Pleiotropic glucose repression-resistant mutation in Saccharomyces carlesbergensis

Abstract

We describe the characterization of a mutation of the locus GLRI. This mutation allowed for (i) the glucose repression-insensitive synthesis of the enzymes maltase, galactokinase, a-galactosidase, reduced nicotinamide adenine dinucleotide-cytochrome c reductase, and cytochrome c oxidase and (ii) growth on maltose in the presence of the gratuitous glucose repressor D-glucosamine. The glucosamine resistance cosegregated with the glucose-insensitive synthesis of the enzymes listed above. In addition, crosses between the glucosamine-resistant mutant and isogenic sensitive strains gave only tetrads containing two resistant and two sensitive spores. Thus, a single pleiotropic mutation is responsible for both phenotypes. We call the locus GLR1, for glucose regulation, and the glucose repression-insensitive mutation glrl-1.

Carrier-free, continuous primary beer fermentation

“…These residual sugars corresponded to maltose and maltotriose (on average 2 and 3 g L À1 , respectively). Not surprisingly, glucose and fructose were not present in the young beer at this phase (Table 1) owing to preferential sugar consumption of monosaccharides by yeast (43)(44)(45)(46). Furthermore, a reduced amount of fermentable sugars is required in the green beer for further carbon dioxide development in the maturation stage.…”

Catabolite repression mutants of yeast1

“…The yeast is plated in the presence of the analogue on a medium whose utilization requires the expression of enzymes sensitive to catabolite repression, e.g., a medium with saccharose or maltose as carbon source. Colonies growing in these conditions are selected as putative mutants [8][9][10][11][12][13]. In some cases diploids were used as starting material to obtain dominant mutants [14,15].…”

“…This is done by testing the activities of a number of enzymes sensitive to catabolite repression under adequate conditions. In cases where resistance to analogues is used as a selection procedure, mutants will frequently be obtained which are resistant to the toxic effect of the analogue but still sensitive to repression by glucose ( [10,12] this laboratory, unpublished).…”

“…Although CCR91 and CCRS0 are in some respect similar they are probably not allelic since glucose fermentation is severely impaired in CCR80 but not in CCR91 mutants. [10] Respiratory enzymes garl, gar2, gar3 [12] ADH II ADR3 [47] MDH, SDH, ICL, MS CCR80 [48] MAL flkl [49,23] iso-2-cytochrome c cyc9 [50] SUC, GAK regl [19] GAK GAL82, GAL83…”

Mixed and diverse metabolic and gene-expression regulation of the glycolytic and fermentative pathways in response to aHXK2deletion inSaccharomyces cerevisiae

“…This signaling pathway senses the concentration of extracellular glucose and transmits this information to the transcription apparatus. Deletion of the HXK2 gene, which encodes the glucose phosphorylating enzyme hexokinase II, alleviated glucose repression (Zimmermann & Scheel, 1977;Entian & Zimmermann, 1980;Michels & Romanowski, 1980) as evidenced by fully respiratory growth at high glucose concentrations , coconsumption of glucose with other sugars , derepression of high affinity hexose transporters (Petit et al, 2000) and increased plasma-membrane H 1 -ATPase activity .…”