Transcriptional reponse of yeast glucose sensing pathway mutants to glucose addition
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA721192 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:While much is known about glucose metabolism in yeast, less is known about the receptors and signaling pathways that indicate glucose availability. Here we compared wildtype and 16 mutants in yeast glucose sensing pathway for their transcriptomics profiles in 0.05% glucose vs 10 min after glucose addition to 2% glucose. With these data, we were able to define various roles of glucose sensing pathway components. We demonstrated that the G protein-coupled receptor (Gpr1/Gpa2) directed early events in glucose utilization, the transceptors (SNF3/RGT2) regulated subsequent processes and downstream products of glucose metabolism. Whereas the large G protein transmits the signal from its cognate receptor, Ras2 (but not Ras1) integrates responses from both receptor pathways. We also determined the relative contributions of the Gα (Gpa2) and Gβ (Asc1) protein subunits to glucose-initiated processes in yeast. We determined that Gpa2 is primarily involved in regulating carbohydratesugar metabolism while Asc1 is primarily involved in amino acid metabolism. Both proteins are involved in regulating purine metabolism. Collectively, our analysis reveals the molecular basis for glucose detection and the earliest events of glucose-dependent signal transduction in yeast.
2021-06-09 | GSE171846 | GEO
Project description:We assessed the impact of glucose transporter Glut2 gene inactivation in adult mouse liver (LG2KO mice). This suppressed hepatic glucose uptake but not glucose output. In the fasted state, expression of carbohydrate responsive element-binding protein (ChREBP) and its glycolytic and lipogenic target genes was abnormally elevated. Feeding, energy expenditure, and insulin sensitivity were identical in LG2KO and control mice. Glucose tolerance was normal early after Glut2 inactivation but intolerance developed at later time. This was caused by progressive impairment of glucose-stimulated insulin secretion even though beta-cell mass and insulin content remained normal. Liver transcript profiling revealed a coordinate down-regulation of cholesterol biosynthesis genes in LG2KO mice. This was associated with reduced hepatic cholesterol in fasted mice and a 30 percent reduction in bile acid production. We showed that chronic bile acids or FXR agonist treatment of primary islets increases glucose-stimulated insulin secretion, an effect not seen in islets from fxr-/- mice. Collectively, our data show that glucose sensing by the liver controls beta-cell glucose competence, through a mechanism that likely depends on bile acid production and action on beta-cells. three replicates each of ps_ctrl_refed, ps_tamox_refed, ps_ctrl_fasted, ps_tamox_fasted
2013-01-18 | E-GEOD-43581 | biostudies-arrayexpress
Project description:Skeletal muscle is a major site of postprandial glucose disposal. Inadequate insulin action in this tissue contributes to hyperglycemia in type 1 and type 2 diabetes. While glucose is known to stimulate insulin secretion by pancreatic b cells, whether it directly engages nutrient-sensing pathways in skeletal muscle to regulate glucose metabolism remains largely unexplored. Here we identified the Baf60c-Deptor-AKT pathway as a target of muscle glucose sensing that augments insulin action in skeletal myocytes. Genetic activation of this pathway improves postprandial glucose disposal in mice, whereas the muscle-specific ablation impaired insulin action and led to glucose intolerance. Mechanistically, glucose triggers a rapid calcium response in myocytes that acts on the class IIa histone deacetylase HDAC5, leading to Baf60c induction and insulin-independent AKT activation. The pathway is engaged by the anti-diabetic drugs sulfonylureas, suggesting that its therapeutic activation may have beneficial effects on glycemic control in diabetes. We used microarrays to elucidate the role of of Baf60c in transcriptional regulation by glucose in skeletal myocytes.
2017-04-20 | GSE79925 | GEO
Project description:We assessed the impact of glucose transporter Glut2 gene inactivation in adult mouse liver (LG2KO mice). This suppressed hepatic glucose uptake but not glucose output. In the fasted state, expression of carbohydrate responsive element-binding protein (ChREBP) and its glycolytic and lipogenic target genes was abnormally elevated. Feeding, energy expenditure, and insulin sensitivity were identical in LG2KO and control mice. Glucose tolerance was normal early after Glut2 inactivation but intolerance developed at later time. This was caused by progressive impairment of glucose-stimulated insulin secretion even though beta-cell mass and insulin content remained normal. Liver transcript profiling revealed a coordinate down-regulation of cholesterol biosynthesis genes in LG2KO mice. This was associated with reduced hepatic cholesterol in fasted mice and a 30 percent reduction in bile acid production. We showed that chronic bile acids or FXR agonist treatment of primary islets increases glucose-stimulated insulin secretion, an effect not seen in islets from fxr-/- mice. Collectively, our data show that glucose sensing by the liver controls beta-cell glucose competence, through a mechanism that likely depends on bile acid production and action on beta-cells.
2013-01-18 | GSE43581 | GEO
Project description:B. thetaiotaomicron was grown in a batch culture fermenter containing tryptone media. Glucose (final concentration 0.2%) was added at OD600 = 0.3. Samples were taken immediately before and 60 minutes after addition. Keywords: time course
2006-09-01 | GSE5274 | GEO
Project description:A nutrient sensing transition at birth triggers glucose-stimulated insulin secretion
| PRJNA613929 | ENA
Project description:It has been strongly argued that plant cells should have a means of sensing sugars at the cell surface, so that extracellular and intracellular sugars can be sensed separately and their metabolism coordinated (Lalonde et al., Plant Cell, 11, 707-26, 2000). There is good evidence for an intracellular hexokinase-dependent pathway of hexose sensing in plants, but very little evidence for a hexokinase-independent signalling pathway, such as that provided by SNF3 or RGT2 in yeast. Many papers on sugar sensing in plants cite work from two laboratories as evidence for hexokinase-independent hexose signalling in plants. The first is that in which cell-wall invertase and sucrose synthase genes were induced by treatment of a Chenopodium suspension culture with 30 mM 6-Deoxyglucose (6DOG) for 24 h (Roitsch et al., Plant Physiol 108, 285-294, 1995; Godt et al., J. Plant Physiol 146, 231-238, 1995). The second is that in which a patatin transgene in Arabidopsis was shown to be weakly induced by growth over several days on a mixture of 30 mM glucose plus 30 mM 3-O-methylglucose (3OMG), but strongly induced by growth on 30 mM Glc plus 90 mM 3OMG (Martin et al., Plant J, 11, 53-62, 1997). We are not aware of any examples of Arabidopsis genes which respond to 6DOG or 3OMG yet this is an area of wide significance. Identification of such a gene would help to establish if a hexokinase-independent signalling system operates in plants, and would provide a basis for establishment of a genetic screen for mutants, using the gene promoter linked to a reporter such as luciferase. The aim of this proposal is to discover any genes which are either activated or repressed by glucose AND by 3OMG and/or 6DOG, but not by mannitol (an osmotic control). The use of both 3OMG and 6DOG will help to identify non-specific effects of either. All substrates will first be analysed by HPLC to confirm that they are pure. Arabidopsis Col-0 seedlings will be grown in vitro for 7 days in the absence of sugars, then treated with 30 mM glucose or glucose analogue for 8 h (these conditions are based on concentrations and time courses of Roitsch et al.). RNA will then be isolated from multiple independent plates to minimise biological variation. Experimenter name = Dorthe Villadsen Experimenter phone = 0131 650 5318 Experimenter fax = 0131 650 5392 Experimenter address = Institute of Cell and Molecular Biology Experimenter address = University of Edinburgh Experimenter address = The King_s Buildings Experimenter address = Mayfield Road Experimenter address = Edinburgh Experimenter zip/postal_code = EH9 3JH Experimenter country = UK Keywords: growth_condition_design
2007-01-08 | GSE5723 | GEO
Project description:It has been strongly argued that plant cells should have a means of sensing sugars at the cell surface, so that extracellular and intracellular sugars can be sensed separately and their metabolism coordinated (Lalonde et al., Plant Cell, 11, 707-26, 2000). There is good evidence for an intracellular hexokinase-dependent pathway of hexose sensing in plants, but very little evidence for a hexokinase-independent signalling pathway, such as that provided by SNF3 or RGT2 in yeast. Many papers on sugar sensing in plants cite work from two laboratories as evidence for hexokinase-independent hexose signalling in plants. The first is that in which cell-wall invertase and sucrose synthase genes were induced by treatment of a Chenopodium suspension culture with 30 mM 6-Deoxyglucose (6DOG) for 24 h (Roitsch et al., Plant Physiol 108, 285-294, 1995; Godt et al., J. Plant Physiol 146, 231-238, 1995). The second is that in which a patatin transgene in Arabidopsis was shown to be weakly induced by growth over several days on a mixture of 30 mM glucose plus 30 mM 3-O-methylglucose (3OMG), but strongly induced by growth on 30 mM Glc plus 90 mM 3OMG (Martin et al., Plant J, 11, 53-62, 1997). We are not aware of any examples of Arabidopsis genes which respond to 6DOG or 3OMG yet this is an area of wide significance. Identification of such a gene would help to establish if a hexokinase-independent signalling system operates in plants, and would provide a basis for establishment of a genetic screen for mutants, using the gene promoter linked to a reporter such as luciferase. The aim of this proposal is to discover any genes which are either activated or repressed by glucose AND by 3OMG and/or 6DOG, but not by mannitol (an osmotic control). The use of both 3OMG and 6DOG will help to identify non-specific effects of either. All substrates will first be analysed by HPLC to confirm that they are pure. Arabidopsis Col-0 seedlings will be grown in vitro for 7 days in the absence of sugars, then treated with 30 mM glucose or glucose analogue for 8 h (these conditions are based on concentrations and time courses of Roitsch et al.). RNA will then be isolated from multiple independent plates to minimise biological variation. Experimenter name = Dorthe Villadsen; Experimenter phone = 0131 650 5318; Experimenter fax = 0131 650 5392; Experimenter address = Institute of Cell and Molecular Biology; Experimenter address = University of Edinburgh; Experimenter address = The King_s Buildings; Experimenter address = Mayfield Road; Experimenter address = Edinburgh; Experimenter zip/postal_code = EH9 3JH; Experimenter country = UK Experiment Overall Design: 6 samples were used in this experiment
2008-06-14 | E-GEOD-5723 | biostudies-arrayexpress
Project description:Previous results suggest that Bmh might inhibit the activity of the transcription factor Adr1 after binding to Adr1-dependent promoters. In a strain lacking the two major histone deacetylases, Hda1 and Rpd3 (hdac∆), Adr1 is bound to its target promoters recruiting what appears to be an inactive RNA ploymerase II preinitiation complex (PIC). To determine whether Bmh activity inhibits this inactive PIC and the generality of this effect on glucose-repressed gene expression, the mRNA profiles of wild type, bmh mutant, hdac mutant, and bmh hdac mutant cells grown in high glucose medium were compared.
2013-01-15 | GSE40116 | GEO
Project description:There are two principal mechanisms underlie sugar perception and signal transduction in biological systems. Direct sensing and signaling is triggered by sugar direct binding sensors such as Hexokiase 1 (HXK1) with a broad range of affinity and specificity, and indirect sensing signaling via a variety of energy and metabolite sensor, such as Target of Rapamycin (TOR). To investigate the intertwined interaction between glucose and plant hormones ethylene, the transcriptome regulated by ethylene, glucose-TOR, and glucose-HXK1 were analyzed and compared. Our results unexpectedly revealed a deep antagonistic interaction between glucose-TOR-energy signaling and the plant stress hormone ethylene.
2020-09-08 | GSE104146 | GEO