Physiological Properties of
            <i>Saccharomyces cerevisiae</i>
            from Which Hexokinase II Has Been Deleted

Diderich, Jasper A.; Raamsdonk, Léonie M.; Kruckeberg, Arthur L.; Berden, J.A.; Dam, K. Van

doi:10.1128/aem.67.4.1587-1593.2001

Cited by 65 publications

(59 citation statements)

References 47 publications

(41 reference statements)

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“…Figures 2A, 2C). This is caused by the much lower ethanol production during the predominantly oxidative growth on glucose and sucrose by the hxk2 deletion strain, whereas the wild-type strain converts glucose mainly to ethanol (see also Diderich et al, 2001). In the first 22 h, the RQ of the hxk2 deletion strain was close to 1, which is characteristic Figure 3.…”

Section: Glucose Repression Through Hxk2 Revisitedmentioning

confidence: 69%

“…Accordingly, the hxk2 deletion strain displayed an increased flux through the TCA cycle and oxidative phosphorylation in the presence of excess glucose. The flux through glycolysis and the fluxes to ethanol and glycerol were decreased, resulting in almost exclusively oxidative growth and thus diminished ethanol production (Diderich et al, 2001). As a consequence, the growth yield of the hxk2 deletion strain during aerobic growth on glucose is much higher than that of its parent strain, since fermentation of glucose to ethanol yields only two ATPs per glucose consumed, whereas complete oxidation of glucose to carbon dioxide and water yields roughly 20 ATPs.…”

Section: Introductionmentioning

confidence: 98%

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Co‐consumption of sugars or ethanol and glucose in a Saccharomyces cerevisiae strain deleted in the HXK2 gene

Raamsdonk¹,

Diderich²,

Kuiper³

et al. 2001

Yeast

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In previous studies it was shown that deletion of the HXK2 gene in Saccharomyces cerevisiae yields a strain that hardly produces ethanol and grows almost exclusively oxidatively in the presence of abundant glucose. This paper reports on physiological studies on the hxk2 deletion strain on mixtures of glucose/sucrose, glucose/galactose, glucose/ maltose and glucose/ethanol in aerobic batch cultures. The hxk2 deletion strain co-consumed galactose and sucrose, together with glucose. In addition, co-consumption of glucose and ethanol was observed during the early exponential growth phase. In S. cerevisiae, co-consumption of ethanol and glucose (in the presence of abundant glucose) has never been reported before. The specific respiration rate of the hxk2 deletion strain growing on the glucose/ethanol mixture was 900 mmolemin x1 e(g protein) x1 , which is four to five times higher than that of the hxk2 deletion strain growing oxidatively on glucose, three times higher than its parent growing on ethanol (when respiration is fully derepressed) and is almost 10 times higher than its parent growing on glucose (when respiration is repressed). This indicates that the hxk2 deletion strain has a strongly enhanced oxidative capacity when grown on a mixture of glucose and ethanol.

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Section: Glucose Repression Through Hxk2 Revisitedmentioning

confidence: 69%

Section: Introductionmentioning

confidence: 98%

Co‐consumption of sugars or ethanol and glucose in a Saccharomyces cerevisiae strain deleted in the HXK2 gene

Raamsdonk¹,

Diderich²,

Kuiper³

et al. 2001

Yeast

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“…The process is blocked in a strain lacking glucose transport genes, and decreased in an hxk2⌬ strain in which fermentation is slowed (11). Furthermore, 2-deoxy glucose, which cannot enter glycolysis, does not substitute for glucose.…”

Section: Discussionmentioning

confidence: 99%

Glucose Regulation of Saccharomyces cerevisiae Cell Cycle Genes

Newcomb

Diderich

Slattery³

et al. 2003

Eukaryot Cell

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Nutrient-limited Saccharomyces cerevisiae cells rapidly resume proliferative growth when transferred into glucose medium. This is preceded by a rapid increase in CLN3, BCK2, and CDC28 mRNAs encoding cell cycle regulatory proteins that promote progress through Start. We have tested the ability of mutations in known glucose signaling pathways to block glucose induction of CLN3, BCK2, and CDC28. We find that loss of the Snf3 and Rgt2 glucose sensors does not block glucose induction, nor does deletion of HXK2, encoding the hexokinase isoenzyme involved in glucose repression signaling. Rapamycin blockade of the Tor nutrient sensing pathway does not block the glucose response. Addition of 2-deoxy glucose to the medium will not substitute for glucose. These results indicate that glucose metabolism generates the signal required for induction of CLN3, BCK2, and CDC28. In support of this conclusion, we find that addition of iodoacetate, an inhibitor of the glyceraldehyde-3-phosphate dehydrogenase step in yeast glycolysis, strongly downregulates the levels CLN3, BCK2, and CDC28 mRNAs. Furthermore, mutations in PFK1 and PFK2, which encode phosphofructokinase isoforms, inhibit glucose induction of CLN3, BCK2, and CDC28. These results indicate a link between the rate of glycolysis and the expression of genes that are critical for passage through G 1 .

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“…Several reports in the literature show that the respiration of cells that accumulate F16bP to different degrees changes proportionally. It has been shown that the rate of oxygen consumption of the ⌬hxk2 mutant, lacking isoform 2 of hexokinase, which has lower levels of F16bP, is not inhibited by high glucose concentrations (25,47). A strain overexpressing phosphofructokinase has lower JO 2 values (48).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Oxidative Phosphorylation Is Regulated by Fructose 1,6-Bisphosphate

Díaz-Ruiz

Avéret

Araiza

et al. 2008

Journal of Biological Chemistry

142

109

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In numerous cell types, tumoral cells, proliferating cells, bacteria, and yeast, respiration is inhibited when high concentrations of glucose are added to the culture medium. This phenomenon has been named the "Crabtree effect." We used yeast to investigate (i) the short term event(s) associated with the Crabtree effect and (ii) a putative role of hexose phosphates in the inhibition of respiration. Indeed, yeast divide into "Crabtree-positive," where the Crabtree effect occurs, and "Crabtree-negative," where it does not. In mitochondria isolated from these two categories of yeast, we found that low, physiological concentrations of glucose 6-phosphate and fructose 6-phosphate slightly (20%) stimulated the respiratory flux and that this effect was strongly antagonized by fructose 1,6-bisphosphate (F16bP). On the other hand, F16bP by itself was able to inhibit mitochondrial respiration only in mitochondria isolated from a Crabtree-positive strain. Using permeabilized spheroplasts from Crabtree-positive yeast, we have shown that the sole effect observed at physiological concentrations of hexose phosphates is an inhibition of oxidative phosphorylation by F16bP. This F16bP-mediated inhibition was also observed in isolated rat liver mitochondria, extending this process to mammalian cells. From these results and taking into account that F16bP is able to accumulate in the cell cytoplasm, we propose that F16bP regulates oxidative phosphorylation and thus participates in the establishment of the Crabtree effect.

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Physiological Properties of Saccharomyces cerevisiae from Which Hexokinase II Has Been Deleted

Cited by 65 publications

References 47 publications

Co‐consumption of sugars or ethanol and glucose in a Saccharomyces cerevisiae strain deleted in the HXK2 gene

Co‐consumption of sugars or ethanol and glucose in a Saccharomyces cerevisiae strain deleted in the HXK2 gene

Glucose Regulation of Saccharomyces cerevisiae Cell Cycle Genes

Mitochondrial Oxidative Phosphorylation Is Regulated by Fructose 1,6-Bisphosphate

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