Transcription profiling of E. coli treated with CHIR-090, an inhibitor of lipid A biosythesis
Ontology highlight
ABSTRACT:
ORGANISM(S): Escherichia coli
SUBMITTER: Matthew Wilmer Frank
PROVIDER: E-GEOD-18623 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:CHIR-090 is an inhibitor of lipid A biosytnesis. CHIR-090 treatment on E. coli sinificantly increased the expression of fatty acid biosythesis gene fabA and fabB. Keywords: Inhibition response
2009-10-20 | GSE18623 | GEO
Project description:Investigation of whole genome gene expression level changes in a E. coli fatty acid overproducing strain with or without heterologous expression of the M. luteus FabH. The strain expressing M. luteus FabH produces more methyl ketones. This study will be further described in Goh, E.B., E.E.K. Baidoo, J.D. Keasling, and H.R. Beller. Engineering of bacterial methyl ketone synthesis for biofuels. A 11 microarray study using total RNA recovered from six separate control cultures of Escherichia coli K-12 DH1 fatty acid overproducing strain with empty vector and five separate cultures of test strain, Escherichia coli K-12 DH1 fatty acid overproducing strain with vector overexpressing M. luteus FabH. Each chip measures the expression level of 4,254 genes from Escherichia coli K-12 with eight 60-mer probe pairs (PM/MM) per gene, with 2-fold technical redundancy.
2012-01-26 | E-GEOD-32561 | biostudies-arrayexpress
Project description:Alteration in metabolic repertoire is commonly associated with resistance phenotype. Although it’s a common phenotype, not much efforts have been undertaken to design effective strategies to target the metabolic drift in such cancerous cells and especially with drug resistant properties. In our study, we identified that drug resistant AML cell line HL-60/MX2 do not follow classical Warburg effect, instead these cells exhibit drastically low levels of aerobic glycolysis. Biochemical analysis confirms reduced glucose consumption and lactic acid production by resistant population with no differences in glutamine consumption. Raman spectroscopy revealed increased lipid and cytochrome content in resistant cells which were also visualized in the form of lipid droplets by Raman mapping, electron microscopy and lipid specific staining. Gene set enrichment analysis data from both the cell lines revealed significant enrichment of lipid metabolic pathways in HL-60/MX2 cells. Further drug resistant cells possess higher mitochondrial activity and increased OXPHOS suggested the role of fatty acid metabolism as energy source which was confirmed by increased rate of fatty acid oxidation. Pharmacological inhibition of fatty acid oxidation using Etomoxir affected the colony formation ability of resistant cells and inhibition of OXPHOS using Antimycin-A increased the sensitivity of resistant cells to chemotherapeutic drug, demonstrating requirement of fatty acid metabolism and increased dependency on OXPHOS by resistant leukemic cells for tumorigenicity.
2021-01-01 | E-MTAB-8981 | biostudies-arrayexpress
Project description:Interventions: omega-3 fatty acid supplement PO 6.5g/day(including lipid 4g and omega-3 fatty acid 2.2g)
No supplement taking
Primary outcome(s): Reduction of systemic inflammatory response, especially C-reactive protein
Study Design: Parallel Non-randomized
| 2647732 | ecrin-mdr-crc
Project description:Canonical Wnt and Nodal signaling are both required for induction of the primitive streak (PS), which guides organization of the early embryo. The Wnt effector β-catenin is thought to function in these early lineage specification decisions via transcriptional activation of Nodal signaling. Here, we demonstrate a broader role for β-catenin in PS formation by analyzing its genome-wide binding in a human embryonic stem cell model of PS induction. β-catenin occupies regulatory regions in numerous PS and neural crest genes, and direct interactions between β-catenin and the Nodal effectors SMAD2/3 are required at these regions for PS gene activation. Furthermore, OCT4 binding in proximity to these sites is likewise required for PS induction, suggesting a collaborative interaction between β-catenin and OCT4. Induction of neural crest genes by β-catenin is repressed by SMAD2/3, ensuring proper lineage specification. This study provides mechanistic insight into how Wnt signaling controls early cell lineage decisions. Examination of β-catenin binding in hESC incubated in media control (RPMI), media containing CHIR or CHIR+SB for 6h and analyzed by ChIP-sequencing
2015-03-31 | E-GEOD-58476 | biostudies-arrayexpress
Project description:Comparative analysis of changes in gene and protein expression and fatty acid profiles between Escherichia coli K-12 MG1655 ΔfadD ΔaraBAD expressing an acyl-acyl carrier protein thioesterase from Umbellularia californica (BTE) or a non-functional mutant thioesterase (BTE-H204A) to determine the functional basis for losses in cell viability, membrane integrity, or other stresses and metabolic perturbations that may be present. New hypotheses obtained from the study will assist in metabolic engineering efforts of improved strains exhibiting higher fatty acid yields and productivities. Cultures of fatty acid overproducing (BTE-expressing) and negative control (non-functional BTE-H204A-expressing) strains of Escherichia coli K-12 MG1655 delta-fadD delta-araBAD (deficient in beta-oxidation and L-arabinose catabolism) were sampled under two different sets of media/induction/antibiotic conditions. These conditions were shake flasks at 37C, 250 rpm shaking, in EZ rich defined medium supplemented with 0.2% glucose and 0.01 mM biotin (EZglu), and in fermentors at 37C with controlled air sparging, agitation, and pH in EZ rich defined medium supplemented with 0.4% glycerol and 0.01 mM biotin (EZgly). Two strains were analyzed in the EZglu experiment, the background strain harboring either pTrc99A-BTE (fatty acid overproducing) or pTrc99A-BTE-H204A (control phenotype). Three strains were analyzed in the EZgly experiment, with the background strain haboring either pBAD35-BTE and pBAD33 (fatty acid overproducing), pBAD35-BTE and pBAD33-ACC (fatty acid overproducing, ACC are the 4 subunits of E. coli K-12 acetyl-CoA carboxylase expressed as an artificial operon accDABC in plasmid pBAD33), and pBAD35-BTE-H204A and pBAD33 (control phenotype). RNA was extracted from harvested cell pellets from biological triplicates (EZglu) or biological duplicates (EZgly) of each strain at three different sampling times as defined in each sample description. Due to a hybridization or scanning problem, biological duplicates rather than triplicates were analyzed at the mid-stationary phase sampling point in the EZglu experiment for the control strain harboring pTrc99A-BTE-H204A. Multiple technical replicates at either the hybridization or sample level were analyzed from the biological duplicates of the fermentor experiment. The form of technical replicate (sample or hybridization) is specified in each EZgly sample description.
2011-05-24 | E-GEOD-29424 | biostudies-arrayexpress
Project description:The role of peroxisome proliferator-activated receptor M-NM-4 (PPARM-NM-4) activation on global gene expression and mitochondrial fuel utilization were investigated in human myotubes. Only 21 genes were up-regulated and 3 genes were down-regulated after activation by the PPARM-NM-4 agonist GW501516. Pathway analysis showed up-regulated mitochondrial fatty acid oxidation, TCA cycle and cholesterol biosynthesis. GW501516 increased oleic acid oxidation and mitochondrial oxidative capacity by 2-fold. Glucose uptake and oxidation were reduced, but total substrate oxidation was not affected, indicating a fuel switch from glucose to fatty acid. Cholesterol biosynthesis was increased, but lipid biosynthesis and mitochondrial content were not affected. This study confirmed that the principal effect of PPARM-NM-4 activation was to increase mitochondrial fatty acid oxidative capacity. Our results further suggest that PPARM-NM-4 activation reduced glucose utilization through a switch in mitochondrial substrate preference by up-regulating pyruvate dehydrogenase kinase isozyme 4 and genes involved in lipid metabolism and fatty acid oxidation. Keywords: Expression profiling by array Human myotubes from four donors were exposed to a PPARM-NM-4 agonist or control for 96 h after which gene expression was profiled.
2014-05-23 | E-GEOD-40789 | biostudies-arrayexpress
Project description:The role of peroxisome proliferator-activated receptor δ (PPARδ) activation on global gene expression and mitochondrial fuel utilization were investigated in human myotubes. Only 21 genes were up-regulated and 3 genes were down-regulated after activation by the PPARδ agonist GW501516. Pathway analysis showed up-regulated mitochondrial fatty acid oxidation, TCA cycle and cholesterol biosynthesis. GW501516 increased oleic acid oxidation and mitochondrial oxidative capacity by 2-fold. Glucose uptake and oxidation were reduced, but total substrate oxidation was not affected, indicating a fuel switch from glucose to fatty acid. Cholesterol biosynthesis was increased, but lipid biosynthesis and mitochondrial content were not affected. This study confirmed that the principal effect of PPARδ activation was to increase mitochondrial fatty acid oxidative capacity. Our results further suggest that PPARδ activation reduced glucose utilization through a switch in mitochondrial substrate preference by up-regulating pyruvate dehydrogenase kinase isozyme 4 and genes involved in lipid metabolism and fatty acid oxidation. Keywords: Expression profiling by array
2014-05-23 | GSE40789 | GEO
Project description:Mesenchymal stem/stromal cells (MSCs) with immunosuppressive properties are increasingly used in advanced cellular therapies. Since the clinical use of hMSCs demands sequential cell expansions, we studied the effect of cell doublings on the phospholipid profile as well as functionality of human bone marrow mesenchymal stem cells (hBMSCs). In addition to the structural role of phospholipids in cell membranes, they provide precursors for eicosanoids and other signalling lipids modulating cellular functions. The hBMSCs, harvested from young adult and old donors (n=5 for both), showed clear compositional changes during cultivation, seen at the level of lipid classes, lipid species and acyl chains. As the main finding at the lipid class level, the ratio of phosphatidylinositol to phosphatidylserine was increased towards the late passage samples. In the species profiles, arachidonic acid (AA) containing species of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) clearly accumulated, while the species containing monounsaturated fatty acids decreased. This was related with an increase of AA, a major n-6 polyunsaturated fatty acid (n-6PUFA), in the total fatty acid pool of the cells, which happened at the expense of n-3PUFAs, especially docosahexenoic acid (DHA). Using hBMSCs from four of the young adult donors and four of the old donors, we found that gene expression of several enzymes involved in fatty acid metabolism (such as FADS1, FADS2 and SCD) was altered. The expression of genes related to the regulation of cell cycle, senescence and immunomodulation were altered. Our findings suggest that multistep expansion of hBMSCs alters their fatty acid metabolism and membrane phospholipid composition, which affects lipid signalling and eventually the immune function of the cells. Cultured undifferentiated bone marrow-derived MSCs from old and young donors. Biological replicates: 4 old donors and 4 young donors, passages 4 and 8 from each.
2013-04-05 | E-GEOD-39035 | biostudies-arrayexpress
Project description:Sirtuins are a family of protein deacetylases, deacylases, and ADP-ribosyltransferases that regulate life span, control the onset of numerous age-associated diseases, and mediate metabolic homeostasis. We have uncovered a novel role for the mitochondrial sirtuin SIRT4 in the regulation of hepatic lipid metabolism during changes in nutrient availability. We show that SIRT4 levels decrease in the liver during fasting and that SIRT4 null mice display increased expression of hepatic peroxisome proliferator activated receptor (PPAR ) target genes associated with fatty acid catabolism. Accordingly, primary hepatocytes from SIRT4 knockout (KO) mice exhibit higher rates of fatty acid oxidation than wild-type hepatocytes, and SIRT4 overexpression decreases fatty acid oxidation rates. The enhanced fatty acid oxidation observed in SIRT4 KO hepatocytes requires functional SIRT1, demonstrating a clear cross talk between mitochondrial and nuclear sirtuins. Thus, SIRT4 is a new component of mitochondrial signaling in the liver and functions as an important regulator of lipid metabolism. SIRT4 knockout (KO) and wild-type (WT) littermates (male; n 6 per genotype; 7- to 8-month-old littermates) were sacrificed after a 16-h overnight fast. Samples were individually hybridized on Affymetrix Mouse Genome 430 2.0 GeneChips by the Biopolymers Facility (Harvard Medical School).
2014-03-28 | E-GEOD-56321 | biostudies-arrayexpress