Open AccessCharacterization of glucose transport mutants of Saccharomyces cerevisiae during a nutritional upshift reveals a correlation between metabolite levels and glycolytic flux
Author(s) -
Bosch Daniel,
Johansson Mikael,
Ferndahl Cecilia,
Franzén Carl Johan,
Larsson Christer,
Gustafsson Lena
Publication year - 2008
Publication title -
fems yeast research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 92
eISSN - 1567-1364
pISSN - 1567-1356
DOI - 10.1111/j.1567-1364.2007.00323.x
Subject(s) - phosphofructokinase , biochemistry , biology , glycolysis , saccharomyces cerevisiae , fructose , sugar phosphates , sugar , glucose 6 phosphate isomerase , hexokinase , mutant , nad+ kinase , metabolism , enzyme , yeast , gene
Saccharomyces cerevisiae shows a marked preference for glucose and fructose, revealed by the repression of genes whose products are involved in processing other carbon sources. This response seems to be driven by sugar phosphorylation in the first steps of glycolysis rather than by the external sugar concentration. To gain a further insight into the role of the internal sugar signalling mechanisms, were measured the levels of upper intracellular glycolytic metabolites and adenine nucleotides in three mutant strains, HXT1, HXT7 and TM6 * , with progressively reduced uptake capacities in comparison with the wild type. Reducing the rate of sugar consumption caused an accumulation of hexose phosphates upstream of the phosphofructokinase (PFK) and a reduction of fructose‐1,6‐bisphosphate levels. Mathematical modelling showed that these effects may be explained by changes in the kinetics of PFK and phosphoglucose isomerase. Moreover, the model indicated a modified sensitivity of the pyruvate dehydrogenase and the trichloroacetic acid cycle enzymes towards the NAD/NADH in the TM6 * strain. The activation of the SNF1 sugar signalling pathway, previously observed in the TM6 * strain, does not correlate with a reduction of the ATP : AMP ratio as reported in mammals. The mechanisms that may control the glycolytic rate at reduced sugar transport rates are discussed.