Comparison of gene expression of WT and PerM mutant M. tuberculosis H37Rv grown in high and reduced magnesium
Ontology highlight
ABSTRACT:
ORGANISM(S): Mycobacterium tuberculosis
SUBMITTER: Sabine Ehrt
PROVIDER: E-GEOD-57263 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:M. tuberculosis membrane protein PerM is required for persistence in chronic mouse infection. In vitro, the perM mutant requires increased magnesium for replication and survival, with elongation and lysis in low-magnesium media. To gain insight into the function of PerM, we compared the transcriptomes of wt and perM mutant Mtb grown in high (2000 μM) and reduced (250 μM) Mg2+ in three independent experiments. Transcriptome analysis of the perM mutant grown in reduced magnesium revealed upregulation of cell division and cell wall biosynthesis genes.
2015-01-05 | GSE57263 | GEO
Project description:Important remodeling of the extracellular matrix is a hallmark of corneal wound healing. Besides the massive secretion of fibronectin (FN) that characterizes the early step of that process, alterations in the secretion of collagens also occurs as part of this wound healingresponse. In this study, we examined whether expression of the gene encoding the M-NM-15 subunit from the FN binding integrin M-NM-15M-NM-21 changes as corneal epithelial cells (CECs) are cultured in the presence of collagens. Responsiveness of the M-NM-15 gene toward collagen was determined by transfection of recombinant plasmids bearing the CAT reporter gene under the control of various segments from the human M-NM-15 promoter into primary cultured rabbit (RCECs) and human (HCECs) CECs cultured on BSA or on collagens. Electrophoretic mobility shift assays (EMSAs) and Western blot analyses were used to monitor both the DNA binding and expression of the transcription factors required to ensure basal transcription of the M-NM-15 gene. The influence collagens on the patterns of genes expressed by HCECs was also studied be gene profiling on microarrays. All collagen types repressed the transcriptional activity directed by the full-length M-NM-15 promoter/CAT construct in confluent CECs. A moderate increase in M-NM-15 promoter activity was observed in subconfluent RCECs grown on CIV but not on CI. These collagen-dependent regulatory influences also correlated with alterations in either the expression or the DNA binding of the transcription factors Sp1/Sp3, NFI and AP-1 that ensure basal transcription of the M-NM-15 gene. Gene profiling on microarray revealed that CI more profoundly alter the pattern of genes expressed by HCECs than what is observed with CIV. Collagens considerably suppressed expression of the M-NM-15 gene in CECs at confluence suggesting that the sustained staining for CI and CIV after corneal injury may play a role in controlling adhesion to the temporary FN matrix and further differentiation of CECs into suprabasal epithelial cells through a mechanism involving the M-NM-15M-NM-21 integrin. Primary cultures of human corneal epithelial cells cultivated on BSA (number of replicates: 2), Collagen type I (number of replicates: 2) and Collagen type IV (number of replicates: 2) matrix.
2015-01-30 | E-GEOD-65421 | biostudies-arrayexpress
Project description:Two long and one truncated isoforms (termed LAP*, LAP, and LIP, respectively) of the transcription factor CCAAT enhancer binding protein beta (C/EBPM-NM-2) are expressed from a single intronless Cebpb gene by alternative translation initiation. Isoform expression is sensitive to mammalian target of rapamycin (mTOR)-mediated activation of the translation initiation machinery and relayed through an upstream open reading frame (uORF) on the C/EBPM-NM-2 mRNA. The truncated C/EBPM-NM-2 LIP, initiated by high mTOR activity, has been implied in neoplasia, but it was never shown whether endogenous C/EBPM-NM-2 LIP may function as an oncogene. In this study, we examined spontaneous tumor formation in C/EBPM-NM-2 knockin mice that constitutively express only the C/EBPM-NM-2 LIP isoform from its own locus. Our data show that deregulated C/EBPM-NM-2 LIP predisposes to oncogenesis in many tissues. Gene expression profiling suggests that C/EBPM-NM-2 LIP supports a protumorigenic microenvironment, resistance to apoptosis, and alteration of cytokine/chemokine expression. The results imply that enhanced translation reinitiation of C/ EBPM-NM-2 LIP promotes tumorigenesis. Accordingly, pharmacological restriction of mTOR function might be a therapeutic option in tumorigenesis that involves enhanced expression of the truncated C/EBPM-NM-2 LIP isoform. A cohort of C/EBPb LIP heterozygous (+/L) and wild type (+/+) mice were kept over 25 months and animals showing palpable lymphoma were sacrificed. The lymphoma developed spontaneously. For each genotype, 5 lymphoma were used for RNA preparation and gene expression profiling analysis.
2014-12-16 | E-GEOD-53770 | biostudies-arrayexpress
Project description:To identify the target gene of M-NM-^TNp63M-NM-1, in osteosarcoma cells, we performed the global gene expression profiling in SaOS- 2 cells stably overexpressing the M-NM-^TNp63M-NM-1 gene (SaOS- 2-M-NM-^TNp63M-NM-1). M-NM-^TNp63M-NM-1 target genes were identified by comparison with genes expressed from SaOS-2-EV transfected with an empty vector ( SaOS-2-EV). Total RNA was extracted from SaOS- 2-M-NM-^TNp63M-NM-1 and SaOS-2-EV cells cultured in three independent replicates for each condition. Cy3-labeled cRNA was synthesized and hybridized to Agilent human 8 x 60K microarrays. Raw data, obtained after array image analysis were normalized and used to retrieve differentially expressed genes in M-NM-^TNp63M-NM-1 overexpressing SaOS- 2 cells and genes from control SaOS-2-EV cells.
2014-02-27 | E-GEOD-54942 | biostudies-arrayexpress
Project description:In our previous work, we showed the positive effect of the magnesium and the negative effect of the copper on yeast fermentation performance. The magnesium increases the ethanol yield and a faster glucose consumption by the yeast, on the other hand, the copper provides an opposite effect in yeast under fermentation condition. Therefore, from this contrasting effect we performed the gene-wide expression analysis in the industrial yeast Saccharomyces cerevisiae JP1 under fermentation condition in order to reveal the gene expression profile upon magnesium and copper supplementation. Fermentation assays was performed with the industrial yeast S. cerevisiae JP1 in reference medium (mineral concentration balanced), in the medium supplemented with 500 mg/L of magnesium (Mg2+ medium) and in the medium supplemented with 1 mg/L of copper (Cu2+ medium).
2015-12-09 | E-GEOD-75803 | biostudies-arrayexpress
Project description:The whole rat genome microarray expression profiling of carotid artery specimen was emplyed to identify the gene expression profile before and after balloon injury. In our study, the neointimal formation of carotid arteries was apparent at day 7 and markedly increased at day 21 after balloon injury. In order to investigate the underlying mechanism of neointimal formationin in injured carotid arteries, all genes involved in signaling pathways whose expression was altered 2-fold in injured carotid arteries at day 7 and day 21 as compared to uninjured arteries were filtered out. Expression of four genes (TLR4, IRAK1, IM-NM-:BM-NM-1, IL-1M-NM-2) from TLR signaling pathway was quantified in the same RNA samples by quantitative real-time PCR, conforming that TLR signaling pathway participated in neointimal formation of carotid arteries after balloon injury. Balloon injury-induced gene expression in wistar rat was measured at day 7 and day 21 after balloon injury as compared with uninjured arteries. Two independent experiments were performed at each time (uninjured, day 7 or day 21) using different wistar rats for each experiment.
2013-06-29 | E-GEOD-48279 | biostudies-arrayexpress
Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. In addition, neurological complications, including depression and restless legs syndrome, occur in almost all CKD patients; however, the mechanisms of these neurological complications remain unclear. Here, we showed the disruptive effect of chronic renal failure in 5/6 nephrectomy mice on an immobility time of forced swim and tail suspension test and the 24-hr rhythm of Drd2 and clock gene expressions in the striatum. These disruptive effects were induced by abnormal signal transduction in high TGF-M-NM-21 expression from the kidney. Abnormal TGF-M-NM-2 signal in the striatum led to TCF7L2 expression and ID2 induced by TCF7L2 led to disruption of the 24-hr rhythm of clock gene expression. These findings suggest that neurological complications in CKD might be overcome by amelioration of the TGF-M-NM-2 signal. Differential gene expression between 5/6 nephrectomized and sham-operated mouse was measured on the brain.
2013-08-01 | E-GEOD-35134 | biostudies-arrayexpress
Project description:Acquired resistance to trastuzumab, a rationally designed HER-2 targeting antibody, remains a major hurdle in management of HER-2 positive breast cancer (HER-2+ BC) patients. Potential resistance mechanisms are numerous, derived primarily from studies where HER-2 positive cell lines are chronically exposed to trastuzumab. Recent evidence suggests a role for epithelial-mesenchymal transition (EMT) in trastuzumab resistance, but a definitive link between the two has been difficult to establish because relevant model systems are lacking. When sub-populations of trastuzumab sensitive SKBR-3 cells were isolated using cloning rings, an (EMT) occurred spontaneously in several (3/8) clones. SKBR-3 EMT-clones featured increased spindle morphology, expressed N-glycosylated M-NM-21-integrin, and decreased HER-2, all characteristics shared by JIMT-1, a cell lines with intrinsic resistance to trastuzumab. SKBR-3 EMT-clones were characterized by gene expression profiling and mammosphere formation. The N-glycosylated isoform of M-NM-2-itnegrin was targeted with M-NM-2-integrin inhibiting antibody, AIIB2. Transcriptional profiling revealed that SKBR-3 EMT-clones underwent a shift from a luminal molecular subtype to a more aggressive mesenchymal/ basal phenotype. Isolating clones from SKBR-3 cells with enforced expression of a M-NM-2-integrin isoform lacking extensive N-glycosylation failed to increase the likelihood for spontaneous EMT in SKBR-3. However, specific inhibition of the heavily N-glycosylated variant of M-NM-21-integrin expressed by SKBR-3 EMT-clones restored epithelial morphology and impaired mammosphere formation. Furthermore, when SKBR-3 EMT-clones were treated with relevant doses of trastuzumab and lapatinib, they showed M-bM-^@M-^\spontaneousM-bM-^@M-^] resistance. In this study we describe a model of spontaneous EMT following clonal selection in HER-2+ cell line, SKBR-3. Using this model we establish the first direct link between EMT and resistance to HER-2 targeted therapies. We also identify the N-glycosylated isoform of M-NM-2-integrin as a potential biomarker and target in HER-2+ BC refractory to HER-2 targeted therapies. RNA was isolated from 10 breast cancer cell lines in triplicate. Pairwise gene expression differences were compared between each of the SKBR-3 cell lines (SKBR-3/ b1, SK-EV-C4, and SK-B1-C1). Features selected had at least a 2X difference in at least one comparison, with a one-way ANOVA corrected p-value of >0.05. In addition, expression profiles from SKBR-3/ EV and SK-B1-C1 cell were compared and a differential gene list was generated to include genes that differed by at least 1.5X, with a t-test p-value of >0.02 (unpaired, Bonferroni corrected). A total of 1940 entities met these criteria and the expression of these genes was investigated in all breast cancer cell lines.
2015-01-01 | E-GEOD-40152 | biostudies-arrayexpress
Project description:To gain insight into the functional mechanisms of an RXR agonist HX630 in murine pituitary corticotroph tumor cells (AtT20 cell), especially concerning cell proliferation and apoptosis, we conducted whole genome microarray analysis to identify gene expression patterns, networks, and pathways in AtT20 cells treated with HX630 at 10 M-NM-<M for 48 hr. 2,173 up-regulated and 3,169 down-regulated genes were identified that demonstrated fold-changes of at least 1.5 and a P-value <0.01 in AtT20 cells with HX630 at 10 uM compared with control. Both the up- and down-regulated differentially expressed genes were submitted to IPA, which groups significant genes according to biological processes in which they function, and identifies various functions, networks, and pathways. These analyses showed that the categories of the biological functions and diseases significantly regulated by HX630 were associated with cell death, growth and cancer. Furthermore, it was identified that a gene network associated with caspase 3 was significantly induced by HX630.These data indicated that HX630 induced cell death and suppressed cell growth in AtT20 cells, consistent with the results of in vitro studies. AtT20 cells grown to 50 % confluence in regular medium in 12-multiwell plates were incubated either without or with HX630 at 10 M-NM-<M in DMEM supplemented with 1 % stripped FBS media for 48 hr. The cells were then lysed and their total RNAs were isolated for microarray analysis.
2013-01-27 | E-GEOD-43783 | biostudies-arrayexpress
Project description:Although regulation of stem cell homeostasis by miRNAs is well studied, it is unclear how individual miRNAs, genomically encoded within an organized polycistron, can interact to induce an integrated phenotype. miR-99a/100, let-7 and miR-125b paralogues are encoded in two tricistrons on human chromosome 11 and 21. They are highly expressed in hematopoietic stem cells (HSCs) and acute megakaryoblastic leukemia (AMKL), an aggressive form of leukemia with poor prognosis. Integrative analysis of global gene expression profiling, miRNA target prediction and pathway architecture revealed that miR-99a/100, let-7 and miR-125b functionally converge at the combinatorial block of the TGFM-NM-2 pathway by targeting four receptor subunits and two SMAD signaling transducers. In addition, downregulation of tumor suppressor genes APC/APC2 stabilizes active M-NM-2-Catenin and enhances Wnt signaling. By switching the balance between Wnt and TGFM-NM-2 signaling the concerted action of these tricistronic miRNAs promoted sustained expansion of murine and human HSCs in vitro or in vivo, while favoring megakaryocytic differentiation. We lentivirally transduced cord blood CD34+-hematopoietic stem and progenitor cells (CB-HSPCs) to ectopically express miR-125b-2, miR-99a, let-7c or miR-99a~125b-2 and cultured them in megakaryocytic differentiation medium for 7 days.
2014-03-28 | E-GEOD-56335 | biostudies-arrayexpress