Regulatory mechanism of host cell contact-dependent T3SS gene expression in Vibrio parahaemolyticus
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ABSTRACT:
PROVIDER: PRJNA1108615 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28926210.fastq.gz | Fastqsanger.gz | |||
| SRR28926211.fastq.gz | Fastqsanger.gz | |||
| SRR28926212.fastq.gz | Fastqsanger.gz | |||
| SRR28926213.fastq.gz | Fastqsanger.gz | |||
| SRR28926214.fastq.gz | Fastqsanger.gz |
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Project description:Many pathogenic bacteria have mechanisms that regulate gene expression in response to the surrounding environment to establish an infection. One such mechanism is the regulation of gene expression in response to contact with host cells. Here, we show that Vibrio parahaemolyticus, a causative agent of foodborne gastroenteritis, has a host cell contact-dependent regulatory mechanism for virulence gene expression. T3SS2, an essential virulence determinant for acute gastroenteritis encoded by V. parahaemolyticus pathogenicity island (Vp-PAI), recognizes host cell contact by sensing high intracellular K+ levels and switches its secretory substrates. This switching of secretory substrates is regulated by proteins called gatekeepers. Mutants deficient in the gatekeeper gene lose the ability to switch secretory substrates and lock their secretory state into contact with the host cell. Transcriptome analysis of T3SS2 gatekeeper gene-deficient strains showed that the genes encoded by Vp-PAI were specifically upregulated, and this upregulation was dependent on T3SS2 secretory activity, implying the presence of a negative regulator secreted by T3SS2. Comparative proteomic analyses identified a previously unidentified T3SS2 secretory substrate, VtrN, that negatively regulates Vp-PAI gene transcription. Secretion of VtrN was promoted under conditions that mimic host cell contact as well as other T3SS2 effectors. vtrN gene deletion specifically upregulated Vp-PAI gene expression, but unlike gatekeeper gene deletion, it was independent of T3SS2 secretory activity. Furthermore, VtrN interacted with VtrB, a transcription factor essential for Vp-PAI-encoded gene expression and repressed its transcriptional activity. Thus, V. parahaemolyticus has a mechanism to upregulate virulence gene expression in response to host-cell contact by utilizing the host-cell recognition mechanism of T3SS2.
2025-06-09 | GSE266863 | GEO
Project description:Here we probe the global response to calcium in the marine bacterium and pathogen Vibrio parahaemolyticus by using transcriptome, reporter and phenotypic analyses. Swarming gene expression and motility were enhanced by calcium. Calcium also stimulated expression and function of one of the organismM-bM-^@M-^Ys two type three secretion systems (T3SS1 but not the T3SS2). Although low calcium is an inducing signal for the T3SS of many organisms, calcium stimulation of T3SS has not been reported before. EGTA was also a stimulus for T3SS1 expression and activity; however this appeared to be the consequence of iron rather than calcium chelation. LafK, a key regulator of swarming genes, was found necessary for calcium induction of T3SS1 gene transcription and cytotoxicity. Regulation of swarming and T3SS1 were additionally linked by a negative feedback loop propagated by ExsA. Overexpression of exsA was used to probe the extent of the T3SS1 regulon and verify its coincident induction by calcium and EGTA. The calcium transcriptome analysis revealed a calcium-repressed LysR-type transcriptional regulator; CalR was shown to repress swarming and T3SS1 gene expression. Thus in V. parahaemolyticus, calcium influences gene expression and behavior and seems a signal pertinent for surface colonization and virulence. The gene expression profiles of Vibrio parahaemolyticus cells grown on rich medium or medium supplemented with CaCl2 or EGTA were compared using Affymetrix custom microarrays.
2010-11-05 | E-GEOD-22190 | biostudies-arrayexpress
Project description:The shrimp aquaculture industry is vulnerable to large losses due to acute hepatopancreatic necrosis disease (AHPND), caused by the bacterium Vibrio parahaemolyticus. The mechanism by which the pathogen causes disease, and the host immune response, is not completely understood. The shrimp hepatopancreas is a multi-functional organ with roles in digestion, immunity, molting and reproduction. Therefore, we set out to characterize the cells of the hepatopancreas and the host response to Vibrio parahaemolyticus infection at single-cell resolution. The hepatopancreas from three individual shrimp were processed to create a single-cell transcriptomic atlas. Then the hepatopancreas from three Vibrio parahaemolyticus infected and two mocked treated shrimp were sampled for infection study. All single-cell libraries were generated using the 10X Genomics platform and sequenced on an Illumina sequencer. Data were aligned to the Litopenaeus vannamei reference genome using Cell Ranger. Seurat and clusterProfiler were used for downstream analyses. Cells of the hepatopancreas were characterized and the transcriptomic response to AHPND-causing V. parahaemolyticus was examined. Data will inform further functional studies and has the potential to aid in the development of novel preventative measures or treatments.
2026-02-18 | GSE306674 | GEO
Project description:In order to gain a better understanding of the impact of Vibrio parahaemolyticus infection on genetic regulation of Litopenaeus vannamei,we performed a miRNA-seq analysis in the hepatopancreas of Litopenaeus vannamei challenged with Vibrio parahaemolyticus, using the Illumina HiSeq 2500 platform.
2020-06-18 | GSE107696 | GEO
Project description:Here we probe the global response to calcium in the marine bacterium and pathogen Vibrio parahaemolyticus by using transcriptome, reporter and phenotypic analyses. Swarming gene expression and motility were enhanced by calcium. Calcium also stimulated expression and function of one of the organism’s two type three secretion systems (T3SS1 but not the T3SS2). Although low calcium is an inducing signal for the T3SS of many organisms, calcium stimulation of T3SS has not been reported before. EGTA was also a stimulus for T3SS1 expression and activity; however this appeared to be the consequence of iron rather than calcium chelation. LafK, a key regulator of swarming genes, was found necessary for calcium induction of T3SS1 gene transcription and cytotoxicity. Regulation of swarming and T3SS1 were additionally linked by a negative feedback loop propagated by ExsA. Overexpression of exsA was used to probe the extent of the T3SS1 regulon and verify its coincident induction by calcium and EGTA. The calcium transcriptome analysis revealed a calcium-repressed LysR-type transcriptional regulator; CalR was shown to repress swarming and T3SS1 gene expression. Thus in V. parahaemolyticus, calcium influences gene expression and behavior and seems a signal pertinent for surface colonization and virulence.
2010-11-05 | GSE22190 | GEO
Project description:Elucidation of host-pathogen interaction is essential for developing effective strategies to combat bacterial infection. Dual RNA-Seq using cultured cells or tissues/organs as the pathogen host has emerged as a novel strategy to understand the response concurrently from both pathogen and host at cellular level. However, bacterial infection mostly causes systematic responses from the host at organism level where the interplay is urgently to be understood but inevitably being neglected by the current practice. Here, we developed an approach that simultaneously monitor the genome-wide infection-linked transcriptional alterations in both pathogenic Vibrio parahaemolyticus and the infection host nematode Caenorhabditis elegans. Besides the dynamic alterations in both transcriptomes of C. elegans and V. parahaemolyticus during infection, we identify a two-component system, BarA/UvrY, that are essential for host colonization. BarA/UvrY not only controls the virulence factors in V. parahaemolyticus including Type III and Type VI secretion systems, but also represses the MAP kinase mediated signaling cascades to attenuate innate immune responses. Thus, our study exemplifies the use of dual RNA-Seq at organism level to uncover previously unrecognized interplay between host and pathogen.
2020-09-10 | GSE138199 | GEO
Project description:In order to gain a better understanding of the impact of Vibrio parahaemolyticus infection on genetic regulation of Litopenaeus vannamei,we performed a transcriptome analysis in the hepatopancreas of Litopenaeus vannamei challenged with Vibrio parahaemolyticus, using the Illumina HiSeq 2500 platform.
2020-06-18 | GSE107697 | GEO
Project description:Comparative proteomics to identify proteins found in the media of Vibrio parahaemolyticus RIMD 2210633 bacteria with an active T6SS2 compared to bacteria with inactive T6SS2. Bacteria with an active T6SS2 are Vibrio parahaemolyticus RIMD 2210633 inwhich hcp1 was deleted to inactivate T6SS1. T6SS2 inactive bacteria are the former strain with an additional deletion in hcp2. Both strains express TfoX from an arabinose-inducible plasmid to induce T6SS2 activity.
2023-02-05 | PXD037980 | Pride
Project description:Vibrio parahaemolyticus an emerging pathogen that is a causative agent of foodborne gastroenteritis when raw or undercooked seafood is consumed. Previous microarray data using a Vibrio parahaemolyticus RIMD2210633 chip has shown the master quorum-sensing regulator OpaR controls virulence, type III and type VI secretion systems, and flagellar and capsule production genes. In a parallel study, RNA-Seq was used to comparatively study the transcriptome changes of wild type Vibrio parahaemolyticus BB22 and a ΔopaR strain directly. Differences in mRNA expression were analyzed using next generation Illumina sequencing and bioinformatics techniques to align and count reads. A comparison with the previous microarray data showed good correlation between the shared genes. The RNA-Seq offered an insight into control of genes specific to the Vibrio parahaemolyticus BB22 strain as well as a new look at the sRNAs that are expressed. Eleven transcriptional regulators with greater than 4 fold regulation in the previous microarray study and 2 fold regulation in the RNA-Seq analysis, were chosen to validate the data using qRT-PCR and further characterized with electrophoretic mobility shift assays (EMSAs) to determine if they are direct targets of OpaR. The transcription factors chosen play key roles in virulence, surface motility, cell to cell interactions, and cell surface characteristics. One small RNA was identified in the RNA-Seq data to be quorum-sensing controlled and unidentified by other programs. The RNA-Seq data has aided in understanding and elucidating the hierarchy of quorum-sensing control of OpaR in Vibrio parahaemolyticus. The wild type Vibrio parahaemolyticus BB22 strain LM5312 and an opaR deletion strain LM5674 were analyzed for mRNA expression using RNA-Seq.
2013-12-31 | E-GEOD-53639 | biostudies-arrayexpress
Project description:V. parahaemolyticus and E. coioides were served as research objects to explore the interaction mechanism between pathogen and host. infection. The mRNA-miRNA integrated analysis of the spleen of E. coioides infected with V. parahaemolyticus was performed, and several crucial pathways were screened, which may contribute to treatment of V. parahaemolyticus infection.
2022-07-03 | GSE207125 | GEO