Ontology highlight
ABSTRACT:
PROVIDER: PRJNA713318 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13925234.fastq.gz | Fastqsanger.gz | |||
| SRR13925235.fastq.gz | Fastqsanger.gz | |||
| SRR13925236.fastq.gz | Fastqsanger.gz | |||
| SRR13925237.fastq.gz | Fastqsanger.gz | |||
| SRR13925238.fastq.gz | Fastqsanger.gz |
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Project description:To determine whether the Vibrio cholerae type VI secretion system (T6SS) is functional during animal infection, derivatives of V52 were used to infect infant mice. In this infection model, a diarrheal response occurred and effector translocation could be detected. These host responses were dependent on a functional T6SS and on the actin cross-linking effector domain of VgrG-1. Gene expression and histological studies showed innate immune activation and immune cell infiltration in the intestinal lumen.
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Project description:Vibrio species are recognized for their role in food- and water-borne diseases in humans, fish, and aquatic invertebrates. We screened bacterial strains isolated from raw food shrimp for those that are bactericidal to Vibrio strains. Here we identify and characterize Aeromonas dhakensis strain A603 which shows robust bactericidal activity specifically towards Vibrio and related taxa but less potency toward other Gram-negative species. Using the A603 genome and genetic analysis, we show that two antibacterial mechanisms account for its vibriocidal activity -- a highly potent Type Six Secretion System (T6SS) and biosynthesis of a vibriocidal phenazine-like small molecule, named here as Ad-Phen. Further analysis indicates coregulation between Ad-Phen and a pore-forming T6SS effector TseC, which potentiates V. cholerae to killing by Ad-Phen.
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Project description:In marine Vibrio species, chitin-induced natural transformation enables bacteria to take up DNA from the external environment and integrate it into their genome via homologous recombination. Expression of the master competence regulator TfoX bypasses the need for chitin induction and drives expression of the genes required for competence in several Vibrio species. Here, we show that TfoX expression in two Vibrio campbellii strains, DS40M4 and NBRC 15631, enables high frequencies of natural transformation. Conversely, transformation was not achieved in the model quorum-sensing strain V. campbellii BB120 (previously classified as Vibrio harveyi). Surprisingly, we find that quorum sensing is not required for transformation in V. campbellii DS40M4. This result is in contrast to Vibrio cholerae that requires the quorum-sensing regulator HapR to activate the competence regulator QstR. However, similar to V. cholerae, QstR is necessary for transformation in DS40M4. To investigate the difference in transformation frequencies between BB120 and DS40M4, we used previously studied V. cholerae competence genes to inform a comparative genomics analysis coupled with transcriptomics. BB120 encodes homologs of all known competence genes, but most of these genes were not induced by ectopic expression of TfoX, which likely accounts for the non-functional natural transformation in this strain. Comparison of transformation frequencies among Vibrio species indicates a wide disparity among even closely related strains, with Vibrio vulnificus having the lowest functional transformation frequency. We show that ectopic expression of both TfoX and QstR is sufficient to produce a significant increase in transformation frequency in Vibrio vulnificus.
2019-11-14 | GSE136941 | 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.
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Project description:We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. C. elegans were exposed to Vibrio cholerae and E.coli then hybridization on Affymetrix microarray chips.
2011-12-02 | E-GEOD-34026 | biostudies-arrayexpress
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
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Project description:Adapting to nutritional downshifts is crucial for the survival of Vibrio cholerae. CgtA, a 50S ribosome-associated essential GTPase, is a bonafide stringent response protein. CgtA, in association with SpoT, modulates the intracellular (p)ppGpp alarmone levels in a nutrient-rich environment. We studied the influence of CgtA during the growth of V. cholerae in a minimal medium in contrast to its pre-defined role in a nutrient-rich medium. Here, we show the pleiotropic effects of CgtA on growth, viability, motility, morphology, and persister phenotype of a V. cholerae strain where the full-length wildtype (Wt) cgtA was deleted. An in-frame deletion of the 52 amino acids long unstructured C-terminal domain of the CgtA GTPase defined its in vivo functionality. Proteomic analyses revealed that loss of CgtA significantly altered 311 proteins involved in diverse cellular processes. However, the CgtA C-terminus deleted strain altered 240 proteins with a major overlap with the full-length cgtA deleted condition. A sustained mRNA expression pattern of CgtA is observed in a minimal medium. Whereas, in nutrient-rich LB medium, intermittent expression of cgtA is observed with the highest expression during the late-logarithmic to early-stationary phase. We propose that minimal media-associated nutrient stress coupled to cgtA depletion aggravates the intracellular stress in V. cholerae, leading to abnormal protein synthesis, altered DNA replication, and transcriptional machinery, negatively affecting cellular energy metabolism and many vital processes. This study suggests that the nutrient-media-dependent controlled expression of CgtA is a mechanism by which V. cholerae can remodel its transcriptome and proteome. Our study reveals an alternative facet of the survival of V. cholerae during nutritional downshift and the consequences concomitantly with cgtA knockdown as evident from the complex altered regulatory network.
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Project description:We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process.
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Project description:We used RNA-seq to determine transcriptional profiles of whole guts or IPCs isolated from guts infected with wild type or type VI secretion system deficient Vibrio cholerae. We found significant differences between guts and progenitor cells infected wild type or type VI secretion system deficient Vibrio cholerae.
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