Recessive mutations conferring resistance to carbon catabolite repression of galactokinase synthesis in Saccharomyces cerevisiae.
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.
D004352:Drug Resistance, Microbial; D004791:Enzyme Inhibitors; D004794:Enzyme Repression; D005686:Galactokinase / Q000096:biosynthesis*; D005947:Glucose / Q000494:pharmacology*; D006026:Glycoside Hydrolases / Q000096:biosynthesis; D009154:Mutation; D012441:Saccharomyces cerevisiae / Q000187:drug effects / Q000235:genetics* / Q000302:isolation & purification; D013997:Time Factors; D043324:beta-Fructofuranosidase
D004791:Enzyme Inhibitors; D005686:Galactokinase; D006026:Glycoside Hydrolases; D043324:beta-Fructofuranosidase; D005947:Glucose