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Vibrio vulnificus CMCP6

ABSTRACT: Transcriptome duplicates of Vibrio vulnificus CMCP6 brpT and brpR brpT mutant strains

PROVIDER: PRJNA695027 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR13557777_1.fastq.gz	Fastqsanger.gz
	SRR13557777_2.fastq.gz	Fastqsanger.gz
	SRR13557778_1.fastq.gz	Fastqsanger.gz
	SRR13557778_2.fastq.gz	Fastqsanger.gz
	SRR13557779_1.fastq.gz	Fastqsanger.gz

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European eel immune response against Vibrio vulnificus challenge

Project description:Vibriosis caused by Vibrio vulnificus on eels represents an important threat for this specie under culture conditions. Development of new transcriptomic tools is essential to increase the knowledge of eel biology, that nowadays is scarcer. Therefore, using previous results obtained by 454 sequencing of the eel immune-enriched transcriptome, an eel-specific custom microarray have been designed. Gills transcriptomic pattern were analyzed as a principal portal of entry for pathogens in fish after 1h of bath infection with Vibrio vulnificus to describe gill immune response. Moreover, two different strains were used, vibro vulnificus wild type (R99) and rtx double mutant (CT285), to asses the virulence of these pathogen caused by MARTX. Adult european eels were bath infected with two Vibrio vulnificus strains, the wild type and double Rtx mutant (CT285). After 0, 3, 12h post-infection eel gills were sampled. Three individuals per experimental point were sampled, including a Control group and a Handling control group. Obtaining a total of 24 samples. The transcriptomic profile was described for each individual sample.

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Project description:Transcriptome duplicates of Vibrio vulnificus MO6-24/O wild type and carR mutant strains

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Project description:IscR is a novel global regulator potentially contributing to the overall success in survival and pathogenesis of V. vulnificus by coordinating the regulation of various virulence factors. The profiles of transcripts from the V. vulnificus iscR mutant and the parental wild type were compared by using a V. vulnificus whole-genome microarray. Two-condition experiment: Wild type vs. iscR mutant. Biological replicates: 3 control, 3 mutant strains, independently grown and harvested. One replicate per array. For transcriptome analysis, the V. vulnificus whole genome TwinChip, manufactured and kindly provided by the 21C Frontier Microbial Genomics and Applications Center (Daejeon, South Korea), was used.

2013-02-27 | E-GEOD-44679 | biostudies-arrayexpress

Vibrio vulnificus: Wild-type vs. smcR mutant (V. vulnificus quorum sensing master regulator)

Project description:Two-condition experiment, Wild-type vs. smcR mutant. Biological replicates: 3 control, 3 mutant strains, independently grown and harvested. One replicate per array. A significant portion of the SmcR regulon predicted on the basis of microarray analysis results is indeed regulated by SmcR and that SmcR is a global regulator in V. vulnificus. For transcriptome analysis, the V. vulnificus whole genome TwinChip, manufactured and kindly provided by the 21C Frontier Microbial Genomics and Applications Center(Daejeon, South Korea), was used.

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Vibrio vulnificus strain:FORC_036

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Project description:Two-condition experiment, Wild-type biofilm cells vs. smcR mutant biofilm cells. Biological replicates: 3 control, 3 mutant strains, independently grown and harvested. One replicate per array. A significant portion of the SmcR regulon predicted on the basis of microarray analysis results is indeed regulated by SmcR and that SmcR functions on biofilm dispersion in V. vulnificus. For transcriptome analysis, the V. vulnificus whole genome TwinChip, manufactured by e-biogen (Seoul, South Korea), was used.

2011-12-31 | E-GEOD-32270 | biostudies-arrayexpress

Vibrio vulnificus: Wild-type vs. smcR mutant (V. vulnificus quorum sensing master regulator)

2011-09-20 | GSE32212 | GEO

Role of AcsR in expression of the acetly-CoA synthetase gene in Vibrio vulnificus

Project description:VarS/A is one of the global factors regulating diverse aspects of metabolism and virulence of bacteria including pathogenic Vibrio spp. An experiment to identify VarS/A-regulon in V. vulnificus revealed that a putative LuxR-type transcriptional regulator was down-regulated in ΔvarA mutant. To investigate the roles of this regulatory cascade from VarS/A to a LuxR-type regulator in V. vulnificus, the target gene regulated by a LuxR-regulator was identified and its expression was characterized.

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Vibrio vulnificus MARTX toxin effector domains differentially remodel the transcriptional response of intestinal epithelial cells

Project description:Vibrio vulnificus is an foodborne pathogen that can cause gastroenteritis and septicemia in humans. V. vulnificus secretes a multifunctional autoprocessing repeats-in-toxin (MARTX) toxin as an essential virulence factor to cause disease. MARTX toxins are pore-forming toxins that translocate multiple functionally independent effector domains into a target cell. MARTX toxins of V. vulnificus can contain anywhere from 3 to 5 of the 10 identified effector domains and strains with different effector repertories having varying virulence potential. The goal of this study was to compare how different effector combinations from an F-type MARTX toxin differentially remodel the transcriptional response of human intestinal epithelial cells (IECs). F-type MARTX toxins contain five effector domains – the actin crosslinking domain (ACD), two copies the makes caterpillar floppy-like domain (MCF), and alpha-beta hydrolase (ABH) domain, and the Ras/Rap1 specific endopeptidase (RRSP). Cultured human IECs were treated with V. vulnificus or strains modified to secrete a toxin with only ACD, ACD with MCF-ABH, ACD with RRSP, or no active effectors. We demonstrate that when no active effectors are present, the bacterium induces minimal changes in the transcriptional profile of IECs. However, the strains containing different effector combinations each uniquely remodeled the transcriptional profile of IECs. These data provide insight into how V. vulnificus strains with varying effector combinations can differentially regulate the host cell response to cause disease.

2021-11-21 | GSE189194 | GEO

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