The transcriptional activator HIyU of <i>Vibrio cholerae</i>: nucleotide sequence and role in virulence gene expression

Williams, Susan G.; Attridge, Stephen R.; Manning, Paul A.

doi:10.1111/j.1365-2958.1993.tb01735.x

Cited by 77 publications

(79 citation statements)

References 46 publications

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“…Like other hemolysins, El Tor hemolysin has been historically described as a pore-forming toxin (14,37), and its effect has been demonstrated on erythrocytes and epithelial cells (38,40). Although its role in diarrhea has been repeatedly suggested (7,21,36,40), there is only one report demonstrating cytolethal activity of El Tor hemolysin on human intestinal cells up to now (39). Here, by means of the experiments conducted in the Ussing chamber, we went on to prove that the deleterious effects introduced in the cells actually induce an inhibition of water absorption concomitant with an increase in Isc in the human small intestine.…”

Section: Discussionmentioning

confidence: 99%

Genetic Diversity of Vibrio cholerae O1 in Argentina and Emergence of a New Variant

et al. 2003

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The genetic diversity of Vibrio cholerae O1 strains from Argentina was estimated by random amplified polymorphic DNA (RAPD) analysis and pulsed-field gel electrophoresis (PFGE). Twenty-nine isolates carrying the virulence genes ctxA, zot, ace, and tcpA appeared to represent a single clone by both typing methods; while 11 strains lacking these virulence genes exhibited several heterogeneous RAPD and PFGE patterns. Among the last group, a set of isolates from the province Tucumán showed a single RAPD pattern and four closely related PFGE profiles. These strains, isolated from patients with diarrhea, did not produce the major V. cholerae O1 virulence determinants, yet cell supernatants of these isolates caused a heat-labile cytotoxic effect on Vero and Y-1 cells and elicited significant variations on the water flux and short-circuit current in human small intestine mounted in an Ussing chamber. All these effects were completely abolished by incubation with a specific antiserum against El Tor hemolysin, suggesting that this virulence factor was responsible for the toxic activity on both the epithelial cells and the small intestine specimens and may hence be involved in the development of diarrhea. We propose "Tucumán variant" as the designation for this new cluster of cholera toxin-negative V. cholerae O1 strains.Cholera reemerged in Latin America after being absent from the continent for around 100 years. The first case occurred in Peru in 1991 and was caused by a Vibrio cholerae O1 biotype El Tor strain that soon spread to the rest of Latin America at the rate of one country a month (4). The disease appeared in Argentina in February 1992 and has caused seven epidemic outbreaks since then. Several studies have demonstrated that a single clone was responsible for the Latin America epidemic (3,26,34). However, this strain appears to have undergone genetic changes in Peru throughout the years (9), and a second strain has been associated with cholera cases occurring in Mexico and Central America (10). Among the different typing techniques, pulsed-field gel electrophoresis (PFGE) has proved to be highly discriminatory for the analysis of V. cholerae O1 and O139 genetic diversity. This method has been successfully used for molecular epidemiology surveillance in monitoring the dissemination of this pathogen and the emergence of new epidemic clones (1,3,9,10,27). Therefore, in this study we applied PFGE to the study of human and environmental V. cholerae O1 isolates referred to our laboratory from different regions of Argentina during the seven epidemic outbreaks. Additionally, we employed random amplified polymorphic DNA (RAPD) analysis as a second typing technique. This methodology has been used in genetic diversity analysis of different bacterial species, including Escherichia coli (22, 23, 25) and V. cholerae (19, 28).The major virulence determinants normally found in epidemic V. cholerae O1 strains are the potent enterotoxin cholera toxin (CT), the colonization factor toxin-coregulated pilus (TCP), and the regulatory ...

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Section: Discussionmentioning

confidence: 99%

Genetic Diversity of Vibrio cholerae O1 in Argentina and Emergence of a New Variant

et al. 2003

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“…It has been reported that expression of the HlyA haemolysin in V. cholerae is regulated by an 11.9 kDa protein designated HlyU (Williams et al, 1993). Insertional inactivation of the hlyU gene inhibited production of the HlyA haemolysin and a 28 kDa Hcp (haemolysin coregulated protein) protein.…”

Section: Discussionmentioning

confidence: 99%

Inactivation of two haemolytic toxin genes in Aeromonas hydrophila attenuates virulence in a suckling mouse model

1998

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The contribution of two unrelated Aeromonas hydrophila fihaemolytic toxins to virulence was assessed in a suckling mouse model. The first haemolysin gene, isolated from an A. hydrophila A6 cosmid bank, encoded a potential gene product of 621 amino acids and a predicted molecular size of 690 kDa. The inferred amino acid sequence showed 89% identity to the AHHI haemolysin of A. hydrophila ATCC 7966, and 51 O/ O identity to the HlyA haemolysin of Vibrio cholerae E l Tor strain 017. The second haemolysin gene (designated aerA), which encodes aerolysin, a pore-forming toxin, was partially cloned by PCR for the purpose of mutant construction. This PCR product was a 1040 bp fragment from the C-terminal region of aerA. It is proposed that the 69.0 kDa V. cholerae-HlyA-like haemolysin gene be termed hlyA to contrast with the aerA terminology for the aerolysin. A suicide vector was used to inactivate both the hlyA and aerA genes in A. hydrophila A6. When assessed in the suckling mouse model, only the hlyA aerA double mutant showed a statistically significant reduction in virulence -a 20-fold change in LD,, (Scheffe test, P < 0 0 5 ) . Cytotoxicity t o buffalo green monkey kidney cell monolayers and haemolysis on horse blood agar were eliminated only in the hlyA aerA double mutants. This is the f i r s t report of cloning and mutagenesis of two unrelated haemolytic toxin genes in the same strain of a mesophilic aeromonad. For A. hydrophila, a two-toxin model provides a more complete explanation of virulence.

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“…Although by examination of their nucleotide sequence, the hlyA, hlyB and hlyC genes do not appear to comprise a classical operon, it is possible they are co-regulated at least in part by HlyU, a recently described transcriptional activator of hlyA (Williams et al, 1993). A strain containing the hlyU mutation was recently shown to be attenuated for virulence in the infant mouse model and furthermore, the observed attenuation was not fully explained by loss of HlyA expression (Williams et al, 1993). Therefore, HlyU may regulate additional virulence factors and, if it is responsible for expression of hlyC, it follows that HlyU may be a regulator that responds to in vivo environmental signals.…”

Section: In Vivo-induced Transcript Coding For a Secreted Lipasementioning

confidence: 99%

Use of recombinase gene fusions to identify Vibrio cholerae genes induced during infection

Camilli

Mekalanos

1995

Molecular Microbiology

259

240

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SummaryA complete understanding of host-parasite interactions must necessarily include the identification and characterization of gene products expressed by both parties during the infectious process. We have developed a new screen to identify bacterial genes that are transcriptionally induced during infection of a host animal. The method is based on pre-selection of strains carrying tnpR operon fusions (encoding resolvase, a site-specific DNA recombinase) which are not expressed in vitro, followed by screening for a subset of these strains that subsequently express resolvase within the host environment. The latter subset was recognized as recombinants that had deleted a resolvasespecific reporter construct. Thirteen transcription units of Vibrio cholerae were identified that were induced during infection in an infant mouse model of cholera. Five of these were predicted to encode polypeptides with diverse functions in metabolism, biosynthesis and motility; one encoded a secreted lipase; two appear to be antisense to genes involved in motility; and five are predicted to encode polypeptides of unknown function. Three of the transcripts were shown to be required for full virulence in infant mice, as assessed by competition experiments.

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The transcriptional activator HIyU of Vibrio cholerae: nucleotide sequence and role in virulence gene expression

Cited by 77 publications

References 46 publications

Genetic Diversity of Vibrio cholerae O1 in Argentina and Emergence of a New Variant

Genetic Diversity of Vibrio cholerae O1 in Argentina and Emergence of a New Variant

Inactivation of two haemolytic toxin genes in Aeromonas hydrophila attenuates virulence in a suckling mouse model

Use of recombinase gene fusions to identify Vibrio cholerae genes induced during infection

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