E-MTAB-3001
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-3001 | ExpressionAtlas | 2018-06-04
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-3001-analysis-methods.tsv | Tabular | |||
| E-MTAB-3001-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-3001-configuration.xml | Xml | |||
| E-MTAB-3001-percentile-ranks.tsv | Tabular | |||
| E-MTAB-3001.condensed-sdrf.tsv | Tabular |
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Project description:The genome-wide transcriptional response of S. cerevisiae cells upon transfer to carbon-limited or carbon-limited and metformin supplemented media is investigated. DHO strain (BY4742 background) was cultivated batch-wise in SDC media at 30C and 180 rpm up to mid-exponential phase (OD600 ~ 0.6). The cells of the main culture were divided in three aliquots at the mid-exponential phase, centrifuged at 6000 rpm for 5 min, washed twice with deionized and distilled sterile water prior to their transfer to the treatment media. Treatment media comprised of SDC + 0.25% glucose for the C-lim control case and SDC +0.25%glucose + 1.66% metformin for the Met case. Control data for the reference condition (glucose limitation) is derived from E-MTAB-3001. Sample collection for transcriptional profiling was done at the 2nd hour of the transfer. The experiments were carried out in biological triplicates.
2019-07-21 | E-MTAB-6847 | biostudies-arrayexpress
Project description:The genome-wide transcriptional response of S. cerevisiae cells upon transfer to carbon-limited or metformin supplemented media is investigated. DHO strain (BY4742 background) was cultivated batch-wise in SDC media at 30C and 180 rpm up to mid-exponential phase (OD600 ~ 0.6). The cells of the main culture were divided in three aliquots at the mid-exponential phase, centrifuged at 6000 rpm for 5 min, washed twice with deionized and distilled sterile water prior to their transfer to the treatment media. Treatment media comprised of fresh SDC (2% glucose) for the control case, SDC + 0.25% glucose for the C-lim case and SDC + 1.66% metformin for the Met case. Samples collection for transcriptional profiling was done at the 2nd hour of the transfer. The experiments were carried out in biological triplicates.
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Project description:The genome-wide transcriptional response of S. cerevisiae cells upon transfer to methionine-restricted media is investigated. DHO strain (BY4742 background) was cultivated batch-wise in SDC media at 30C and 180 rpm up to mid-exponential phase (OD600 ~ 0.6). The cells of the main culture were divided in three aliquots at the mid-exponential phase, centrifuged at 6000 rpm for 5 min, washed twice with deionized and distilled sterile water prior to their transfer to the treatment media. Treatment media comprised of SDC + 0.75% methionine for the methionine-restricted case while SDC is used for the control case. Sample collection for transcriptional profiling was done at the 2nd hour of the transfer. The experiments were carried out in biological triplicates.
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Project description:Transcriptional response of S. cerevisiae to metformin treatment in carbon-limited medium
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Project description:Transcriptional profiles of S. cerevisiae strains with deletions of mth1, std1, or both were compared to that of a wild-type strain during growth on synthetic complete media with galactose as the carbon source, with the intent to understand each protein's contribution to the cells' response to glucose.
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Project description:In this study we investigated the transcriptional response of the yeast Saccharomyces cerevisiae to potassium starvation. To this end yeast cells were grown for 60 min in media without potassium or in media with a standard potassium concnetration (50 mM KCl). Using Serial Analysis of Gene Expression (SAGE)-tag sequencing the effect of potassium starvation on the transcriptome was determined.
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Project description:Metformin is a type 2 diabetes medication which extends life span across species when given from young adulthood onwards; late life effects of metformin are not well understood. Here we used C. elegans to investigate the outcome of metformin treatment initiated late in life. We found that, contrary to young age administration, old age metformin treatment interferes with energy homeostasis and shortens life span by aggravating age-associated mitochondrial dysfunction. Nematode mutants defective in mitochondrial respiration, mitochondrial biogenesis and mitochondrial quality control were highly susceptible to metformin killing already at young age while insulin receptor deficient nematodes carrying healthier mitochondria were protected from late life metformin toxicity. In the mammalian cell culture model of replicative senescence metformin killing correlated with loss of mitochondrial membrane potential and strong reduction of systemic ATP levels. Reduced ATP levels and depletion of lipid stores consistent with energy deficit were observed also in nematodes following late life metformin treatment. At the molecular level young animals responded to metformin by inducing adaptive stress responses and longevity-assurance pathways while old nematodes demonstrated a protein expression signature consistent with lipid turnover and energy deficit. Ectopic ATP supplementation was sufficient to alleviate metformin toxicity in human skin fibroblasts highlighting the key contribution of energy deficit to the detrimental effect of metformin. Also, co-exposure with rapamycin, known to stabilize cellular ATP levels under conditions of mitochondrial failure, significantly reduced metformin-inflicted lethality in both cells and old animals. In summary we uncovered a novel negative synergism between metformin treatment and mitochondrial dysfunction which gains importance late in life and may limit therapeutic benefits of metformin for older patients; these side effects can partially be overcome by co-treatment with agents stabilizing cellular ATP levels such as rapamycin.
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Project description:<p class='ql-align-justify'>Several studies indicated anti-cancer effects of metformin in liver cancer. This was attributed to the activation of LKB-AMPK axis, which is associated with anti-hyperglycaemic effect and cytotoxicity. However, glucose- and central carbon-independent effects of metformin and their reversibility remain unexplored. The dose-dependent effects of metformin on HepG2 cells were examined in presence and absence of glucose. The longitudinal evolution of metabolome was analyzed along with gene and protein expression as well as their correlations with and reversibility of cellular phenotype and metabolic signatures. Metformin concentrations ≤2.5mM were found to be non-cytotoxic but anti-proliferative irrespective of presence of glucose. Mitochondrial impairment along with derangement of one-carbon, glutathione and polyamine metabolism was associated with non-cytotoxic metformin treatment irrespective of glucose supplementation. Depletion of pantothenic acid, upregulation of fatty acid desaturation and downregulation of essential amino acid uptake, metabolism and purine salvage were identified as novel glucose-independent effects of metformin. These were significantly correlated with cMyc expression and reduction in proliferation. Rescue experiments established reversibility upon metformin withdrawal and tight association between proliferation, metabotype and cMyc expression. Taken together, derangement of novel glucose-independent pathways and concomitant cMyc downregulation coordinately contribute to anti-proliferative effect, which is reversible and may influence therapeutic utility of metformin.</p>
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Project description:We investigated the transcriptional response of yeast Saccharomyces cerevisiae bmh1 and bmh2 deletion mutants to potassium starvation. To this end yeast strains were grown for 60 min in media without potassium or in media with a standard potassium concentration (50 mM KCl). Using Serial Analysis of Gene Expression (SAGE)-tag sequencing the effect of potassium starvation on the transcriptome was determined. This study is a follow-up of our previous study (Anemaet IG and van Heusden GPH. 2014. BMC Genomics:1040)( GEO accession number GSE57093).
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