Shavlovskiĭ G M, Sibirnyĭ A A, Ksheminskaia G P, Pinchuk G E
Mikrobiologiia. 1980 Sep-Oct;49(5):702-7.
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.
从对多种抗生素和抗代谢物具有多重敏感性的季也蒙毕赤酵母菌株MS14 - A10中筛选出对7 - 甲基 - 8 - 三氟甲基 - 10 -(1'-D - 核糖基)异咯嗪具有抗性的突变体。许多此类突变体表现出较高的黄素生成活性。对黄素生成活性最高的三个突变体,即RZ4、RZ7和RZ11的特性研究表明,它们过量生产核黄素的能力并非源于嘌呤从头生物合成的调节紊乱、铁离子向细胞内转运受损或GTP环化水解酶变构性质的改变。在两个突变体RZ4和RZ11中观察到GTP环化水解酶和核黄素合酶的比活性增加了两倍。这些数据表明,在这些突变体中,涉及铁离子的黄素生成酶合成的抑制机制受到了损害。突变体RZ7中核黄素过量生产的原因仍然不明。