q000378:metabolism*; D005127:Eye Color; D005838:Genotype; D007444:Inulin / Q000378:metabolism; D007737:Kynurenine / Q000031:analogs & derivatives / Q000378:metabolism*; D007814:Larva / Q000378:metabolism; D008317:Malpighian Tubules / Q000378:metabolism; D009154:Mutation
D007737:Kynurenine; D007444:Inulin