Michels C A, Hahnenberger K M, Sylvestre Y
J Bacteriol. 1983 Jan;153(1):574-8. doi: 10.1128/jb.153.1.574-578.1983.
Previously, we described a mutation glr1-1 in Saccharomyces carlsbergensis which pleiotropically relieves the synthesis of the following enzymes from glucose repression: maltase, galactokinase, alpha-galactosidase, NADH:cytochrome c reductase, and cytochrome c oxidase (C. A. Michels and A. Romanowski, J. Bacteriol, 143:674-679, 1980.) In this report, we demonstrate that glr1-1 and two other alleles, glr1-3 and glr1-16, are also insensitive to the glucose repression of invertase synthesis. Determinations of the levels of hexokinase activity and the rate of glucose transport in these mutants show that both are reduced as compared with the parent strain. Complementation tests and genetic analysis indicate that the glr1 mutations are allelic to HXK2, the structural gene for hexokinase B. The significance of this result is discussed with regard to the mechanism of glucose repression in S. carlsbergensis.
先前,我们描述了卡尔斯伯酵母中的一种突变体glr1-1,它能多效性地解除葡萄糖对以下几种酶合成的阻遏作用:麦芽糖酶、半乳糖激酶、α-半乳糖苷酶、NADH:细胞色素c还原酶和细胞色素c氧化酶(C.A. 米歇尔和A. 罗曼诺夫斯基,《细菌学杂志》,143:674 - 679,1980年)。在本报告中,我们证明glr1-1以及另外两个等位基因glr1-3和glr1-16对蔗糖酶合成的葡萄糖阻遏也不敏感。对这些突变体中己糖激酶活性水平和葡萄糖转运速率的测定表明,与亲本菌株相比,二者均有所降低。互补试验和遗传分析表明,glr1突变与己糖激酶B的结构基因HXK2等位。结合卡尔斯伯酵母中葡萄糖阻遏的机制对这一结果的意义进行了讨论。