AAF3+5
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB18579 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR1755173_1.fastq.gz | Fastqsanger.gz | |||
| ERR1755173_2.fastq.gz | Fastqsanger.gz | |||
| ERR1755174_1.fastq.gz | Fastqsanger.gz | |||
| ERR1755174_2.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:We performed a high-throughput mapping of the 5’ end transcriptome of the pAA plasmid of the clinical Escherichia coli O104:H4 (E. coli O104:H4) isolate LB226692. We employed differential RNA-sequencing (dRNA-seq), a terminator exonuclease (TEX)-based RNA-seq approach allowing for the discrimination of primary and processed transcripts. This method has proven to be a powerful tool for the mapping of transcription start sites (TSS) and detection of non-coding RNAs (ncRNAs) in bacteria. We catalogued pAA-associated TSS and processing sites on a plasmid-wide scale and performed a detailed analysis of the primary transcriptome focusing on pAA virulence gene expression.
2016-10-19 | GSE78041 | GEO
Project description:Purpose: In this work, we evaluated the role of two indicative species, Citrobacter werkmanii (CW) and Escherichia albertii (EA), in the virulence of two DEC pathotypes, Shiga toxin-producing (STEC) and enteroaggregative (EAEC) Escherichia coli. Methods: To determine the effect of supernatant obtained from CW and EA cultures in STEC strain 86-24 and EAEC strain 042 gene expression, a RNA-seq analysis was performed. T84 cells were infected with DEC strains in the presence or absence of supernatant from EA and IL-8 secretion was evaluated. The effect of supernatant from EA on the growth and adherence of STEC and EAEC to T84 cells was also evaluated. Finally, we studied the participation of long polar fimbriae (Lpf) in STEC and plasmid-encoded toxin (Pet) in EAEC during DEC infection in the presence of supernatant from EA. Results: RNA-seq analysis revealed that several virulence factors in STEC and EAEC were up-regulated in the presence of supernatants from CW and EA. Interestingly, an increase in the secretion of IL-8 was observed in T84 cells infected with STEC or EAEC in the presence of a supernatant from EA. Similar results were observed with the supernatants obtained from clinical strains of E. albertii. Supernatant from EA had no effect on the growth of STEC and EAEC, or on the ability of these DEC strains to adhere to intestinal epithelial cells. Finally, we found that Pet toxin in EAEC was up-regulated in the presence of a supernatant from EA. In STEC, using mutant strains for Lpf fimbriae, our data suggested that these fimbriae might be participating in the increase of IL-8 induced by STEC on intestinal epithelial cells in the presence of a supernatant from EA. Conclusion:Supernatant obtained from an indicative species of DEC-positive diarrhea could modulate gene expression in STEC and EAEC, and IL-8 secretion induced by these bacteria. These data provide new insights into the effect of gut microbiota species in the pathogenicity of STEC and EAEC.
2022-07-22 | GSE197797 | GEO
Project description:A common genomic feature of most EAEC strains is the presence of a virulence plasmid termed pAA. Plasmid-encoded virulence determinants are, among others, a transcriptional activator termed AggR, a member of the AraC-XylS family of transcription factors. We have previously determined the direct correlation between (p)ppGpp, expression of AggR and biofilm development in strain EAEC 042 (https://doi.org/10.3389/fmicb.2018.00717). In this work we characterize a novel variant of the aggR gene. We modified its 3´UTR by insertion of a FRT sequence, which have generated a series of different phenotypes. We used RNA-seq to compare the transcriptome of the wt strain and its aggR3UTRFRT variant grown at 37ºC in LB medium.
2021-10-29 | GSE160448 | GEO
Project description:Curli are adhesive fimbriae of Enterobactericaeae and are involved in surface attachment, cell aggregation and biofilm formation. We previously reported that natural curli variants of E. coli O157:H7 (EcO157) displayed distinct acid resistance; however, this difference was not linked to the curli fimbriae per se. Here, we investigated the underlying molecular basis of this phenotypic divergence between the curli variants. Among curli-producing (C+) variants isolated from the 1993 U.S. hamburger-associated outbreaks strains, we identified large deletions in the rcsB gene that encodes the response regulator of RcsCDB two-component signal transduction system of rcsB ,. Further comparison of stress fitness revealed that C+ variants were also significantly more sensitive to heat shock, but remained similar resistance to osmotic stress and oxidative damage as curli-deficient (C-) variants. Transcriptomics analysis uncovered a large number of differentially expressed genes between the curli variants, characterized by the enhanced expression of genes related to biofilm formation, virulence, catabolic activity and nutrients uptake, but marked decrease in transcription of genes related to various stress resistance in C+ variants. Supplying C+ variants with a functional rcsB restored cells resistance to heat shock and acid challenge, but blocked the curli production, confirming that inactivation of RcsB in C+ variants was the basis of fitness segregation within the EcO157population. This study provides an example of how genome instability of EcO157promotes the intra-population diversification, generating sub-populations carrying an array of distinct phenotypes that may confer the pathogen survival advantages in host and nonhost environments.
2012-08-31 | GSE39439 | GEO
Project description:Salmonella enterica serovar Typhimurium produces type 1 fimbriae on the outer membrane and such hair-like appendages is proposed to play a significant role in the attachment of the bacteria to host cells and tissues. S. Typhimurium cultured in static broth favors expression of type 1 fimbriae. Conversely, solid agar medium represses type 1 fimbrial expression. Production of type 1 fimbriae is cooperatively regulated by fimZ, fimY, stm0551, fimW, and fimU within the fim gene cluster. FimZ belongs to the response regulator of the two-component regulatory system in bacteria and functions as a DNA binding protein. FimZ can bind to the promoter of the fimbrial major subunit gene fimA to activate its expression and produce type 1 fimbriae. A fimZ mutant in LB5010 strain constructed by allelic exchange was found to be non-fimbriate. Total RNA was extracted from the parental LB5010 and the fimZ mutant strain cultured in static broth and analyzed by hybridization to a S. Typhimurium LT2 DNA microarray. Transcriptomic analysis indicated that the stress response related gene cpxP, soxS and type 1 fimbriae related genes were down-regulated, whereas plasmid-encoded fimbriae, flagella associated genes and virulence genes like virK and mgtC were up-regulated in the fimZ mutant strain. It is possible that FimZ protein may play a role to interact with other genes besides fim genes. Mechanisms of this crosstalk warrant further elucidation.
2017-01-20 | GSE93882 | 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: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:P. aeruginosa is known to cause acute cytotoxicity against various human and animal cells and tissues. We identified bacterial metabolite - phenylacetic acid (PAA) which acts as an inhibitory molecule counteracting its pathogenic infection. Microarray and genetic analyses were conducted to investigate the inhibitory mechanism of the identified inhibitor PAA on bacterial virulence. Microarray analysis revealed that treatment of P. aeruginosa with PAA down-regulated the transcriptional expression of type 3 secretion systems (T3SS) genes and related regulatory genes including rsmA and vfr, which were confirmed by transcriptional and translational analysis. Our findings present a new insight to the puzzle of high-cell-density-modulated virulence attenuation in P. aeruginosa and the regulatory mechanisms of T3SS which is associated with bacterial acute infection.
2013-02-21 | GSE43641 | GEO
Project description:Enteroaggregative Escherichia coli (EAEC) is a significant cause of acute and chronic diarrhea, foodborne outbreaks, infections of the immunocompromised, and growth stunting in children in developing nations. There is no vaccine and resistance to antibiotics is rising. Unlike related E. coli pathotypes that are often associated with acute bouts of infection, EAEC is associated with persistent diarrhea and subclinical long-term colonization. Several secreted virulence factors have been associated with EAEC pathogenesis and linked to disease in humans, less certain are the molecular drivers of adherence to the intestinal mucosa. We previously established human intestinal enteroids (HIEs) as a model system to study host-EAEC interactions and aggregative adherence fimbriae A (AafA) as a major driver of EAEC adherence to HIEs. Here, we report a large-scale assessment of the host response to EAEC adherence from all four segments of the intestine across at least three donor lines for five E. coli pathotypes.
2021-10-30 | GSE182426 | GEO
Project description:Many species of pathogenic bacteria harbor critical plasmid-encoded virulence factors, and yet the regulation of plasmid replication is often poorly understood despite playing key role in plasmid-encoded gene expression. Human pathogenic Yersinia, including the plague agent Yersinia. pestis and its close relative Y. pseudotuberculosis, require the type III secretion system (T3SS) virulence factor to subvert host defense mechanisms and colonize host tissues. The Yersinia T3SS is encoded on the IncFII plasmid for Yersinia virulence (pYV). Several layers of gene regulation enables a large increase in expression of Yersinia T3SS genes at mammalian body temperature. Surprisingly, T3SS expression is also controlled at the level of gene dosage. The number of pYV molecules relative to the number of chromosomes per cell, referred to as plasmid copy number, increases with temperature. The ability to increase and maintain elevated pYV plasmid copy number, and therefore T3SS gene dosage, at 37˚C is important for Yersinia virulence. In addition, pYV is highly stable in Yersinia at all temperatures, despite being dispensable for growth outside the host. Yet how Yersinia reinforces elevated plasmid replication and plasmid stability remains unclear. In this study, we show that the chromosomal gene pcnB encoding the polyadenylase PAP I is required for regulation of pYV plasmid copy number (PCN), maintenance of pYV in the bacterial population outside the host, robust T3SS activity, and Yersinia virulence in a mouse infection model. Likewise, pcnB/PAP I is also required for robust expression of the Shigella flexneri virulence plasmid-encoded T3SS that, similar to Yersinia, is encoded on a virulence plasmid whose replication is regulated by sRNA. Furthermore, Yersinia and Shigella pcnB/PAP I is required for maintaining normal PCN of model antimicrobial resistance (AMR) plasmids whose replication is regulated by sRNA, thereby increasing antibiotic resistance by ten-fold. These data suggest that pcnB/PAP I contributes to the spread and stabilization of sRNA-regulated virulence and AMR plasmids in bacterial pathogens, and is essential in maintaining the gene dosage required to mediate plasmid-encoded traits. Importantly pcnB/PAP I has been bioinformatically identified in many species of bacteria despite being studied in only a few species to date. Our work highlights the potential importance of pcnB/PAP I in antibiotic resistance, and shows for the first time that pcnB/PAP I reinforces PCN andpromotes virulence plasmid stability in natural pathogenic hosts with a direct impact on bacterial virulence.
2025-03-20 | GSE292107 | GEO