Vibrio cholerae 623-39
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA18493 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| AAWG02.dat.gz | Other | |||
| AAWG02.fasta.gz | Fasta.gz | |||
| AAWG02.master.dat | Other | |||
| AAWG01.dat.gz | Other |
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Project description:Understanding gene expression by bacteria during the actual course of human infection may provide important insights into microbial pathogenesis. In this study, we evaluated the transcriptional profile of Vibrio cholerae, the causative agent of cholera, in clinical specimens from cholera patients. We collected samples of human stool and vomitus that were positive by dark-field microscopy for abundant vibrios and used a microarray to compare gene expression in organisms recovered directly from the early and late stages of human infection. Our results reveal that V. cholerae gene expression within the human host environment differs from patterns defined in in vitro models of pathogenesis. tcpA, the major subunit of the essential V. cholerae colonization factor, was significantly more highly expressed in early compared with late infection; however, the genes encoding cholera toxin were not highly expressed in either phase of human infection. Furthermore, expression of the virulence regulators, toxRS and tcpPH, was uncoupled. Interestingly, the pattern of gene expression indicates that the human upper intestine may be a uniquely suitable environment for the transfer of genetic elements that are important in the evolution of pathogenic strains of V. cholerae. These findings provide a more detailed assessment of the transcriptome of V. cholerae in the human host than previous studies of organisms in stool alone and have implications for cholera control and the design of improved vaccines. Keywords: comparative gene expression analysis
2005-08-17 | GSE2775 | GEO
Project description:Bacteria use quorum sensing (QS) to monitor cell density and coordinate group behaviours. In Vibrio cholerae, the causative agent of cholera disease, QS is linked to virulence gene expression via the autoinducer molecules, AI-2 and CAI-1. Both autoinducers share one signal transduction pathway to control AphA production, a key transcriptional activator of virulence genes. In this study, we demonstrate that the recently identified autoinducer, DPO, also controls AphA production in V. cholerae. DPO acts through the transcriptional activator, VqmA, and the VqmR small RNA to reduce AphA levels at the post-transcriptional level. Consequently, DPO inhibits virulence gene expression in V. cholerae, including repression of the cholera toxin, a key factor required for disease in humans. VqmR-mediated repression of AphA links the AI-2/CAI-1 and DPO-dependent QS pathways of V. cholerae and global transcriptome analysis indicate that all three autoinducers are required for full QS function. Together, our data provide the first view on autoinducer interplay in V. cholerae and highlight the importance of post-transcriptional gene regulation for collective functions in this major human pathogen.
2018-06-25 | GSE115711 | GEO
Project description:Understanding gene expression by bacteria during the actual course of human infection may provide important insights into microbial pathogenesis. In this study, we evaluated the transcriptional profile of Vibrio cholerae, the causative agent of cholera, in clinical specimens from cholera patients. We collected samples of human stool and vomitus that were positive by dark-field microscopy for abundant vibrios and used a microarray to compare gene expression in organisms recovered directly from the early and late stages of human infection. Our results reveal that V. cholerae gene expression within the human host environment differs from patterns defined in in vitro models of pathogenesis. tcpA, the major subunit of the essential V. cholerae colonization factor, was significantly more highly expressed in early compared with late infection; however, the genes encoding cholera toxin were not highly expressed in either phase of human infection. Furthermore, expression of the virulence regulators, toxRS and tcpPH, was uncoupled. Interestingly, the pattern of gene expression indicates that the human upper intestine may be a uniquely suitable environment for the transfer of genetic elements that are important in the evolution of pathogenic strains of V. cholerae. These findings provide a more detailed assessment of the transcriptome of V. cholerae in the human host than previous studies of organisms in stool alone and have implications for cholera control and the design of improved vaccines. The V. cholerae microarray consists of 3,890 full-length PCR products representing the annotated open reading frames from the initial release of the V. cholerae N16961 genome. Each labeling and hybridization was performed in duplicate. Genomic DNA was used as a universal internal control for the quality of the microarray and to allow for the comparison of results across multiple experiments. Data were normalized using locally-weighted regression (Lowess) to obtain the relative abundance of each transcript as an intensity ratio with respect to that of genomic DNA. High correlation coefficients were observed between technical replicates (Pearsonâs correlation coefficient (r) > 0.80) and between results of separate clinical specimens of vomitus (r > 0.77) and of stool (r > 0.80). Hence, the results from the two clinical vomitus specimens and the five clinical stool specimens were pooled. Fold changes for the relative expression of a given gene between the two clinical specimens were calculated by dividing the normalized median intensity ratios with respect to genomic DNA.
2010-06-09 | E-GEOD-2775 | biostudies-arrayexpress
Project description:Temperature is a crucial environmental signal that govers the occurrence of Vibrio cholerae and cholera outbreaks. To understand how temperature impacts the transcriptome of V. cholerae we performed whole-genome level transcriptional profiling using custom microarrays on cells grown at human body temperature (37 C) then shifted to temperatures V. cholerae experience in the environment (15 C and 25 C).
2016-05-09 | GSE81158 | GEO
Project description:Many, if not all, bacteria use quorum sensing (QS) to control gene expression and collective behaviours, and more recently QS has also been discovered in bacteriophages (phages). Phages can produce communication molecules of their own, or “listen in” on the host’s communication processes, in order to switch between lytic and lysogenic modes of infection. In this project, we studied the interaction of Vibrio cholerae, the causative agent of cholera disease, with the lysogenic vibriophage VP882. The lytic cycle of VP882 is induced by the QS molecule DPO (3,5-dimethylpyrazin-2-ol), however, the global regulatory consequences of DPO-mediated VP882 activation have remained unclear.
2023-11-23 | GSE247770 | GEO
Project description:Quorum sensing (QS) is a process of cell-cell communication that enables bacteria to transition between individual and collective lifestyles. QS controls virulence in Vibrio cholerae, the causative agent of the disease cholera. Differential RNA-sequencing (dRNA-seq) analyses of wild-type V. cholerae and a locked low cell density QS-mutant strain identified a total of 7641 transcriptional start sites (TSS) with ~40% initiated in the antisense direction. Genome-wide TSS mapping combined with phylogenetic comparisons enabled re-annotation of 129 genes from the NCBI database. 107 of the transcripts we identified do not appear to encode proteins suggesting they could specify non-coding RNAs. We focused on one such transcript that we name VqmR. vqmR is located upstream of the vqmA gene that encodes a DNA-binding transcription factor. Mutagenesis and microarray analyses demonstrate that VqmA activates vqmR transcription; that vqmR encodes a regulatory RNA, and VqmR directly controls at least eight mRNA targets including the rtxBA toxin genes and the vpsT transcriptional regulator of biofilm production. We show that VqmR inhibits biofilm formation through repression of vpsT. Together, these data provide the first global annotation of the V. cholerae transcription landscape and they highlight the importance of post-transcriptional regulation for collective behaviors in this human pathogen.
2014-12-08 | GSE62084 | GEO
Project description:Quorum sensing (QS) is a process of cell-cell communication that enables bacteria to transition between individual and collective lifestyles. QS controls virulence in Vibrio cholerae, the causative agent of the disease cholera. Differential RNA-sequencing (dRNA-seq) analyses of wild-type V. cholerae and a locked low cell density QS-mutant strain identified a total of 7641 transcriptional start sites (TSS) with ~40% initiated in the antisense direction. Genome-wide TSS mapping combined with phylogenetic comparisons enabled re-annotation of 129 genes from the NCBI database. 107 of the transcripts we identified do not appear to encode proteins suggesting they could specify non-coding RNAs. We focused on one such transcript that we name VqmR. vqmR is located upstream of the vqmA gene that encodes a DNA-binding transcription factor. Mutagenesis and microarray analyses demonstrate that VqmA activates vqmR transcription; that vqmR encodes a regulatory RNA, and VqmR directly controls at least eight mRNA targets including the rtxBA toxin genes and the vpsT transcriptional regulator of biofilm production. We show that VqmR inhibits biofilm formation through repression of vpsT. Together, these data provide the first global annotation of the V. cholerae transcription landscape and they highlight the importance of post-transcriptional regulation for collective behaviors in this human pathogen. Global mapping TSS in V. cholerae
2014-12-08 | E-GEOD-62084 | biostudies-arrayexpress
Project description:Vibrio cholerae is a Gram negative, motile, facultative anaerobic bacterium, and the causative agent of cholera, a severe diarrhoeal disease, which untreated can rapidly lead to dehydration, hypotensive shock, and death. Cholera is a significant human disease that is estimated to affect 3-5 million people each year. The mechanism by which V. cholerae regulates virulence gene expression in vivo is unknown, but a number of studies have suggested that low molecular weight signally molecules may be important in modulating gene expression. cFP is a low molecular weight cyclic dipeptide produced by multiple Vibrio species. Evidence previously generated in our laboratory showed that cFP inhibited the production of the virulence factors cholera toxin (CT) and the toxin coregulated pilus (TCP) in O1 El Tor V. cholerae strain N16961 during growth under virulence gene inducing conditions. cFP inhibition of CT and TCP production correlated with reduced transcription of several regulators that belong to the ToxR regulon. To identify additional cFP-responsive genes we performed microarray experiments with the O1 El Tor V. cholerae strain N16961. In these experiments N16961 was grown under virulence gene inducing conditions in the presence and absence of cFP before RNA was extracted and hybridized to microarrays. The results showed that cFP positively affected the expression of the LysR-family regulatory protein LeuO. This finding suggests the possibility that LeuO may be mediating cFP-dependent regulation of gene expression in response to environmental cFP.
2013-08-13 | GSE38272 | GEO
Project description:Pandemic and endemic strains of Vibrio cholerae arise from toxigenic conversion by the CTXφ bacteriophage, a process by which CTXφ infects non-toxigenic strains of V. cholerae. CTXφ encodes the cholera toxin, an enterotoxin responsible for the watery diarrhea associated with cholera infections. Despite the critical role of CTXφ during infections, signals that affect CTXφ-driven toxigenic conversion or expression of the CTXφ-encoded cholera toxin remain poorly characterized, particularly in the context of the gut mucosa. Here, we identify mucin polymers as potent regulators of CTXφ-driven pathogenicity in V. cholerae. Our results indicate that mucin-associated O-glycans block toxigenic conversion by CTXφ and suppress the expression of CTXφ-related virulence factors, including the toxin co-regulated pilus and cholera toxin, by interfering with the TcpP/ToxR/ToxT virulence pathway. By synthesizing individual mucin glycan structures de novo, we identify the Core 2 motif as the critical structure governing this virulence attenuation. Overall, our results highlight a novel mechanism by which mucins and their associated O-glycan structures affect CTXφ-mediated evolution and pathogenicity of V. cholerae, underscoring the potential regulatory power housed within mucus.
2022-12-01 | GSE213598 | GEO