Escherichia coli 8624
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ABSTRACT:
PROVIDER: PRJNA186946 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of effect of deletion of the two transcriptional factors KdpE and Cra on gene expression of EHEC 8624 A double mutant of kdpE and cra in the EHEC 8624 was grown to OD600=1.0 in DMEM then processed according to manufacturer's specifications: http//www.affymetrix.com/support/technical/manual/expression_manual.affx
2013-07-03 | E-GEOD-43659 | biostudies-arrayexpress
Project description:Enterohemorrhagic Escherichia coli (EHEC)8624 double deletions of qseC and qseE grown in DMEM
| PRJNA148335 | ENA
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:Analysis of effect of deletion of the two transcriptional factors KdpE and Cra on gene expression of EHEC 8624
2013-07-03 | GSE43659 | GEO
Project description:Enteric pathogens with low infectious doses rely on the ability to orchestrate expression of virulence and metabolism-associated genes in response to environmental cues for successful infection. Accordingly, the human pathogen enterohemorrhagic Escherichia coli (EHEC) employs a complex multifaceted regulatory network to link expression of type III secretion system (T3SS) factors to nutrient availability. While phosphorylation of histidine and aspartate on two-component system response regulators is recognized as an integral part of signaling, the involvement of phosphotyrosine-mediated control is minimally explored in Gram-negative pathogens. Our recent phosphotyrosine profiling study of E. coli revealed 342 proteins, indicating that phosphotyrosine modifications in bacteria are more prevalent than previously anticipated. Here, we demonstrate that tyrosine phosphorylation of a metabolite-responsive LacI/GalR family regulator, Cra, negatively affects T3SS expression in glycolytic conditions typical for the colon lumen environment where production of the T3SS is unnecessary. Our data suggest that Cra phosphorylation affects T3SS expression by modulating expression of ler, encoding the major activator of EHEC virulence gene expression. Phosphorylation of the Cra Y47 residue diminishes DNA-binding, thereby altering expression of metabolism and virulence-associated genes including those of the LEE pathogenicity island encoding the T3SS. Hence, phosphotyrosine-mediated regulation provides a mechanism to regulate Cra activity. Our data further suggest that tyrosine phosphorylation influences DNA binding by PurR and LacI, thereby phosphotyrosine-mediated control could provide a means to regulate DNA-binding of LacI/GalR family regulators in general. Our study provides an initial effort to unravel the role of phosphotyrosine-mediated global signaling in controlling the EHEC virulence potential
2018-02-02 | GSE103764 | GEO
Project description:Enterohemorrhagic Escherichia coli (EHEC) is a gram negative enteric bacterial pathogen that can cause hemorrhagic colitis and heamolytic uremic syndrome (HUS) in humans and is the cause of bloody diarrhoea and acute renal failure in children. We have studied the transcriptional response of a colon cell line (CaCo2) to infection by EHEC and another closely related enteric pathogen Enteropathogenic Escherichia coli (EPEC) and compared its response to a cervical cell line (Hela). We carried out microarray analysis on CaCo2 infected with EHEC O157H:7 EDL933 and EPEC E2348/69 at 4 hours of infection and analysis on Hela infected with EHEC also at 4 hours of infection
2016-09-01 | GSE13403 | GEO
Project description:Enterohemorrhagic Escherichia coli (EHEC) is a gram negative enteric bacterial pathogen that can cause hemorrhagic colitis and heamolytic uremic syndrome (HUS) in humans and is the cause of bloody diarrhoea and acute renal failure in children. We have studied the transcriptional response of a colon cell line (CaCo2) to infection by EHEC and another closely related enteric pathogen Enteropathogenic Escherichia coli (EPEC) and compared its response to a cervical cell line (Hela). We carried out microarray analysis on CaCo2 infected with EHEC O157H:7 EDL933 and EPEC E2348/69 at 4 hours of infection and analysis on Hela infected with EHEC also at 4 hours of infection CaCo2 cells and Hela cells were grown to 80% confluency and infected with the bacteria for 4 hours before samples were collected for microarray analysis.
2016-09-01 | E-GEOD-13403 | biostudies-arrayexpress
Project description:Enterohemorrhagic Escherichia coli (EHEC), including serotype O157:H7, cause severe food-borne illness. On route to the human colon, they encounter and resist, numerous anti-microbial ingestion stresses. We hypothesize that these stresses cue EHEC to alter virulence properties. This study investigated the impact of bile salts on virulence properties and examined the genetic basis of the phenotypes. Established assays were used to examine adhesion to human epithelial cells, motility, verotoxin (VT) production and antimicrobial resistance with/without bile salt stress. Bacteria treated for 90 minute in DMEM plus 0.15% (w/v) bile salt mix demonstrated significantly enhanced adhesion to epithelial cells and resistance to several antibiotics but did not increase motility or VT production. To determine the genetic basis of these phenotypes a microarray experiment was conducted. EHEC strain 86-24, in mid-log phase of growth, were grown in DMEM pH 7.4 (control), or DMEM plus bile salt mix (0.15% w/v), for 90 minutes, statically at 37˚C, 5% CO2 prior to harvesting RNA for the microarray study. Four biological replicates were produced for each treatment. Microarray and gene expression analysis (semi-quantitative RT-PCR and beta-galactosidase reporter assays) of bile salt-treated EHEC revealed significant up-regulation of genes for lipid A modification, fimbriae, an efflux pump, and a two-component regulatory system relative to the bacteria grown in DMEM alone. This work points to several mechanisms that EHEC employs to resist the stresses of the human small intestine, notably efflux, antimicrobial resistance, and outer membrane alterations. Bile salts enhanced the virulence-related properties of increased adhesion and resistance to antimicrobials but not VT production or motility. This research contributes to our understanding of how EHEC senses and responds to host environmental signals and the mechanisms this pathogen uses to successfully colonize and infect the human host.
2011-09-06 | GSE22060 | GEO
Project description:Enterohemorrhagic Escherichia coli (EHEC) deletions of glmY and glmZ
| PRJNA267534 | ENA
Project description:Enterohemorrhagic Escherichia coli (EHEC) induces the attachment and effacement of intestinal microvilli. While the molecular mechanisms contributed to the attachment of EHEC have been thoroughly studied, the underlying mechanisms for the effacement of intestinal microvilli induced by EHEC remained elusive. By focus RNAi screening and genetic analysis in C. elegans and further reconfirmed in human Caco-2 intestinal epithelial cells, we demonstrate that the CDK1-formin signal axis is required for this EHEC-induced microvillar effacement in vitro and in vivo.
2020-11-11 | GSE142507 | GEO