Open AccessMixed and diverse metabolic and gene‐expression regulation of the glycolytic and fermentative pathways in response to a HXK2 deletion in Saccharomyces cerevisiae
Author(s) -
Rossell Sergio,
Lindenbergh Alexander,
Van Der Weijden Coen C.,
Kruckeberg Arthur L.,
Van Eunen Karen,
Westerhoff Hans V.,
Bakker Barbara M.
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.1567-1364.2007.00282.x
Subject(s) - biology , hexokinase , phosphofructokinase , glycolysis , biochemistry , saccharomyces cerevisiae , mutant , enzyme , yeast , gene
In Saccharomyces cerevisiae the HXK2 gene, which encodes the glycolytic enzyme hexokinase II, is involved in the regulatory mechanism known as ‘glucose repression’. Its deletion leads to fully respiratory growth at high glucose concentrations where the wild type ferments profusely. Here we describe that deletion of the HXK2 gene resulted in a 75% reduction in fermentative capacity. Using regulation analysis we found that the fluxes through most glycolytic and fermentative enzymes were regulated cooperatively by changes in their capacities ( V max ) and by changes in the way they interacted with the rest of the metabolism. Glucose transport and phosphofructokinase were regulated purely at the metabolic level. The reduction of fermentative capacity in the mutant was accompanied by a remarkable resilience of the remaining capacity to nutrient starvation. After starvation, the fermentative capacity of the hxk2 Δ mutant was similar to that of the wild type. Based on our results and previous reports, we suggest an inverse correlation between glucose repression and the resilience of fermentative capacity towards nutrient starvation. Only a limited number of glycolytic enzyme activities changed upon starvation of the hxk2 Δ mutant and we discuss to what extent this could explain the stability of the fermentative capacity.