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accession-icon GSE7439
Escherichia coli strain 8624 and Escherichia coli strain VS94 with signaling molecules
  • organism-icon Escherichia coli
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

These E. coli strains were grown with various signaling molecules and the expression profiles were determined.

Publication Title

Global effects of the cell-to-cell signaling molecules autoinducer-2, autoinducer-3, and epinephrine in a luxS mutant of enterohemorrhagic Escherichia coli.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE18118
QseA regulation of virulence factors in EHEC
  • organism-icon Escherichia coli
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Enterohemorrhagic E. coli (EHEC) colonizes the large intestine and causes attaching and effacing lesions (AE). Most of the genes involved in the formation of AE lesions are encoded within a chromosomal pathogenicity island termed the Locus of Enterocyte Effacement (LEE). The LysR-like transcriptional factor QseA regulates the LEE by binding directly to the regulatory region of ler. Here, we performed transcriptome analyses comparing WT EHEC and the isogenic qseA mutant in order to elucidate the extent of QseAs role in gene regulation in EHEC. The following results compare genes that were up-regulated and down-regulated ! 2-fold in the qseA mutant strain compared to the WT strain. At mid-exponential growth, 222 genes were up-regulated and 1874 were downregulated. At late-exponential growth, a total of 55 genes were up-regulated and 605 genes were down-regulated. During mid-exponential growth, QseA represses its own transcription, whereas during late-logarithmic growth, QseA activates expression of the LEE genes as well as non-LEE encoded effector proteins. During both growth phases, several genes carried in O-islands, were activated by QseA, whereas genes involved in cell metabolism were repressed. We also performed electrophoretic mobility shift assays, competition experiments, and DNAseI footprints, and the results suggested that QseA directly binds both the ler proximal and distal promoters, its own promoter, as well as promoters of genes encoded in EHEC-specific O-islands. Additionally, we mapped the transcriptional start site of qseA, leading to the identification of two promoter sequences. Taken together, these results indicate that QseA acts as a global regulator in EHEC, coordinating expression of virulence genes.

Publication Title

The LysR-type regulator QseA regulates both characterized and putative virulence genes in enterohaemorrhagic Escherichia coli O157:H7.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12831
The role of qseE, qseF and qseG in the regulation of EHEC virulence
  • organism-icon Escherichia coli
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Escherichia coli 8624 and the isogenic mutants in qseE, qseF and qseG are compared to determine the role that each of the genes play in regulation of the transcriptome. These results are verified by qRT-PCR and reveal the important role of this three-component signaling system.

Publication Title

The two-component system QseEF and the membrane protein QseG link adrenergic and stress sensing to bacterial pathogenesis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15050
Bacterial Adrenergic signaling
  • organism-icon Escherichia coli
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

The ability to respond to stress is at the core of an organisms survival. The hormones epinephrine and norepinephrine play a central role in stress responses in mammals, which require the synchronized interaction of the whole neuroendocrine system. Bacteria also sense and respond to epinephrine and norepinephrine as a means to gauge the metabolic and immune state of the host. Mammalian adrenergic receptors are G-coupled protein receptors (GPCRs), bacteria, however, sense these hormones through histidine sensor kinases (HKs). HKs autophosphorylate in response to multiple signals and transfer this phosphate to response regulators (RRs). Two bacterial adrenergic receptors have been identified in EHEC, QseC and QseE, with QseE being downstream of QseC in this signaling cascade. We mapped the QseC signaling cascade in the deadly pathogen enterohemorrhagic E. coli (EHEC), which exploits this signaling system to promote disease. Through QseC, EHEC activates expression of metabolic, virulence and stress response genes, synchronizing the cell response to these stress hormones. Coordination of these responses is achieved by QseC phosphorylating three of the thirty two EHEC RRs. The QseB RR, which is QseCs cognate RR, activates the flagella regulon which controls bacteria motility and chemotaxis. The QseF RR, which is phosphorylated by the QseE adrenergic sensor, coordinates expression of virulence genes involved in formation of lesions in the intestinal epithelia by EHEC, and the bacterial SOS stress response. The third RR, KdpE, controls potassium uptake, osmolarity response, and also the formation of lesions in the intestine. Adrenergic regulation of bacterial gene expression shares several parallels with mammalian adrenergic signaling having profound effects in the whole organism. Understanding adrenergic regulation of a bacterial cell is a powerful approach to study the underlying mechanisms of stress and cellular survival.

Publication Title

The QseC adrenergic signaling cascade in Enterohemorrhagic E. coli (EHEC).

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE57624
Identification of nuclear-enriched miRNAs during mouse granulopoiesis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of nuclear-enriched miRNAs during mouse granulopoiesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE57622
Gene expression data from mouse hemopoietic stem cells (LSKs), promyelocytes, myelocytes and granulocytes.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Differentiation of hemopoietic stem cells into granulocytes is characterized by distinct changes in the transcriptome.

Publication Title

Identification of nuclear-enriched miRNAs during mouse granulopoiesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE13562
Effects of sidA and AHL on EHEC virulence
  • organism-icon Escherichia coli
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

A study on the effects of an sdiA mutant and the AHL molecule on the virulence of EHEC

Publication Title

Chemical sensing in mammalian host-bacterial commensal associations.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11927
RCV02 (cadA deficient) v wild-type enterohemorrhagic E. coli (EHEC)
  • organism-icon Escherichia coli
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Adherence of pathogenic Escherichia coli strains to intestinal epithelia is essential for infection. For enterohemorrhagic E. coli (EHEC) serotype O157:H7, we have previously demonstrated that multiple factors govern this pathogens adherence to HeLa cells (39). One of these factors is CadA, a lysine decarboxylase, and this protein has been proposed to negatively regulate virulence in several enteric pathogens. In the case of EHEC strains, CadA modulates expression of the intimin, an outer membrane adhesin involved in pathogenesis. Here, we experimentally inactivated cadA in O157:H7 strain 86-24 to investigate the role of this gene in EHEC adhesion to tissue culture monolayers, global gene expression patterns, and colonization of the infant rabbit intestine. As expected, the cadA mutant did not possess lysine decarboxylation activity and was hyper-adherent to tissue-culture cells. Adherence of the cadA mutant was nearly 2-fold greater than that of the wt and complementation of the cadA defect reduced adherence back to wt levels. Furthermore, the cadA mutant affected the expression of intimin protein. Disruption of the eae gene (encoding the intimin protein) in the cadA mutant significantly reduced its adherence to tissue-culture cells. However, adherence of the cadA eae double mutant was greater than that of an 86-24 eae mutant, suggesting that the enhanced adherence of the cadA mutant is not entirely attributable to enhanced expression of intimin in this background. Gene array analysis revealed that the cadA mutation significantly altered EHEC gene expression patterns; expression of 1332 genes was down-regulated and 132 genes up-regulated in the mutant compared to the wild type strain. Interestingly, the gene expression variation shows an EHEC-biased gene alteration including intergenic regions. Two putative adhesins: flagella and F9 fimbriae were up-regulated in the cadA mutant, suggestive of their association with adherence in absence of the Cad regulatory mechanism. Remarkably, in the infant rabbit model, the cadA mutant out-competed the wild type strain in the ileum but not in the cecum or mid-colon, raising the possibility that CadA negatively regulates EHEC pathogenicity in a tissue-specific fashion.

Publication Title

CadA negatively regulates Escherichia coli O157:H7 adherence and intestinal colonization.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE79623
Gene expression analysis in the aorta from non-diabetic or STZ-induced diabetic apolipoprotein E deficient (ApoE-/-) mice fed with high fat diet in the presence or absence of PKC inhibitor, ruboxistaurin (RBX, or LY333531)
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We found that hyperglycemia and elevated fatty acids in diabetes could activate protein kinase C- isoforms and selectively induce insulin resistance via inhibiting vascular insulin signaling.

Publication Title

Insulin decreases atherosclerosis by inducing endothelin receptor B expression.

Sample Metadata Fields

Age, Specimen part, Disease, Disease stage, Treatment

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accession-icon GSE48307
Orchestrated intron retention regulates normal granulocyte differentiation
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Orchestrated intron retention regulates normal granulocyte differentiation.

Sample Metadata Fields

Specimen part

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
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Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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