Ontology highlight
ABSTRACT:
PROVIDER: PRJNA575075 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10208200_1.fastq.gz | Fastqsanger.gz | |||
| SRR10208201_1.fastq.gz | Fastqsanger.gz | |||
| SRR10208197_1.fastq.gz | Fastqsanger.gz | |||
| SRR10208198_1.fastq.gz | Fastqsanger.gz | |||
| SRR10208199_1.fastq.gz | Fastqsanger.gz |
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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: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. V. cholerae N16961 was grown under AKI growth condition in the presence or absence of 1 mM cFP for 2.5 or 3 hours when total RNA was extracted, differentially labelled and hybridized to microarrays. Four independent experiments were performed.
2013-08-13 | E-GEOD-38272 | biostudies-arrayexpress
Project description:Cholera is a diarrheal disease caused by Vibrio cholerae of serogroups O1 and O139 that affects impoverished populations worldwide. The histone-like nucleoid structuring protein (H-NS) is a global regulator of environmentally-regulated gene expression that plays a fundamental role in V. cholerae adaptation to disparate ecological niches. We used RNA-seq to characterize the hns transcriptome of El Tor biotype V. cholerae. H-NS affected the expression of 18% of all predicted genes in a growth phase-dependent manner. It silenced the transcription of genes encoding virulence regulators and cytotoxic factors such as the VieSAB regulatory system, the repeat in toxin (RTX) and hemolysin. H-NS was 10 times more effective in silencing the vieSAB promoter in El Tor compared to classical biotype V. cholerae. In the El Tor biotype hns mutant, VieSAB significantly enhanced the expression of cholera toxin genes. For the RTX and hemolysin, we found that overexpression of the transcription activator HlyU diminished H-NS occupancy at the hlyA promoter but not at the rtxCA and rtxBDE promoters. H-NS had a significant impact on the cell envelope and the mutant expressed elevated rpoE encoding the extracytoplamic sigma factor E (sE), though this effect was indirect. A remarkable feature of the hns transcriptome was the down-regulation of numerous methyl-accepting chemotaxis proteins in early stationary phase that translated into diminished chemotaxis toward the amino acids glycine and serine. Our study suggests that H-NS transcriptional silencing can contribute to multiple phenotypic differences observed between V. cholerae biotypes, mainly by differentially repressing the VieSAB sensory pathway.
2015-02-16 | GSE62785 | GEO
Project description:Cholera is a diarrheal disease caused by Vibrio cholerae of serogroups O1 and O139 that affects impoverished populations worldwide. The histone-like nucleoid structuring protein (H-NS) is a global regulator of environmentally-regulated gene expression that plays a fundamental role in V. cholerae adaptation to disparate ecological niches. We used RNA-seq to characterize the hns transcriptome of El Tor biotype V. cholerae. H-NS affected the expression of 18% of all predicted genes in a growth phase-dependent manner. It silenced the transcription of genes encoding virulence regulators and cytotoxic factors such as the VieSAB regulatory system, the repeat in toxin (RTX) and hemolysin. H-NS was 10 times more effective in silencing the vieSAB promoter in El Tor compared to classical biotype V. cholerae. In the El Tor biotype hns mutant, VieSAB significantly enhanced the expression of cholera toxin genes. For the RTX and hemolysin, we found that overexpression of the transcription activator HlyU diminished H-NS occupancy at the hlyA promoter but not at the rtxCA and rtxBDE promoters. H-NS had a significant impact on the cell envelope and the mutant expressed elevated rpoE encoding the extracytoplamic sigma factor E (sE), though this effect was indirect. A remarkable feature of the hns transcriptome was the down-regulation of numerous methyl-accepting chemotaxis proteins in early stationary phase that translated into diminished chemotaxis toward the amino acids glycine and serine. Our study suggests that H-NS transcriptional silencing can contribute to multiple phenotypic differences observed between V. cholerae biotypes, mainly by differentially repressing the VieSAB sensory pathway. Transcriptome profiles of wild type and M-NM-^Thns mutant cells of the V. cholerae strain C7258 grown in LB medium were generated by Next Generation Sequencing using the Illumina HiSeq2000 platform. Samples from mid-exponential phase (OD600 0.5) and early stationary phase (OD600 2.0) were analyzed in duplicate
2015-02-16 | E-GEOD-62785 | biostudies-arrayexpress
Project description:Purpose: to characterize the regulatory targets of an AraC-like transcriptional regulator (VC0513) encoded on the Vibrio Seventh Pandemic Island -II (VSP-II) in V. cholerae O1 El Tor N16961 Methods: RNA was isolated from a wild-type N16961 carrying an IPTG-inducible copy of vc0513, vc0515, or an empty vector control Results: vc0513 induction significantly increased expression of other VSP-II encoded genes relative to the empty vector control Conclusions: our study represents the first analysis of a transcriptional regulator encoded on the VSP-II island
2021-05-08 | GSE174028 | GEO
Project description:These experiments were performed to show a serogroup conversion of Vibrio cholerae from O1 to O139. For this purpose, V. cholerae O1 El Tor (A1552) was grown on crab shell fragments to induce natural competence for transformation. Purified DNA (4 ug each) from strain MO10, an O139 serogroup strain, was added after 24h and the cells were further grown for 24h. After detachment from the crab shell fragments, bacteria were poured into soft-agar and overlaid onto LB plates. Mukerjees El Tor phage V (a gift of Dr. M.S. Islam) was dropped onto the surface of the bacteria containing soft-agar. The plaques formed by killing non-transformed A1552 cells possessed resistant clones which were picked and further selected for opaque morphotype and agglutination by O139-specific antiserum. Four clones were selected from each independent experiment and analyzed by microarray hybridization (BioPrime. Array CGH Genomic Labeling from Invitrogen). Two microarray replicates were done per clone. Strain Names: AIIIpO139#1 / AIIIpO139#3 / AIIIpO139#4 / AIIIpO139#5 are four clones analyzed after the second experiment; AIVpO139#2 / AIVpO139#4 / AIVpO139#5 / AIVpO139#8 are four clones analyzed after the fourth independent experiment. Two MA replicates for each clone were done.
2007-07-25 | E-SMDB-3821 | biostudies-arrayexpress
Project description:These experiments were performed to show a serogroup conversion of Vibrio cholerae from O1 to O139. For this purpose, V. cholerae O1 El Tor (A1552) was grown on crab shell fragments to induce natural competence for transformation. Purified DNA (4 ug each) from strain MO10, an O139 serogroup strain, was added after 24h and the cells were further grown for 24h. After detachment from the crab shell fragments, bacteria were poured into soft-agar and overlaid onto LB plates. Mukerjeee's El Tor phage V (a gift of Dr. M.S. Islam) was dropped onto the surface of the bacteria containing soft-agar. The plaques formed by killing non-transformed A1552 cells possessed resistant clones which were picked and further selected for opaque morphotype and agglutination by O139-specific antiserum. Four clones were selected from each independent experiment and analyzed by microarray hybridization (BioPrime. Array CGH Genomic Labeling from Invitrogen). Two microarray replicates were done per clone. Strain Names: ApO139#2 / ApO139#4 / ApO139#6 / ApO139#8 are four clones analyzed after the first experiment; AIIpO139#3 / AIIpO139#4 / AIIpO139#5 / AIIpO139#6 are four clones analyzed after the second independent experiment. Two MA replicates for each clone were done. CGHs of A1552 versus MO10 are provided as control.
2007-08-01 | E-SMDB-3752 | biostudies-arrayexpress
Project description:These experiments were performed to show serogroup conversion in Vibrio cholerae from O1 to O139 in a mixed communities / biofilms. For this purpose, V. cholerae O1 El Tor A1552 and VCO139-Kan strain (a MO10 derivative; O139 serogroup) were grown on crab shell fragments to induce natural competence for transformation. Transformants were selected on LB+Kan+Rif plates. O139 positive transformants have undergone a full exchange of the O1 region by the O139 region. This implies an exchange of an at least 32 kb spanning O1 genomic region by more than 42 kb of the O139 region. The transformation experiment was done at least five independent times; data from four experiments are shown; per experiment one to three clones were analysed by CGH with two experimental replicates each.
2007-07-25 | E-SMDB-3820 | biostudies-arrayexpress
Project description:Vibrio cholerae El Tor O1 Genome sequencing
| PRJNA279011 | ENA