scholarly journals The virulence gene activator ToxT from Vibrio cholerae is a member of the AraC family of transcriptional activators.

1992 ◽  
Vol 174 (21) ◽  
pp. 6974-6980 ◽  
Author(s):  
D E Higgins ◽  
E Nazareno ◽  
V J DiRita
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Gene ◽  
Transcriptional Activators ◽  
Arac Family

Prevalence and Molecular Characterization of Vibrio cholerae from Ice and Beverages Sold in Jakarta, Indonesia, Using Most Probable Number and Multiplex PCR

2012 ◽  
Vol 75 (4) ◽  
pp. 651-659 ◽  
Author(s):  
DIANA E. WATURANGI ◽  
NATANIA PRADITA ◽  
JESSICA LINARTA ◽  
SWAPAN BANERJEE
Keyword(s):  
Multiplex Pcr ◽  
Vibrio Cholerae ◽  
Virulence Gene ◽  
Watery Diarrhea ◽  
Most Probable Number ◽  
Intestinal Infection ◽  
Safety Measures ◽  
Probable Number ◽  
Tropical Regions

Vibrio cholerae is well recognized as the causative agent of cholera, an acute intestinal infection characterized by watery diarrhea that may lead to dehydration and death in some cases. V. cholerae is a natural inhabitant of the aquatic environment in the tropical regions. Jakarta has the highest percentage of individuals affected by sporadic diarrheal illness compared with other areas in Indonesia. Inadequate safety measures for drinking water supplies, improper sanitation, and poor hygiene can increase the risk of cholera outbreaks. Few studies have been conducted on the prevalence of these bacteria in ice and beverages that are popularly sold and consumed in Jakarta. In this study, we detected and quantified V. cholerae from ice and beverages collected from several areas in five regions of Jakarta. Levels of V. cholerae in both ice and beverages were determined with the three-tube most-probable-number (MPN) method and ranged from <0.3 to >110 MPN/ml. The presence of regulatory and virulence gene sequences was determined by using uniplex and multiplex PCR assays. Of 110 samples tested, 33 (30%) were positive for V. cholerae; 21 (64%) were ice samples and the remaining 12 (36%) were beverages. A total of 88 V. cholerae strains were isolated, based on the presence of the toxR gene sequence identified by PCR. Other genetic markers, such as hlyA (59%), ompU (16%), and ctxA (19%), also were found during the search for potential pathogenic strains. The detection and isolation of potentially harmful V. cholerae from ice and beverages in Jakarta indicate that these products pose a health risk from choleragenic vibrios, particularly because of the emergence of classical biotypes of V. cholerae O1 and potentially harmful non-O1 serovars of this species.

scholarly journals Cyclo(valine–valine) inhibits Vibrio cholerae virulence gene expression

Microbiology ◽  
2014 ◽  
Vol 160 (6) ◽  
pp. 1054-1062 ◽  
Author(s):  
Amit Vikram ◽  
Vanessa M. Ante ◽  
X. Renee Bina ◽  
Qin Zhu ◽  
Xinyu Liu ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Factor ◽  
Inhibitory Activity ◽  
Virulence Gene ◽  
Side Chains ◽  
Cyclic Dipeptides ◽  
Virulence Gene Expression ◽  
Factor Production ◽  
Virulence Regulator ◽  
Virulence Factor Production

Vibrio cholerae has been shown to produce a cyclic dipeptide, cyclo(phenylalanine–proline) (cFP), that functions to repress virulence factor production. The objective of this study was to determine if heterologous cyclic dipeptides could repress V. cholerae virulence factor production. To that end, three synthetic cyclic dipeptides that differed in their side chains from cFP were assayed for virulence inhibitory activity in V. cholerae. The results revealed that cyclo(valine–valine) (cVV) inhibited virulence factor production by a ToxR-dependent process that resulted in the repression of the virulence regulator aphA. cVV-dependent repression of aphA was found to be independent of known aphA regulatory genes. The results demonstrated that V. cholerae was able to respond to exogenous cyclic dipeptides and implicated the hydrophobic amino acid side chains on both arms of the cyclo dipeptide scaffold as structural requirements for inhibitory activity. The results further suggest that cyclic dipeptides have potential as therapeutics for cholera treatment.

scholarly journals The Cpx System Regulates Virulence Gene Expression in Vibrio cholerae

2015 ◽  
Vol 83 (6) ◽  
pp. 2396-2408 ◽  
Author(s):  
Nicole Acosta ◽  
Stefan Pukatzki ◽  
Tracy L. Raivio
Keyword(s):  
Vibrio Cholerae ◽  
Response Regulator ◽  
Bacterial Species ◽  
Virulence Gene ◽  
Receptor Protein ◽  
Virulence Determinants ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Envelope Stress ◽  
El Tor

Bacteria possess signal transduction pathways capable of sensing and responding to a wide variety of signals. The Cpx envelope stress response, composed of the sensor histidine kinase CpxA and the response regulator CpxR, senses and mediates adaptation to insults to the bacterial envelope. The Cpx response has been implicated in the regulation of a number of envelope-localized virulence determinants across bacterial species. Here, we show that activation of the Cpx pathway inVibrio choleraeEl Tor strain C6706 leads to a decrease in expression of the major virulence factors in this organism, cholera toxin (CT) and the toxin-coregulated pilus (TCP). Our results indicate that this occurs through the repression of production of the ToxT regulator and an additional upstream transcription factor, TcpP. The effect of the Cpx response on CT and TCP expression is mostly abrogated in a cyclic AMP receptor protein (CRP) mutant, although expression of thecrpgene is unaltered. Since TcpP production is controlled by CRP, our data suggest a model whereby the Cpx response affects CRP function, which leads to diminished TcpP, ToxT, CT, and TCP production.

scholarly journals Integration Host Factor Positively Regulates Virulence Gene Expression in Vibrio cholerae

2008 ◽  
Vol 190 (13) ◽  
pp. 4736-4748 ◽  
Author(s):  
Emily Stonehouse ◽  
Gabriela Kovacikova ◽  
Ronald K. Taylor ◽  
Karen Skorupski
Keyword(s):  
Gene Expression ◽  
Vibrio Cholerae ◽  
Virulence Gene ◽  
Toxin Production ◽  
Dnase I ◽  
Integration Host Factor ◽  
Host Factor ◽  
Mobility Shift ◽  
Virulence Gene Expression ◽  
Dnase I Footprinting

ABSTRACT Virulence gene expression in Vibrio cholerae is dependent upon a complex transcriptional cascade that is influenced by both specific and global regulators in response to environmental stimuli. Here, we report that the global regulator integration host factor (IHF) positively affects virulence gene expression in V. cholerae. Inactivation of ihfA and ihfB, the genes encoding the IHF subunits, decreased the expression levels of the two main virulence factors tcpA and ctx and prevented toxin-coregulated pilus and cholera toxin production. IHF was found to directly bind to and bend the tcpA promoter region at an IHF consensus site centered at position −162 by using gel mobility shift assays and DNase I footprinting experiments. Deletion or mutation of the tcpA IHF consensus site resulted in the loss of IHF binding and additionally disrupted the binding of the repressor H-NS. DNase I footprinting revealed that H-NS protection overlaps with both the IHF and the ToxT binding sites at the tcpA promoter. In addition, disruption of ihfA in an hns or toxT mutant background had no effect on tcpA expression. These results suggest that IHF may function at the tcpA promoter to alleviate H-NS repression.

scholarly journals Structural basis for virulence regulation in Vibrio cholerae by unsaturated fatty acid components of bile

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Justin T. Cruite ◽  
Gabriela Kovacikova ◽  
Kenzie A. Clark ◽  
Anne K. Woodbrey ◽  
Karen Skorupski ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Structural Model ◽  
Unsaturated Fatty Acids ◽  
Diarrheal Disease ◽  
Bacterial Pathogen ◽  
Virulence Gene ◽  
Structural Basis ◽  
Active Conformation ◽  
Structural Mechanism ◽  
Virulence Gene Regulation

AbstractThe AraC/XylS-family transcriptional regulator ToxT is the master virulence activator of Vibrio cholerae, the gram-negative bacterial pathogen that causes the diarrheal disease cholera. Unsaturated fatty acids (UFAs) found in bile inhibit the activity of ToxT. Crystal structures of inhibited ToxT bound to UFA or synthetic inhibitors have been reported, but no structure of ToxT in an active conformation had been determined. Here we present the 2.5 Å structure of ToxT without an inhibitor. The structure suggests release of UFA or inhibitor leads to an increase in flexibility, allowing ToxT to adopt an active conformation that is able to dimerize and bind DNA. Small-angle X-ray scattering was used to validate a structural model of an open ToxT dimer bound to the cholera toxin promoter. The results presented here provide a detailed structural mechanism for virulence gene regulation in V. cholerae by the UFA components of bile and other synthetic ToxT inhibitors.

scholarly journals Effect of Fatty Acids and Cholesterol Present in Bile on Expression of Virulence Factors and Motility of Vibrio cholerae

2007 ◽  
Vol 75 (4) ◽  
pp. 1946-1953 ◽  
Author(s):  
Arpita Chatterjee ◽  
Pradeep K. Dutta ◽  
Rukhsana Chowdhury
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Unsaturated Fatty Acids ◽  
Virulence Gene ◽  
Gene Repression ◽  
Heterogeneous Mixture ◽  
Independent Manner ◽  
Regulatory Cascade

ABSTRACT Bile induces pleiotropic responses that affect production of virulence factors, motility, and other phenotypes in the enteric pathogen Vibrio cholerae. Since bile is a heterogeneous mixture, crude bile was fractionated, and the components that mediate virulence gene repression and enhancement of motility were identified by nuclear magnetic resonance, gas chromatography (GC), and GC-mass spectrometry analyses. The unsaturated fatty acids detected in bile, arachidonic, linoleic, and oleic acids, drastically repressed expression of the ctxAB and tcpA genes, which encode cholera toxin and the major subunit of the toxin-coregulated pilus, respectively. The unsaturated fatty acid-dependent repression was due to silencing of ctxAB and tcpA expression by the histone-like nucleoid-structuring protein H-NS, even in the presence of the transcriptional activator ToxT. Unsaturated fatty acids also enhanced motility of V. cholerae due to increased expression of flrA, the first gene of a regulatory cascade that controls motility. H-NS had no role in the fatty acid-mediated enhancement of motility. It is likely that the ToxR/ToxT system that negatively regulates motility is rendered nonfunctional in the presence of unsaturated fatty acids, leading to an increase in motility. Motility and flrA expression were also increased in the presence of cholesterol, another component of bile, in an H-NS- and ToxR/ToxT-independent manner.

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