Ethanolamine gene regulation in EHEC
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ABSTRACT:
ORGANISM(S): Escherichia coli
PROVIDER: GSE34046 | GEO | 2012/06/18
SECONDARY ACCESSION(S): PRJNA149913
REPOSITORIES: GEO
Similar Datasets
Project description:Bacterial pathogens must be able to both recognize suitable niches within the host for colonization and successfully compete with commensal flora for nutrients in order to establish infection. Ethanolamine (EA) is a major component of mammalian and bacterial membranes and may be used by pathogens as a carbon and/or nitrogen source in the gastrointestinal tract. We examined how EA influences gene expression in the human pathogen enterohemorrhagic Escherichia coli O157:H7 (EHEC). Our results indicate EA is not only important for nitrogen metabolism, but that EA is used in cell-to-cell signaling to activate virulence gene expression. Genes encoding for the global regulatory proteins QseC, QseE, and QseA, as well as for attaching and effacement (AE) lesion formation and Shiga toxin are differentially regulated when EHEC is grown with micromolar concentrations of EA. We also constructed a deletion of eutR that encodes the regulator of the eut (EA utilization) operon and examined virulence gene expression. These results suggest that EutR is important in regulating gene expression in response to EA, but that EA signaling does not occur solely through EutR. This is the first report linking EA to cell-to-cell signaling and pathogenesis. Design of the study was to compare the transcriptional response of WT cells grown with ethanolamine to that of wild type cells grown without ethanolamine.
2012-06-17 | E-GEOD-34046 | biostudies-arrayexpress
Project description:The ability to respond to stress is at the core of an organismâs 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 QseCâs 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. Experiment Overall Design: Microarray comparisons reveal some trends with respect to signaling cascades. Comparative methods were used to identify networks.
2009-11-16 | E-GEOD-15050 | biostudies-arrayexpress
Project description:The ability to respond to stress is at the core of an organism’s 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 QseC’s 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.
2009-09-15 | GSE15050 | GEO
Project description:Atypical EPEC (aEPEC) strains are part of group of pathogens capable of forming the Attaching and Effacing (A/E) lesion. This lesion is characterized by intimate adherence of bacteria to enterocytes, and microvilli destruction. The genes responsible to cause that lesion are located in a pathogenicity island called Locus of Enterocyte Effacement (LEE). Transcription of LEE genes is subjected to various levels of regulation, including quorum sensing through autoinducer 3 (AI-3) system. AI-3 is an aromatic compound with similar characteristics to the epinephrine and norepinephrine hormones. This similarity allows bacteria to use these hormones and AI-3 to perform cell M-bM-^@M-^S to M-bM-^@M-^S cell signaling processes and bacteria - host communication processes in order to modulate its virulence. AI-3, epinephrine and norepinephrine are detected by a sensor kinase named quorum sensing E.coli regulator (QseC). In order to investigate the role of QseC and epinephrine in atypical EPEC O55:H7 virulence, we constructed a QseC mutant of this strain and performed transcription and phenotypic analyses in the presence or absence of epinephrine. We have reported here, for the first time, the quorum sensing QseC regulation of virulence genes in atypical EPEC. Our results shown that QseC is a global regulator of gene expression in aEPEC and positively regulates flagellar genes, LEE and non-LEE encoded factors. We also have shown that the presence of epinephrine could be sensed by other receptor that acts as negative regulator of LEE4 and LEE5 genes. Comparison of transcriptional regulation of enteropathogenic E. coli serotype O55:H7 wild type and the qseC mutant in the absence or presence of epinephrine signal to identify the regulated targets
2013-01-08 | E-GEOD-43325 | biostudies-arrayexpress
Project description:Atypical EPEC (aEPEC) strains are part of group of pathogens capable of forming the Attaching and Effacing (A/E) lesion. This lesion is characterized by intimate adherence of bacteria to enterocytes, and microvilli destruction. The genes responsible to cause that lesion are located in a pathogenicity island called Locus of Enterocyte Effacement (LEE). Transcription of LEE genes is subjected to various levels of regulation, including quorum sensing through autoinducer 3 (AI-3) system. AI-3 is an aromatic compound with similar characteristics to the epinephrine and norepinephrine hormones. This similarity allows bacteria to use these hormones and AI-3 to perform cell – to – cell signaling processes and bacteria - host communication processes in order to modulate its virulence. AI-3, epinephrine and norepinephrine are detected by a sensor kinase named quorum sensing E.coli regulator (QseC). In order to investigate the role of QseC and epinephrine in atypical EPEC O55:H7 virulence, we constructed a QseC mutant of this strain and performed transcription and phenotypic analyses in the presence or absence of epinephrine. We have reported here, for the first time, the quorum sensing QseC regulation of virulence genes in atypical EPEC. Our results shown that QseC is a global regulator of gene expression in aEPEC and positively regulates flagellar genes, LEE and non-LEE encoded factors. We also have shown that the presence of epinephrine could be sensed by other receptor that acts as negative regulator of LEE4 and LEE5 genes.
2013-01-08 | GSE43325 | GEO
Project description:Analysis of effect of deletion of the two adrenergic kinases QseC and QseE on gene expression of EHEC 8624 in the absence and presence of epinephrine A double mutant of qseC and qseE in the EHEC 8624 was grown in the absence or presence of epinephrine to OD600=1.0 in DMEM then processed according to manufacturer's specifications: http//www.affymetrix.com/support/technical/manual/expression_manual.affx
2012-03-15 | E-GEOD-33895 | biostudies-arrayexpress
Project description:“Stress, survival and virulence: the multi-faceted host/microbial interactions.” Bacteria employ epinephrine and norepinephrine, which converge to distinct bacterial crucial processes, like survival and pathogenicity. A novel stress periplasmic membrane protein belonging to previously described BOF family, protein renamed here SrpP, and together with membrane sensor kinase QseC has an essential role in stress response and virulence of S. Typhimurium. SrpP employs its predicted binding pocket, specifically the SrpPE110 residue, and interacts with lipid A modification enzyme, LpxO dioxygenase. Upon this interaction SrpP in S. Typhimurium finely manages multiple membrane functions to culminate in survival upon stress and pathogenesis in vivo, connecting host-stress chemical signaling to cell stress in bacteria. Comparison of sensor histidine kinase qseC mutant expression levels versus wild type strain.
2012-05-31 | E-GEOD-38353 | biostudies-arrayexpress
Project description:Analysis of effect of deletion of the two adrenergic kinases QseC and QseE on gene expression of EHEC 8624 in the absence and presence of epinephrine
2012-03-15 | GSE33895 | GEO
Project description:Escherichia coli O157:H7 is a food-borne pathogen that causes bloody diarrhea and hemolytic uremic syndrome. Hfq is an sRNA chaperone protein that is involved in post-transcriptional regulation of virulence genes in pathogenic bacteria. In EHEC strain EDL933, Hfq acts a negative regulator of the locus of enterocyte effacement (LEE) that encodes most of the proteins involved in type three secretion and attaching and effacing lesions. We deleted hfq in E. coli O157:H7 strain 86-24 and compared global transcription profiles of the hfq mutant to the wild type strain in exponential growth phase. Deletion of hfq affected transcription of genes common to nonpathogenic and pathogenic strains of E. coli as well as pathogen-specific genes. Downregulated genes in the hfq mutant included ler as well as genes encoded in LEE2-5 that encode for type three secretion and AE lesion formation. Decreased expression of the LEE genes in the hfq mutant occurred at mid-, late, and stationary growth phases in both LB and DMEM media as detected by qRT-PCR. We also confirmed decreased regulation of the LEE genes by examining secreted proteins and AE lesion formation by the hfq mutant and WT strains. Deletion of hfq also caused decreased expression of the two-component system qseBC involved in inter-kingdom signaling and virulence gene regulation in EHEC as well as an increase in stx2AB expression that encodes for the deadly Shiga toxin. Altogether, these data indicate that Hfq plays a different regulatory role in EHEC 86-24 from what has been reported for EHEC strain EDL933 and that the role of Hfq in EHEC virulence regulation extends beyond the LEE. Comparison of transcriptional regulation of the WT 86-24 isolate and the hfq mutant for the identification of regulated targets that were followed up by functional analysis.
2012-01-06 | E-GEOD-30893 | biostudies-arrayexpress
Project description:Escherichia coli O157:H7 is a food-borne pathogen that causes bloody diarrhea and hemolytic uremic syndrome. Hfq is an sRNA chaperone protein that is involved in post-transcriptional regulation of virulence genes in pathogenic bacteria. In EHEC strain EDL933, Hfq acts a negative regulator of the locus of enterocyte effacement (LEE) that encodes most of the proteins involved in type three secretion and attaching and effacing lesions. We deleted hfq in E. coli O157:H7 strain 86-24 and compared global transcription profiles of the hfq mutant to the wild type strain in exponential growth phase. Deletion of hfq affected transcription of genes common to nonpathogenic and pathogenic strains of E. coli as well as pathogen-specific genes. Downregulated genes in the hfq mutant included ler as well as genes encoded in LEE2-5 that encode for type three secretion and AE lesion formation. Decreased expression of the LEE genes in the hfq mutant occurred at mid-, late, and stationary growth phases in both LB and DMEM media as detected by qRT-PCR. We also confirmed decreased regulation of the LEE genes by examining secreted proteins and AE lesion formation by the hfq mutant and WT strains. Deletion of hfq also caused decreased expression of the two-component system qseBC involved in inter-kingdom signaling and virulence gene regulation in EHEC as well as an increase in stx2AB expression that encodes for the deadly Shiga toxin. Altogether, these data indicate that Hfq plays a different regulatory role in EHEC 86-24 from what has been reported for EHEC strain EDL933 and that the role of Hfq in EHEC virulence regulation extends beyond the LEE.
2012-01-06 | GSE30893 | GEO