Abstract
The X-linked, xanthine dehydrogenase (XDH) deficient cinnamon (cin, 1-0.0) eye color mutant of Drosophila melanogaster is a female sterile and as a result, cannot be maintained as a homozygous stock. Since the eye color of cin progeny from heterozygous females is maternally affected, genotypically cin flies have a wild type eye color. Supplementation of the culture medium with 0.02% allopurinol (4-hydroxypyrazolo (3,4-d), pyrimidine) (an XDH inhibitor) causes maternally affected cin flies to express a fully mutant eye color while it has no effect on the eye color of wild type flies. Using an allopurinol screening system we successfully induced two new alleles cin3 and cin4 with ethyl methane sulfonate (EMS). cin3 is more severe than cin4 and cin with respect to three cin phenotypes suggesting that cin and cin4 are leaky. cin3 mutants have no greater levels of XDH throughout development than do maternally affected ma-l flies while cin and cin4 have higher XDH levels as late as the 96 h pupa. Using overlapping deficiencies and duplications, an unequivocal order of genes mapping at the tip of the X-chromosome (1-0.0) was obtained: l(1)J1, cin, arth, y, ac, sc and svr. Gynandromorphs marked with cin and y were employed to demonstrate that the action of cin+ is non-autonomous. A selection scheme using a combination of allopurinol and purine which renders cin flies conditionally lethal is described.
Published Version
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