Vibrio cholerae VttR
            <sub>A</sub>
            and VttR
            <sub>B</sub>
            Regulatory Influences Extend beyond the Type 3 Secretion System Genomic Island

Chaand, Mudit; Dziejman, Michelle

doi:10.1128/jb.02151-12

Cited by 12 publications

(14 citation statements)

References 79 publications

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“…Previous results from our laboratory showed that VttR A and VttR B modulate T3SS island gene expression in vitro in the presence of bile (31,34). Data also support a model for hierarchical regulation whereby VttR A regulates the expression of vttR B , since both a ⌬vttR A single-deletion strain and a ⌬vttR A ⌬vttR B double-deletion strain can be complemented for T3SS gene expression by providing vttR B in trans (32).…”

Section: Resultssupporting

confidence: 61%

Regulation by ToxR-Like Proteins Converges on vttR _B Expression To Control Type 3 Secretion System-Dependent Caco2-BBE Cytotoxicity in Vibrio cholerae

et al. 2016

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Genes carried on the type 3 secretion system (T3SS) pathogenicity island of Vibrio cholerae non-O1/non-O139 serogroup strain AM-19226 must be precisely regulated in order for bacteria to cause disease. Previously reported results showed that both T3SS function and the presence of bile are required to cause Caco2-BBE cell cytotoxicity during coculture with strain AM-19226. We therefore investigated additional parameters affecting in vitro cell death, including bacterial load and the role of three transmembrane transcriptional regulatory proteins, VttR A , VttR B , and ToxR. VttR A and VttR B are encoded on the horizontally acquired T3SS genomic island, whereas ToxR is encoded on the ancestral chromosome. While strains carrying deletions in any one of the three transcriptional regulatory genes are unable to cause eukaryotic cell death, the results of complementation studies point to a hierarchy of regulatory control that converges on vttR B expression. The data suggest both that ToxR and VttR A act upstream of VttR B and that modifying the level of either vttR A or vttR B expression can strongly influence T3SS gene expression. We therefore propose a model whereby T3SS activity and, hence, in vitro cytotoxicity are ultimately regulated by vttR B expression. IMPORTANCEIn contrast to O1 and O139 serogroup V. cholerae strains that cause cholera using two main virulence factors (toxin-coregulated pilus [TCP] and cholera toxin [CT]), O39 serogroup strain AM-19226 uses a type 3 secretion system as its principal virulence mechanism. Although the regulatory network governing TCP and CT expression is well understood, the factors influencing T3SS-associated virulence are not. Using an in vitro mammalian cell model to investigate the role of three ToxR-like transmembrane transcriptional activators in causing T3SS-dependent cytotoxicity, we found that expression levels and a hierarchical organization were important for promoting T3SS gene expression. Furthermore, our results suggest that horizontally acquired, ToxR-like proteins act in concert with the ancestral ToxR protein to orchestrate T3SS-mediated pathogenicity. P athogenic bacteria must effectively control the expression of virulence factors in order to achieve productive infection. As a waterborne pathogen, Vibrio cholerae senses and responds to signals from two distinct environments, the aquatic reservoir and the human host, requiring appropriate temporospatial changes in gene expression. Epidemic-causing O1 and O139 serogroup strains use the ToxR-ToxT regulatory hierarchy to modulate the expression of genes encoding factors responsible for colonization (toxin-coregulated pilus [TCP]) and diarrhea (cholera toxin [CT]) (1, 2). Whereas toxR is an ancestral gene found in all V. cholerae strains, toxT is carried on horizontally acquired Vibrio pathogenicity island 1 (VPI-1), which encodes the TCP. ToxR can directly activate transcription from the toxT promoter (3, 4). VPI-1 also encodes the TcpPH proteins, which can increase toxT transcription and are required for...

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Section: Resultssupporting

confidence: 61%

Regulation by ToxR-Like Proteins Converges on vttR _B Expression To Control Type 3 Secretion System-Dependent Caco2-BBE Cytotoxicity in Vibrio cholerae

et al. 2016

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“…Recently genetic, biochemical, and transcriptome analyses have been used to reveal the role of bile salts in inducing the pathogenesis of different enteric bacteria (Joyce & Gahan, ; Sistrunk et al, ). Bile salts mediate reciprocal host‐pathogen crosstalk (Chaand & Dziejman, ; Gotoh et al, ), and there is increasing evidence supporting the role of bile salts in regulating bacterial virulence gene expression (Li et al, ; Xue et al, ; Yang et al, ). ST plays an important role in inducing V .…”

Section: Discussionmentioning

confidence: 99%

The bile salt sodium taurocholate inducesCampylobacter jejuniouter membrane vesicle production and increases OMV-associated proteolytic activity

Elmi

Dorey

Watson

et al. 2017

Cellular Microbiology

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Campylobacter jejuni, the leading cause of bacterial acute gastroenteritis worldwide, secretes an arsenal of virulence-associated proteins within outer membrane vesicles (OMVs). C. jejuni OMVs contain three serine proteases (HtrA, Cj0511, and Cj1365c) that cleave the intestinal epithelial cell (IEC) tight and adherens junction proteins occludin and E-cadherin, promoting enhanced C. jejuni adhesion to and invasion of IECs. C. jejuni OMVs also induce IECs innate immune responses. The bile salt sodium taurocholate (ST) is sensed as a host signal to coordinate the activation of virulence-associated genes in the enteric pathogen Vibrio cholerae. In this study, the effect of ST on C. jejuni OMVs was investigated. Physiological concentrations of ST do not have an inhibitory effect on C. jejuni growth until the early stationary phase. Coculture of C. jejuni with 0.1% or 0.2% (w/v) ST stimulates OMV production, increasing both lipid and protein concentrations. C. jejuni ST-OMVs possess increased proteolytic activity and exhibit a different protein profile compared to OMVs isolated in the absence of ST. ST-OMVs exhibit enhanced cytotoxicity and immunogenicity to T84 IECs and enhanced killing of Galleria mellonella larvae. ST increases the level of mRNA transcripts of the OMVs-associated serine protease genes and the cdtABC operon that encodes the cytolethal distending toxin. Coculture with ST significantly enhances the OMVs-induced cleavage of E-cadherin and occludin. C. jejuni OMVs also cleave the major endoplasmic reticulum chaperone protein BiP/GRP78 and this activity is associated with the Cj1365c protease. These data suggest that C. jejuni responds to the presence of physiological concentrations of the bile salt ST that increases OMV production and the synthesis of virulence-associated factors that are secreted within the OMVs. We propose that these events contribute to pathogenesis.

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“…Although functions of VPA1351 and VPA1353 are not yet determined, VPA1351 is predicted to have structural homology with an MS ring protein of Salmonella enterica SPI‐1 T3SS . In addition, V. cholerae VopH and VopA are required for T3SS effector translocation by the V. cholerae strain AM‐19226 . Based on these observations, VPA1351 and VPA1353 are probably T3SS2‐apparatus‐related proteins, rather than functional effectors in host cells.…”

Section: T3ss2 Effectors: Repertoire and Mechanisms Of Actionmentioning

confidence: 99%

Advances on Vibrio parahaemolyticus research in the postgenomic era

Matsuda

Hiyoshi

Tandhavanant

et al. 2020

Microbiology and Immunology

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Vibrio parahaemolyticus is a leading cause of seafood‐borne bacterial gastroenteritis in humans. Since its discovery in 1950, this bacterium has been isolated in widespread outbreaks and in sporadic cases of gastroenteritis worldwide. Although the exotoxin, thermostable direct hemolysin, had been the focus of extensive research on the pathogenicity of V. parahaemolyticus, the whole‐genome sequencing of a clinical isolate, RIMD2210633 strain, was a breakthrough in this field. The possession of two sets of gene clusters for type III secretion systems (T3SS1 and T3SS2) was unveiled by that genome project. T3SS is a protein export apparatus that delivers bacterial proteins, called effectors, directly into the host's cytosol, to disrupt host cell function. The subsequent studies have established that T3SS2, which is encoded in an 80 kb pathogenicity island called V. parahaemolyticus pathogenicity island (Vp‐PAI), is closely related to enteropathogenicity. Recent functional analyses of Vp‐PAI‐encoded genes revealed the sophisticated mechanisms in V. parahaemolyticus for sensing the intestinal environment and host cell contact, and a dozen T3SS2‐exported proteins encoded in Vp‐PAI. In this review, we summarize recent advances in V. parahaemolyticus research regarding the control of the expression of Vp‐PAI‐encoded genes, structural components and the secretory regulation of T3SS2, and the biological activities of T3SS2‐exported effectors. Thus, Vp‐PAI‐encoded T3SS2 becomes an important key in the postgenomic era to shed light on the enteropathogenic mechanism of V. parahaemolyticus.

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Vibrio cholerae VttR _A and VttR _B Regulatory Influences Extend beyond the Type 3 Secretion System Genomic Island

Cited by 12 publications

References 79 publications

Regulation by ToxR-Like Proteins Converges on vttR _B Expression To Control Type 3 Secretion System-Dependent Caco2-BBE Cytotoxicity in Vibrio cholerae

Regulation by ToxR-Like Proteins Converges on vttR _B Expression To Control Type 3 Secretion System-Dependent Caco2-BBE Cytotoxicity in Vibrio cholerae

The bile salt sodium taurocholate inducesCampylobacter jejuniouter membrane vesicle production and increases OMV-associated proteolytic activity

Advances on Vibrio parahaemolyticus research in the postgenomic era

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Vibrio cholerae VttR A and VttR B Regulatory Influences Extend beyond the Type 3 Secretion System Genomic Island

Cited by 12 publications

References 79 publications

Regulation by ToxR-Like Proteins Converges on vttR B Expression To Control Type 3 Secretion System-Dependent Caco2-BBE Cytotoxicity in Vibrio cholerae

Regulation by ToxR-Like Proteins Converges on vttR B Expression To Control Type 3 Secretion System-Dependent Caco2-BBE Cytotoxicity in Vibrio cholerae

The bile salt sodium taurocholate inducesCampylobacter jejuniouter membrane vesicle production and increases OMV-associated proteolytic activity

Advances on Vibrio parahaemolyticus research in the postgenomic era

Contact Info

Product

Resources

About

Vibrio cholerae VttR _A and VttR _B Regulatory Influences Extend beyond the Type 3 Secretion System Genomic Island

Regulation by ToxR-Like Proteins Converges on vttR _B Expression To Control Type 3 Secretion System-Dependent Caco2-BBE Cytotoxicity in Vibrio cholerae

Regulation by ToxR-Like Proteins Converges on vttR _B Expression To Control Type 3 Secretion System-Dependent Caco2-BBE Cytotoxicity in Vibrio cholerae