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A cytosolic Arabidopsis D-xylulose kinase catalyzes the phosphorylation of 1-deoxy-D-xylulose into a precursor of the plastidial isoprenoid pathway.

Plants are able to integrate exogenous 1-deoxy-D-xylulose (DX) into the 2C-methyl-D-erythritol 4-phosphate pathway, implicated in the biosynthesis of plastidial isoprenoids. Thus, the carbohydrate needs to be phosphorylated into 1-deoxy-D-xylulose 5-phosphate and translocated into plastids, or vice versa. An enzyme capable of phosphorylating DX was partially purified from a cell-free Arabidopsis (Arabidopsis thaliana) protein extract. It was identified by mass spectrometry as a cytosolic protein bearing D-xylulose kinase (XK) signatures, already suggesting that DX is phosphorylated within the cytosol prior to translocation into the plastids. The corresponding cDNA was isolated and enzymatic properties of a recombinant protein were determined. In Arabidopsis, xylulose kinases are encoded by a small gene family, in which only two genes are putatively annotated. The additional gene is coding for a protein targeted to plastids, as was proved by colocalization experiments using green fluorescent protein fusion constructs. Functional complementation assays in an Escherichia coli strain deleted in xk revealed that the cytosolic enzyme could exclusively phosphorylate xylulose in vivo, not the enzyme that is targeted to plastids. xk activities could not be detected in chloroplast protein extracts or in proteins isolated from its ancestral relative Synechocystis sp. PCC 6803. The gene encoding the plastidic protein annotated as "xylulose kinase" might in fact yield an enzyme having different phosphorylation specificities. The biochemical characterization and complementation experiments with DX of specific Arabidopsis knockout mutants seedlings treated with oxo-clomazone, an inhibitor of 1-deoxy-D-xylulose 5-phosphate synthase, further confirmed that the cytosolic protein is responsible for the phosphorylation of DX in planta.

Arabidopsis↗

Synthesis of 1-Deoxy-D-xylulose and 1-Deoxy-D-xylulose-5-phosphate.

1-Deoxy-D-xylulose (4) and the corresponding 5-phosphate (5) are substrates for the first pathway-specific enzymes in the biosynthesis of thiamine diphosphate (vitamin B(1)), pyridoxol phosphate (vitamin B(6)), and the nonmevalonate family of isoprenoid compounds recently discovered in bacteria and plant chloroplasts. Both 4 and 5 were synthesized from commercially available (-)-2,3-O-isopropylidene-D-threitol (10). The protected tetraol was converted to (-)-3,4-O-isopropylidene-5-triisopropylsilyl-1-deoxy-D-xylulose (14) in four steps. Treatment of 14 with acetic acid gave 4 in an overall yield of 69%. The corresponding 5-phosphate was obtained by protection the carbonyl group in 14, removal of the triisopropylsilyl moiety, and treatment of the resulting alcohol with trimethyl phosphite/TeCl(4), trimethylsilyl bromide, water, and HCl in successive steps to give 5 in 58% overall yield from 10.

Journal Article↗

Rapid and flexible synthesis of 1-deoxy-D-xylulose-5-phosphate, the substrate for 1-deoxy-D-xylulose-5-phosphate reductoisomerase.

1-Deoxy-D-xylulose-5-phosphate (DXP) is a key intermediate in the non-mevalonate pathway to terpenoids in bacteria, and it is the substrate for the enzyme 1-deoxy-D-xylulose-5-phosphate reductoisomerase (DXP-R). In order to study the mechanism of DXP-R, we required a flexible synthesis of the substrate which would allow the incorporation of isotopic labels, and the variation of the two stereocentres. Thus 1,4-dihydroxypent-2-yne was selectively reduced to give the E-olefin, and selective phosphorylation of the primary alcohol followed by oxidation of the secondary alcohol gave a substrate suitable for dihydroxylation. Dihydroxylation using stoichiometric OsO4 in the presence of chiral ligands gave protected DXP in high ee. Final hydrogenolysis gave DXP in quantitative yield and high purity. DXP-R was produced by rapid cloning of the dxr gene from Escherichia coli through controlled expression and ion exchange chromatography. The synthetic DXP was fully active in enzyme assays catalysed by recombinant DXP-R.

Alcohols↗

Isoprenoid biosynthesis via the MEP pathway. Synthesis of (3,4)-3,4-dihydroxy-5-oxohexylphosphonic acid, an isosteric analogue of 1-deoxy-D-xylulose 5-phosphate, the substrate of the 1-deoxy-D-xylulose 5-phosphate reducto-isomerase.

(3,4)-3,4-Dihydroxy-5-oxohexylphosphonic acid, an isosteric analogue of 1-deoxy-D-xylulose 5-phosphate (DXP), was obtained in enantiomerically pure form from (+)-2,3--benzylidene--threitol by a seven-step sequence. This phosphonate did not affect the growth of. It did not inhibit the 1-deoxy-D-xylulose 5-phosphate reductoisomerase (DXR), but was converted by this enzyme into (3,4)-3,4,5-trihydroxy-3-methylpentylphosphonic acid, an isosteric analogue of 2-C-methyl-D-erythritol 4-phosphate. The enzyme was, however, less efficient with the methylene phosphonate analogue than with the natural substrate.

Aldose-Ketose Isomerases↗

Identification of class 2 1-deoxy-D-xylulose 5-phosphate synthase and 1-deoxy-D-xylulose 5-phosphate reductoisomerase genes from Ginkgo biloba and their transcription in embryo culture with respect to ginkgolide biosynthesis.

Diterpenoid ginkgolides having potent platelet-activating factor antagonist activity are major active ingredients of ginkgo extract. Class 2-type 1-deoxy-D-xylulose 5-phosphate synthase (GbDXS2) and 1-deoxy-D-xylulose 5-phosphate reductoisomerase (GbDXR), the first two enzymes in 2-C-methyl-D-erythritol 4-phosphate (MEP) pathway, operating in the earlier step of ginkgolide biosynthesis, were cloned from embryonic roots of Ginkgo biloba through a homology-based polymerase chain reaction for role assessment of the enzymes. Plasmids harboring each gene rescued the respective knockout E. coli mutants. The levopimaradiene synthase gene (LPS), responsible for the first committed step in ginkgolide biosynthesis, and GbDXS2 were transcribed exclusively in embryonic root, suggesting a specific role of GbDXS2 in ginkgolide biosynthesis. GbDXR retained a higher transcription level in roots than in leaves, whereas class 1 DXS (GbDXS1) showed 30 to 50 % higher level in leaves. Ginkgolides and bilobalide were found both in leaves and roots from an earlier stage of the embryo culture. Exclusive transcription of ginkgolide biosynthesis-specific LPS and GbDXS2 in roots and the appearance of ginkgolides in leaves was consistent with translocation of the compounds from roots to leaves.

Aldose-Ketose Isomerases↗

Xylulose 5-phosphate mediates glucose-induced lipogenesis by xylulose 5-phosphate-activated protein phosphatase in rat liver.

Carbohydrate-responsive element binding protein (ChREBP) is a transcription factor that activates lipogenic genes in liver in response to excess carbohydrate in the diet. ChREBP is regulated in a reciprocal manner by glucose and cAMP. cAMP-dependent protein kinase (protein kinase A) phosphorylates two physiologically important sites in ChREBP, Ser-196, which is located near nuclear localization signal sequence (NLS), and Thr-666, within the basic helix-loop-helix (bHLH) site, resulting in inactivation of nuclear translocation of ChREBP and of the DNA-binding activity, respectively. We demonstrate here that crude cytosolic extracts from livers of rats fed a high carbohydrate diet contained protein phosphatase (PPase) activity that dephosphorylated a peptide containing Ser-196, whereas a PPase in the nuclear extract catalyzed dephosphorylation of Ser-568 and Thr-666. All these PPases are activated specifically by xylulose 5-phosphate (Xu5P), but not by other sugar phosphates. Furthermore, addition of Xu5P elevated PPase activity to the level observed in extracts of fed liver cells. These partially purified PPases were characterized as PP2A-AB delta C by immunoblotting with specific antibodies. These results suggest that (ia) Xu5P-dependent PPase is responsible for activation of transcription of the L-type pyruvate kinase gene and lipogenic enzyme genes, and (ii) Xu5P is the glucose signaling compound. Thus, we propose that the same Xu5P-activated PPase controls both acute and long-term regulation of glucose metabolism and fat synthesis.

Amino Acid Sequence↗

The involvement of liver fructokinase in the metabolism of D-xylulose and xylitol in isolated rat hepatocytes.

Hepatocytes isolated from fed, male, Sprague-Dawley rats accumulate xylulose-1-phosphate and glycolaldehyde as well as xylulose-5-phosphate when incubated with 2-20 mM D-xylulose. Fructokinase inhibitors (fructose and 1-deoxyfructose) decreased xylulose-1-phosphate and glycolaldehyde (but not xylulose-5-phosphate) levels in xylulose-treated hepatocytes, demonstrating the role of fructokinase in xylulose-1-phosphate and glycolaldehyde formation. As the fructokinase inhibitors had no overall effects on the conversion of D-xylulose to glucose, the overall flux through the pathway involving fructokinase was less than 27% of the total D-xylulose utilized. In hepatocytes from fed or fasted rats there was no detectable accumulation of either xylulose-1-phosphate or glycolaldehyde after treatment with 20 mM xylitol. Other differences between xylitol and D-xylulose metabolism in rat hepatocytes included a slower rate of xylitol metabolism in all preparations and a difference in the relative conversion of xylitol to glucose in hepatocytes from fasted rats. Rats adapted to 20% xylitol (diarrhea-free) had a lower water consumption than those fed a control cornstarch diet; there were no differences in weight gain, food consumption or in rates or metabolite patterns of xylitol metabolism in hepatocytes isolated from these rats. Despite the minor role of fructokinase in the overall metabolism of xylitol and of D-xylulose as shown by these results, it is not possible to exclude the possibility of some flux through the pathway involving xylulose-1-phosphate and glycolaldehyde formation as a possible route for oxalate formation.

Acetaldehyde↗

Intermediary Metabolite Concentrations in Xylulose- and Glucose-Fermenting Saccharomyces cerevisiae Cells.

Glucose and xylulose fermentation and product formation by Saccharomyces cerevisiae were compared in batch culture under anaerobic conditions. In both cases the main product was ethanol, with glycerol, xylitol, and arabitol produced as by-products. During glucose and xylulose fermentation, 0.74 and 0.37 g of cell mass liter, respectively, were formed. In glucose-fermenting cells, the carbon balance could be closed, whereas in xylulose-fermenting cells, about 25% of the consumed sugar carbon could not be accounted for. The rate of sugar consumption was 3.94 mmol g of initial biomass h for glucose and 0.39 mmol g of initial biomass h for xylulose. Concentrations of the intermediary metabolites fructose-1,6-diphosphate (FDP), pyruvate (PYR), sedoheptulose 7-phosphate (S7P), erytrose 4-phosphate, citrate (CIT), fumarate, and malate were compared for both types of cells. Levels of FDP, PYR, and CIT were lower, and levels of S7P were higher in xylulose-fermenting cells. After normalization to the carbon consumption rate, the levels of FDP were approximately the same, whereas there was a significant accumulation of S7P, PYR, CIT, and malate, especially of S7P, in xylulose-fermenting cells compared with in glucose-fermenting cells. In the presence of 15 muM iodoacetate, an inhibitor of the enzyme glyceraldehyde-3-phosphate dehydrogenase (EC 1.2.1.12), FDP levels increased and S7P levels decreased in xylulose-assimilating cells compared with in the absence of the inhibitor, whereas fermentation was slightly slowed down. The specific activity of transaldolase (EC 2.2.1.2), the pentose phosphate pathway enzyme reacting with S7P and glyceraldehyde-3-phosphate, was essentially the same for both glucose- and xylulose-fermenting cells. It was, however, several orders of magnitude lower than that reported for a Torula yeast and Candida utilis. The presence of iodoacetate did not influence the activity of transaldolase in xylulose-fermenting cells. The results are discussed in terms of a competition between the pentose phosphate pathway and glycolysis for the common metabolite, glyceraldehyde-3-phosphate, which would explain the low rates of xylulose assimilation and ethanol production from xylulose by S. cerevisiae.

Journal Article↗

A novel NADH-linked l-xylulose reductase in the l-arabinose catabolic pathway of yeast.

An NADH-dependent l-xylulose reductase and the corresponding gene were identified from the yeast Ambrosiozyma monospora. The enzyme is part of the yeast pathway for l-arabinose catabolism. A fungal pathway for l-arabinose utilization has been described previously for molds. In this pathway l-arabinose is sequentially converted to l-arabinitol, l-xylulose, xylitol, and d-xylulose and enters the pentose phosphate pathway as d-xylulose 5-phosphate. In molds the reductions are NADPH-linked, and the oxidations are NAD(+)-linked. Here we show that in A. monospora the pathway is similar, i.e. it has the same two reduction and two oxidation reactions, but the reduction by l-xylulose reductase is not performed by a strictly NADPH-dependent enzyme as in molds but by a strictly NADH-dependent enzyme. The ALX1 gene encoding the NADH-dependent l-xylulose reductase is strongly expressed during growth on l-arabinose as shown by Northern analysis. The gene was functionally overexpressed in Saccharomyces cerevisiae and the purified His-tagged protein characterized. The reversible enzyme converts l-xylulose to xylitol. It also converts d-ribulose to d-arabinitol but has no activity with l-arabinitol or adonitol, i.e. it is specific for sugar alcohols where, in a Fischer projection, the hydroxyl group of the C-2 is in the l-configuration and the hydroxyl group of C-3 is in the d-configuration. It also has no activity with C-6 sugars or sugar alcohols. The K(m) values for l-xylulose and d-ribulose are 9.6 and 4.7 mm, respectively. To our knowledge this is the first report of an NADH-linked l-xylulose reductase.

Arabinose↗

D-xylulose-induced depletion of ATP and Pi in isolated rat hepatocytes.

Xylitol is known to cause hepatic ATP catabolism by inducing the trapping of Pi in the form of glycerol 3-P as a consequence of an increase in the NADH:NAD+ ratio, resulting from the oxidation of xylitol to D-xylulose. The question was therefore raised whether D-xylulose also depletes hepatic ATP. In isolated rat hepatocytes, 5 mM D-xylulose decreased ATP by 80% within 5 min compared to 40% with 5 mM xylitol. Intracellular Pi decreased by 70% within the same time interval with both compounds, but was restored three-fold faster with D-xylulose. The rate of utilization of D-xylulose reached 5 mumol.min-1.g-1 of cells, as compared with 1.5 for xylitol, indicating that reduction of xylitol into D-xylulose is a rate-limiting step in the metabolism of the polyol. D-Xylulose barely modified the concentration of glycerol 3-P but increased xylulose 5-P from 0.02 to 0.5 mumol/g within 5 min. The main cause of the ATP- and Pi-depleting effects of D-xylulose was found to be an accumulation of sedoheptulose 7-P from a basal value of 0.1 to 5 mumol/g of cells after 10 min. Ribose 5-P increased from 0.03 to 0.5 mumol/g at 5 min. Ribose 1-P also accumulated, albeit outside of the cells. This extracellular accumulation can be explained by the release of intracellular purine nucleoside phosphorylase from damaged hepatocytes acting on inosine that had diffused out of the cells. Smaller increases in the concentrations of sedoheptulose 7-P and pentose phosphates were recorded after incubations of the cells with xylitol.

Adenosine Triphosphate↗

Enzymatic and Microbial Preparation of d-Xylulose from d-Xylose.

A high-d-xylulose mixture (d-xylose-d-xylulose = 33:67) was prepared from the cold ethanol extract of preisomerized d-xylose solution (d-xylose-d-xylulose = 77:23). Fusarium oxysporum f. sp. lini and Aspergillus niger were demonstrated to preferentially utilize d-xylose in the mixture of d-xylose and d-xylulose. Chromatographically pure d-xylulose was thus obtained in 90% yield. A high-d-xylulose mixture was also incubated with Rhodotorula toruloides, Klebsiella pneumoniae, Candida utilis, or Mucor rouxii.d-Xylose and d-xylulose were simultaneously consumed. When borate was added to the mixture, a d-xylulose-borate complex was formed, and it could be used to protect d-xylulose from being utilized.

Journal Article↗

Xylulose fermentation by Saccharomyces cerevisiae and xylose-fermenting yeast strains.

Xylulose fermentation by four strains of Saccharomyces cerevisiae and two strains of xylose-fermenting yeasts, Pichia stipitis CBS 6054 and Candida shehatae NJ 23, was compared using a mineral medium at a cell concentration of 10 g (dry weight)/l. When xylulose was the sole carbon source and fermentation was anaerobic, S. cerevisiae ATCC 24860 and CBS 8066 showed a substrate consumption rate of 0.035 g g cells-1 h-1 compared with 0.833 gg cells-1 h-1 for glucose. Bakers' yeast and S. cerevisiae isolate 3 consumed xylulose at a much lower rate although they fermented glucose as rapidly as the ATCC and the CBS strains. While P. stipitis CBS 6054 consumed both xylulose and glucose very slowly under anaerobic conditions, C. shehatae NJ 23 fermented xylulose at a rate of 0.345 gg cells-1 h-1, compared with 0.575 gg cells-1 h-1 for glucose. For all six strains, the addition of glucose to the xylulose medium did not enhance the consumption of xylulose, but increased the cell biomass concentrations. When fermentation was performed under oxygen-limited conditions, less xylulose was consumed by S. cerevisiae ATCC 24860 and C. shehatae NJ 23, and 50%- 65% of the assimilated carbon could not be accounted for in the products determined.

Anaerobiosis↗

Xylulose fermentation by mutant and wild-type strains of Zygosaccharomyces and Saccharomyces cerevisiae.

Anaerobic xylulose fermentation was compared in strains of Zygosaccharomyces and Saccharomyces cerevisiae, mutants and wild-type strains to identify host-strain background and genetic modifications beneficial to xylose fermentation. Overexpression of the gene (XKS1) for the pentose phosphate pathway (PPP) enzyme xylulokinase (XK) increased the ethanol yield by almost 85% and resulted in ethanol yields [0.61 C-mmol (C-mmol consumed xylulose)(-1)] that were close to the theoretical yield [0.67 C-mmol (C-mmol consumed xylulose)(-1)]. Likewise, deletion of gluconate 6-phosphate dehydrogenase (gnd1delta) in the PPP and deletion of trehalose 6-phosphate synthase (tps1delta) together with trehalose 6-phosphate phosphatase (tps2delta) increased the ethanol yield by 30% and 20%, respectively. Strains deleted in the promoter of the phosphoglucose isomerase gene (PGI1) - resulting in reduced enzyme activities - increased the ethanol yield by 15%. Deletion of ribulose 5-phosphate (rpe1delta) in the PPP abolished ethanol formation completely. Among non-transformed and parental strains S. cerevisiae ENY. WA-1A exhibited the highest ethanol yield, 0.47 C-mmol (C-mmol consumed xylulose)(-1). Other non-transformed strains produced mainly arabinitol or xylitol from xylulose under anaerobic conditions. Contrary to previous reports S. cerevisiae T23D and CBS 8066 were not isogenic with respect to pentose metabolism. Whereas, CBS 8066 has been reported to have a high ethanol yield on xylulose, 0.46 C-mmol (C-mmol consumed xylulose)(-1) (Yu et al. 1995), T23D only formed ethanol with a yield of 0.24 C-mmol (C-mmol consumed xylulose)(-1). Strains producing arabinitol did not produce xylitol and vice versa. However, overexpression of XKS1 shifted polyol formation from xylitol to arabinitol.

Anaerobiosis↗

Activation of a cryptic gene encoding a kinase for L-xylulose opens a new pathway for the utilization of L-lyxose by Escherichia coli.

A silent gene encoding a kinase that specifically phosphorylates L-xylulose was activated and rendered constitutive in mutant cells of Escherichia coli. L-Xylulose kinase was purified to homogeneity and found to be a dimer of two subunits of 55 kDa, highly specific for L-xylulose with a Km of 0.8 mM, a Vmax of 33 mumol/min/mg, and an optimum pH of 8.4. Physical (thin layer chromatography) and spectroscopic (nuclear magnetic resonance and optical rotation) characterization of the product of L-xylulose kinase indicated that the enzyme phosphorylated the sugar at position 5. The gene encoding L-xylulose kinase was mapped in the 80.2 min region of the chromosome by conjugation and transduction. Cloning and comparison of the restriction map with the Kohara map (Kohara, Y., Akiyame, K., and Isono, K. (1987) Cell 50, 495-501) located the gene between positions 3963 and 3965 kilobases. The molecular and functional features of L-xylulose kinase together with the location of the corresponding gene indicate that this enzyme did not derive from mutation of any other known kinase. The new kinase opens a route for the utilization of L-lyxose through the action of rhamnose permease, rhamnose isomerase, and the phosphorylation of the L-xylulose formed to L-xylulose 5-phosphate, which is then introduced into the pentose phosphate pathway for subsequent metabolism.

Cloning, Molecular↗

A mechanism for fatty acid inhibition of glucose utilization in liver. Role of xylulose 5-P.

The glucose-stimulated rise in Fru-2,6-P2 in liver results from xylulose 5-P activation of a specific protein phosphatase 2A which dephosphorylates Fru-6-P,2-kinase:Fru-2,6-bisphosphatase (Nishimura, M., and Uyeda, K. (1994) J. Biol. Chem. 269, 26100-26106). In order to determine the role of xylulose 5-P in regulating Fru-2, 6-P2 in liver, the effect of fatty acids, various hexoses, and hormones was examined in perfused rat liver and in intact rats. When 24-h starved rat livers were perfused with acetate, butyrate, or propionate, Fru-2,6-P2 and xylulose 5-P decreased to the same extent and at similar rates. The activity ratios of the kinase and the phosphatase changed in a reciprocal manner, indicating that the phosphorylated form of the enzyme was increased by the fatty acids perfusion. The fatty acids caused the similar changes in the metabolites and the phosphorylation state of the bifunctional enzyme in livers of fed animals. Fructose, galactose, or mannose perfusion in starved rat liver increased both Fru-2,6-P2 and xylulose 5-P and converted the bifunctional enzyme to the dephospho form. Both the Fru-2,6-P2 and xylulose 5-P levels in rats fed a high fat diet decreased over 50% compared to that in control rats. These results indicated a close correlation between Fru-2,6-P2 and xylulose 5-P levels and the phosphorylation state of fructose 6-P, 2-kinase:fructose 2,6-bisphosphatase. Fatty acid inhibition of glucose metabolism can be explained by a decrease in xylulose 5-P, which lowers xylulose 5-P-activated protein phosphatase 2A activity, resulting in more phosphorylated form of the bifunctional enzyme and consequently lower Fru-2,6-P2.

Animals↗

Growth of yeasts on D-xylulose 1.

Nine of eleven yeasts of different species or genera grew in the presence of air on the intermediate of D-xylose catabolism, D-xylulose (D-threo-pentulose). Growth on this substrate was efficient as judged by the optical density in stationary phase being generally similar to that after growth on glucose. Yeasts which grew on D-xylose also did so on D-xylulose, but among those which grew are included several which utilise neither D-xylose nor xylitol: Saccharomyces cerevisiae, Saccharomyces carlsbergensis, and Schizosaccharomyces pombe. Since catabolism of a sugar generally requires an initial phosphorylation step, growth of these strains suggests that they contain an enzyme which can function as a D-xylulose kinase. The D-xylulose-5-phosphate formed thereby is considered to enter the pentose-phosphate pathway. Glucose-grown inocula of S. carlsbergensis and Schizosaccharomyces pombe, and of several other yeasts, began to grow logarithmically when placed on D-xylulose with no apparent delay, or one which was minimal, suggesting that the D-xylulose kinase was already present in such cells, or was rapidly induced. Petites of S. cerevisiae did not grow on D-xylulose indicating that, in this species, mitochondria are involved in its utilisation.

Ascomycota↗

Elevated L-xylulose concentrations in serum: a difference between type I and type II diabetes.

L-Xylulose, which can be derived from glucose directly or from mucopolysaccharide degradation, was measured in serum samples from 61 diabetics and 42 controls. All serum samples from the controls were negative for L-xylulose. Fifteen of 30 adult-onset diabetics, in contrast to only four of 31 juvenile-onset diabetics, had detectable L-xylulose levels. This difference between adult-onset and juvenile-onset diabetics was significant at the 0.001 level. Detectability of L-xylulose in serum did not appear to be influenced by the fasting mean or peak serum concentration of glucose. Mean serum concentrations of growth hormone did not correlate with L-xylulose levels. The reason for the variation of L-xylulose between type-I and type-II diabetic subjects could not be identified. We would postulate a variation in the degradation of glycosaminoglycan. These results support the view that type-I and type-II diabetes are different diseases.

Blood Glucose↗

Effects of xylulokinase activity on ethanol production from D-xylulose by recombinant Saccharomyces cerevisiae.

AIMS: Recombinant Saccharomyces cerevisiae strains harbouring different levels of xylulokinase (XK) activity and effects of XK activity on utilization of xylulose were studied in batch and fed-batch cultures. METHODS AND RESULTS: The cloned xylulokinase gene (XKS1) from S. cerevisiae was expressed under the control of the glyceraldehyde 3-phosphate dehydrogenase promoter and terminator. Specific xylulose consumption rate was enhanced by the increased specific XK activity, resulting from the introduction of the XKS1 into S. cerevisiae. In batch and fed-batch cultivations, the recombinant strains resulted in twofold higher ethanol concentration and 5.3- to six-fold improvement in the ethanol production rate compared with the host strain S. cerevisiae. CONCLUSIONS: An effective conversion of xylulose to xylulose 5-phosphate catalysed by XK in S. cerevisiae was considered to be essential for the development of an efficient and accelerated ethanol fermentation process from xylulose. SIGNIFICANCE AND IMPACT OF THE STUDY: Overexpression of the XKS1 gene made xylulose fermentation process accelerated to produce ethanol through the pentose phosphate pathway.

Aerobiosis↗