TYROSINASE INHERITANCE IN STREPTOMYCES SCABIES. II. INDUCTION OF TYROSINASE DEFICIENCY BY ACRIDINE DYES

Abstract

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 mug 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 mug/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.