Matsumoto K, Yoshimatsu T, Oshima Y
J Bacteriol. 1983 Mar;153(3):1405-14. doi: 10.1128/jb.153.3.1405-1414.1983.
A total of 37 recessive mutations showing enhanced resistance to the glucose repression of galactokinase synthesis have been isolated by a selection procedure with a GAL81 gal7 double mutant. These mutations were grouped into three different complementation classes. One class, reg1, contains mutants arising from mutations at a site close to, but complementing, the gal3 locus. The reg1 mutant also showed resistance to the glucose repression of invertase synthesis but not to that of alpha-D-glucosidase. The two other classes were identified as arising from recessive mutations at the GAL82 locus and the GAL83 locus, respectively, at which various dominant mutations were isolated previously. When in a constitutive background due to the GAL81 or gal80 mutation, the GAL82 and GAL83 mutations did not show a mutually additive effect on the resistance to glucose repression of galactokinase synthesis, while the reg1 and GAL82 (or GAL83) mutations did. Based upon the specific behavior of cells with various genotypes for the above genes in response to the concentration of galactose and glucose in the medium, we propose a model involving three independent circuits for glucose signals in the regulation of the structural genes for the galactose pathway enzymes.
通过使用GAL81 gal7双突变体的筛选程序，总共分离出37个对半乳糖激酶合成的葡萄糖阻遏具有增强抗性的隐性突变。这些突变被分为三个不同的互补群。其中一个互补群reg1包含由靠近gal3位点但与之互补的位点发生突变产生的突变体。reg1突变体对蔗糖酶合成的葡萄糖阻遏也具有抗性，但对α-D-葡萄糖苷酶的葡萄糖阻遏不具有抗性。另外两个互补群分别被鉴定为是由GAL82位点和GAL83位点的隐性突变产生的，之前在这些位点分离出了各种显性突变。当处于由于GAL81或gal80突变导致的组成型背景中时，GAL82和GAL83突变对半乳糖激酶合成的葡萄糖阻遏抗性没有表现出相互累加效应，而reg1和GAL82（或GAL83）突变则表现出这种效应。基于上述基因的各种基因型细胞对培养基中半乳糖和葡萄糖浓度的特定反应行为，我们提出了一个模型，该模型涉及在半乳糖途径酶结构基因调控中葡萄糖信号的三个独立回路。
