TYROSINASE INHERITANCE IN STREPTOMYCES SCABIES II. : Induction of Tyrosinase Deficiency by Acridine Dyes

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Gregory, Kenneth F. (Ontario Agricultural College, Guelph, Ontario, Canada), and Jay C. C. Huang. Tyrosinase inheritance in Streptomyces scabies. II. Induction of tyrosinase deficiency by acridine dyes. J. Bacteriol. 87:1287–1294. 1964.—Growth in minimal medium containing 1 μg of acriflavine per ml resulted in a large increase (up to 62%) in the frequency of tyrosinase-deficient (tye−) mutants in all of ten strains of Streptomyces scabies and eight unidentified streptomycetes studied. This increased frequency did not result from the selection of preformed mutants, since tye− clones were usually inhibited by lower concentrations of acriflavine than were tyrosinase-producing (tye+) clones, and no significant difference in mycelial yields occurred between the two types growing in a 1 μg/ml concentration of the dye. The mutations induced by X rays and acriflavine were either allelic or closely linked. This tye− phenotype was not caused by the production of an enzyme inhibitor, lack of a cofactor, or defect in the conversion of a protyrosinase to tyrosinase. Tye− mutants formed no detectable tyrosinase under a variety of conditions, including the presence of possible inducers. Mutants were able to oxidize glucose and succinate. The S. scabies tyrosinase was heat-labile (half-life at 59 C = 1.6 min) and not particle-bound. We conclude that acriflavine induces the loss of, or alteration in, a structural gene for tyrosinase production present as an extrachromosomal factor.

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