Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR179390.fastq.gz | Fastqsanger.gz | |||
| ERR179391.fastq.gz | Fastqsanger.gz | |||
| ERR179392.fastq.gz | Fastqsanger.gz | |||
| ERR179393.fastq.gz | Fastqsanger.gz | |||
| ERR179394.fastq.gz | Fastqsanger.gz |
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Project description:Comparative genome sequencing of E.coli EHEC isolated from an outbreak
| PRJEB588 | ENA
Project description:Temperate bacteriophages play a pivotal role in the biology of their bacterial host. Of particular interest are bacteriophages infecting enterohemorrhagic E. coli (EHEC) due to their significant contribution in the pathogenicity of these pathogens, most notably by encoding the key virulence factor of this pathogen, the Shiga toxin. To better understand the role of EHEC phages on the functionality of its host, we isolated eight temperate phages from clinical EHEC isolates and characterized their genomic composition, morphology and receptor targeting. Morphological analysis identified one long-tailed member from the Siphoviridae family, targeting the OmpC receptor for host recognition, while the other seven phages are short-tailed (Podoviridae) and target the essential BamA protein. Genomic characterization revealed significant variation between the long- and short-tailed phages. Five of the eight isolated phages encode the potent Shiga toxin. Comparative analysis displays the typical lambdoid mosaicism, indicative of horizontal gene transfer driving evolution. These findings provide insights into the genetic and morphologic diversity and receptor specificity of EHEC phages, highlighting their role in evolution and pathogenicity of clinical EHEC strains
2025-08-26 | PXD061229 | Pride
Project description:Transcriptional profiling of E.coli SE15 comparing wild type E.coli SE15 with Autoindecur 2 synthesis gene LuxS mutnat E.coli SE15. E.coli SE15 is isolated from indwelling catheter of urinary tract infected patient. Examine change of quorum sensing related gene by deleting autoinducer 2 synthesis gene LuxS in E.coli
2013-08-02 | GSE49474 | GEO
Project description:While significant advances have been made in EHEC pathogenesis, we still do not fully understand the impact of environmental stress on EHEC virulence. During the course of infection, EHEC must evade or overcome several biological barriers, the first of which is the gastric acidity encountered during passage through the stomach. EHEC is remarkable in its ability to tolerate this acidity. There are four different acid resistance systems that provide E. coli O157:H7 protection against exposure to low pH (2-2.5). Interestingly, EHEC uses these acid resistance systems differentially for survival in foods versus the bovine intestinal tract. The glutamate-dependent acid-resistance system is thought to offer the best protection below pH 3. Since the infectious dose of EHEC is so low (50-100 organisms), acid resistance becomes an important virulence trait. Studies of EHEC response to acid stress have focused primarily on levels of acid tolerance and the molecular basis of tolerance. However, the impact of acid stress on EHEC virulence is less well understood. In the related pathogen, EPEC, the plasmid-encoded regulator, Per, that regulates expression of many EPEC virulence factors, is regulated negatively at pH 5.5 and positively at pH 8.0, suggesting that virulence gene expression is repressed during mild acid stress and enhanced in alkaline pH typical of the small intestine. Expression of EPEC type III secreted factors involved in A/E lesion formation has been shown to be influenced by factors including culture media, iron and calcium levels. Protein secretion was inhibited at pH 6 and 8. In a third study, a gadE (encoding acid resistance regulator) mutation resulted in increased adhesion of E.coli O157:H7 to colonic epithelial cells, suggesting negative regulation of one or more adhesins. Other studies have reported that shiga toxin production is sensitive to culture conditions including pH. However, there are no studies of EHEC virulence changes after more severe acid stress nor studies linking stressed EHEC virulence phenotype with transcriptional changes. The goal of this study was to determine how acid stress affects EHEC virulence properties and through microarray analysis, define the genetic basis for these changes. Understanding how acid stress modulates the virulence potential of this pathogen is essential for delineating the pathogenesis of disease caused by EHEC infection and may offer novel approaches to prevent and treat EHEC infections.
2009-06-26 | GSE14069 | GEO
Project description:Background: Enterohemorrhagic Escherichia coli (EHEC) O157 causes severe food-bone illness in humans. The chromosome of O157 consists of 4.1-Mb backbone sequences shared by benign E. coli K-12, and 1.4-Mb O157-specific sequences encoding many virulence determinants such as Shiga toxin genes (stxs) and the locus of enterocyte effacement (LEE). Non-O157 EHECs belonging to clonal lineages distinct from O157 also cause similar illness in humans. According to the parallel evolution model, they have independently acquired the major virulence determinants, stxs and LEE. However, the genomic differences between O157 and non-O157 EHECs have not yet systematically been analyzed. Results: By using the microarray and Whole Genome PCR scanning analyses, we performed a whole genome comparison of 20 EHEC strains of O26, O111, and O103 serotypes with O157. In non-O157 EHEC strains, although genome sizes were similar with or rather larger than O157 and the backbone regions were well conserved, O157-specific regions were very poorly conserved. Only around 20% of the O157-specific genes were fully conserved in each non-O157 serotype. However, the non-O157 EHECs contained a significant number of virulence genes found on prophages and plasmids in O157, and also multiple prophages similar but significantly divergent from those in O157. Conclusion: Although O157 and non-O157 EHECs have independently acquired a huge amount of serotype- or strain-specific genes by lateral gene transfer, they share an unexpectedly large number of virulence genes. Independent infections of similar but distinct bacteriophages carrying these virulence determinants appear to be involved in the parallel evolution of EHEC. Keywords: comparative genomic hybridization, CGH
2007-08-23 | GSE7931 | GEO
Project description:A recently isolated phage, vB_EcoP_SU10 (SU10) with unusual elongated C3 morphotype, can infect a wide range of E.coli strains. We have sequenced the genome of SU10, and further characterization has been conducted by MS-based proteomics.
2015-06-18 | PXD002278 | Pride
Project description:We applied ChIP-seq to identify genome wide binding targets of NsrR in E.coli CFT073. NsrR is a nitric oxide sensitive regulator of transcription. Genome wide binding targets of NsrR have been identified in E.coli K12 using ChIP-chip. The genome of CFT073 is about 0.6Mb larger than that of K12. In this study, we identify the novel NsrR binding sites in CFT073.
2015-06-15 | GSE69829 | GEO
Project description:In 2011, in Germany, Escherichia coli O104:H4 caused the enterohemorrhagic E. coli (EHEC) outbreak with the highest incidence rate of hemolytic uremic syndrome. This pathogen carries an exceptionally potent combination of EHEC- and enteroaggregative E. coli (EAEC)-specific virulence factors. Here, we identified an E. coli O104:H4 isolate that carried a single nucleotide polymorphism (SNP) in the start codon (ATG>ATA) of rpoS, encoding the alternative sigma factor S. The rpoS ATG>ATA SNP was associated with enhanced EAEC-specific virulence gene expression. Deletion of rpoS in E. coli O104:H4 Dstx2 and typical EAEC resulted in a similar effect. Both rpoS ATG>ATA and DrpoS strains exhibited stronger virulence-related phenotypes in comparison to wild type. Using promoter-reporter gene fusions, we demonstrated that wild-type RpoS repressed aggR, encoding the main regulator of EAEC virulence. In summary, our work demonstrates that RpoS acts as a global repressor of E. coli O104:H4 virulence, primarily through an AggR-dependent mechanism.
2024-04-04 | GSE243699 | GEO
Project description:We applied ChIP-seq to identify genome wide binding targets of NsrR in E.coli CFT073. NsrR is a nitric oxide sensitive regulator of transcription. Genome wide binding targets of NsrR have been identified in E.coli K12 using ChIP-chip. The genome of CFT073 is about 0.6Mb larger than that of K12. In this study, we identify the novel NsrR binding sites in CFT073. The nsrR gene was modified by the addition of DNA sequences encoding a C-terminal 3X-Flag tag, and the tagged gene was integrated into the chromosome. NsrR bound DNA was isolated by chromatin immunoprecipitation and it was sequenced using Miseq platform.
2015-06-15 | E-GEOD-69829 | biostudies-arrayexpress