Mutants resistant to 7-methyl-8-trifluoromethyl-10-(1'-D-ribityl)isoalloxazine were selected from the yeast Pichia guilliermondii, strain MS14-A10, possessing a multiple sensitivity to antibiotics and antimetabolites. A lot of such mutants displayed an elevated flavinogenic activity. The investigation of the properties of three mutants with the highest flavinogenic activity, viz. RZ4, RZ7 and RZ11, has shown that their capability for riboflavin overproduction does not stem from disordered regulation of the de novo purine biosynthesis, from the damaged transport of iron ions into the cell, or from changes in the allosteric properties of GTP cyclohydrolase. A twofold increase in the specific activities of GTP cyclohydrolase and riboflavin synthase was observed in the two mutants, RZ4 and RZ11. These data suggest that the mechanism for repression of the synthesis of flavinogenic enzymes, in which iron ions are involved, is impaired in these mutants. The reason for riboflavin overproduction in the mutant RZ7 remains obscure.
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