Expression data of enterohemorrhagic E. coli (EHEC) dicF mutant
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA507958 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8271740_1.fastq.gz | Fastqsanger.gz | |||
| SRR8271740_2.fastq.gz | Fastqsanger.gz | |||
| SRR8271741_1.fastq.gz | Fastqsanger.gz | |||
| SRR8271741_2.fastq.gz | Fastqsanger.gz | |||
| SRR8271736_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project 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 pathogen’s 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.
2008-09-18 | GSE11927 | GEO
Project 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 pathogenâs 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. Experiment Overall Design: Arrays used as a starting point for further examination of the effects of the cadA deficiency. A limited number of biologically significant phenotypes and gene expression profiles were examined using qRT-PCR
2008-10-25 | E-GEOD-11927 | biostudies-arrayexpress
Project description:Fimbriae are important virulence traits that promote bacterial adhernece to surfaces. Here, we assessed whether fimbriae modulate gene expression using microarrays. We used microarrays to compare gene expression in wild-type of fimbrial deletion strains of EHEC
2024-06-07 | GSE100200 | GEO
Project description:Regulation of EHEC gene expression by the gut commensal bacterium B. thetaiotaomicron. EHEC is a human pathogen that colonizes in the colon where B. thetaiotaomicron is a predominant commensal. We used microarrays to evaluate global regulation of EHEC when cultured with B. thetaiotaomicron. EHEC and B. thetaiotaomicron were co-cultured in vitro under strict anaerobic conditions in low-glucose Dulbecco's modified Eagle's medium (DMEM). Total RNA from bacteria grown to mid-logarithmic phase was extracted and hybridized to an Affymetrix E. coli 2.0 gene chip according to manufacturer's specifications: http//www.affymetrix.com/support/technical/manual/expression_manual.affx
2013-05-29 | E-GEOD-47418 | biostudies-arrayexpress
Project description:We used arrays to examine the overall transcriptional differences between WT K-12 E. coli, and EHEC 86-24 and their corresponding QseD (yjiE) mutants.
2010-03-01 | GSE20413 | GEO
Project description:Global regulation of the effects of deletion of phage cro gene in EHEC
2016-09-29 | GSE86271 | GEO
Project description:Transcriptional analysis of the effects of the deletion of the sRNAs glmY and glmZ in EHEC
2015-02-01 | GSE63336 | GEO
Project description:Regulation of EHEC gene expression by the gut commensal bacterium B. thetaiotaomicron. EHEC is a human pathogen that colonizes in the colon where B. thetaiotaomicron is a predominant commensal. We used microarrays to evaluate global regulation of EHEC when cultured with B. thetaiotaomicron.
2013-05-29 | GSE47418 | GEO
Project description:Enterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes diarrheal disease and the potentially lethal hemolytic uremic syndrome. Here, we used an infant rabbit model of EHEC infection that recapitulates many aspects of human intestinal disease to comprehensively assess the host colonic epithelial and lamina propria cell transcriptional responses to EHEC infection. Furthermore, comparisons of colonic pathology and intestinal transcriptomic profiles in animals infected with EHEC strains containing or lacking Shiga toxins (∆∆stx) were carried out to investigate how these potent toxins shape the host response to the pathogen. We found that Stx is required for severe, multi-focal hemorrhage and extensive apoptosis in the colon. RNA-sequencing revealed that EHEC infection elicits a robust innate immune response in the colonic epithelium that is dramatically shaped by Stx. Over 1400 genes were differentially expressed in animals infected with WT versus ∆∆stx EHEC strains. Several pathways linked to innate immune responses were dependent on Stx. Upregulated genes in the presence of toxin included cytokines IL23a and CXCL8, as well as F3, the gene encoding the coagulation initiator Tissue Factor. RNA FISH revealed that these elevated transcripts were found almost exclusively in epithelial cells, suggesting that Stx remodels the transcriptional profile of the epithelium. Collectively, these findings reveal that Stx potently modulates the innate immune response to EHEC in the intestine, and suggest that Stx drives the response to infection towards type 3 immunity.
2021-01-14 | GSE156056 | GEO
Project description:The enterohemorrhagic Escherichia (E.) coli (EHEC) is a pathogen of great concern for public health and the meat industry all over the world. High economic losses in meat industry and the high cost of the illness evidence the necessity of additional efforts to control this pathogen. Previous studies demonstrated inhibitory activity towards EHEC, of a bioprotective strain, Enterococcus mundtii CRL35, it showing also a specific proteomic response during the co-culture. In the present work additional studies of the EHEC-Ent. mundtii interaction were carried out: i) differential protein expression of E. coli O157:H7 NCTC12900 when growing in co-culture with Enterococcus mundtii in a meat environment, ii) the reciprocal influence between these two microorganisms in the adhesion to extracellular matrix (ECM) proteins and iii) the possible induction of the phage W933, coding for Shiga toxin (Stx1), by the presence of Ent. mundtii CRL35. When compared the co-culture with individual growth, proteomic results showed significant repression of E. coli NCTC12900 proteins related mostly to the metabolism and transport of amino acids and nucleotides. However, statistically significant over expression of EHEC proteins involved in stress, energy production, amino acid metabolism and transcription was observed at 30 h respect to 6 h when EHEC grew in co-culture. On the other hand, EHEC showed a decreased adhesion capacity to ECM proteins in the presence of the bioprotective strain. Finally, Ent. mundtii CRL35 did not induce the lytic cycle of W933 bacteriophage, thus indicating its potential safe use for eliminating this pathogen. Overall, this study expands the knowledge of EHEC- Ent. mundtii CRL35 interaction in a meat environment, as an attempt to find out effective biological strategies to eliminate this pathogen.
2019-09-30 | PXD014588 | Pride