scholarly journals Expression of the Vibrio cholerae gene encoding aldehyde dehydrogenase is under control of ToxR, the cholera toxin transcriptional activator.

1991 ◽  
Vol 173 (9) ◽  
pp. 2842-2851 ◽  
Author(s):  
C Parsot ◽  
J J Mekalanos
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Aldehyde Dehydrogenase ◽  
Transcriptional Activator ◽  
Gene Encoding

scholarly journals 1.65 Å resolution structure of the AraC-family transcriptional activator ToxT fromVibrio cholerae

2016 ◽  
Vol 72 (9) ◽  
pp. 726-731 ◽  
Author(s):  
Jiaqin Li ◽  
Graham Wehmeyer ◽  
Scott Lovell ◽  
Kevin P. Battaile ◽  
Susan M. Egan
Keyword(s):  
Crystal Structure ◽  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Causative Agent ◽  
Transcriptional Activator ◽  
Current Structure ◽  
Transcriptional Activator Protein ◽  
Resolution Structure ◽  
Arac Family

ToxT is an AraC-family transcriptional activator protein that controls the expression of key virulence factors inVibrio cholerae, the causative agent of cholera. ToxT directly activates the expression of the genes that encode the toxin-coregulated pilus and cholera toxin, and also positively auto-regulates its own expression from thetcppromoter. The crystal structure of ToxT has previously been solved at 1.9 Å resolution (PDB entry 3gbg). In this study, a crystal structure of ToxT at 1.65 Å resolution with a similar overall structure to the previously determined structure is reported. However, there are distinct differences between the two structures, particularly in the region that extends from Asp101 to Glu110. This region, which can influence ToxT activity but was disordered in the previous structure, can be traced entirely in the current structure.

scholarly journals Enterotoxigenicity of Mature 45-Kilodalton and Processed 35-Kilodalton Forms of Hemagglutinin Protease Purified from a Cholera Toxin Gene-Negative Vibrio cholerae Non-O1, Non-O139 Strain

2006 ◽  
Vol 74 (5) ◽  
pp. 2937-2946 ◽  
Author(s):  
A. Ghosh ◽  
D. R. Saha ◽  
K. M. Hoque ◽  
M. Asakuna ◽  
S. Yamasaki ◽  
...  
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Hela Cells ◽  
Histopathological Examination ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Toxin Gene ◽  
Dependent Manner ◽  
A Cell

ABSTRACT Cholera toxin gene-negative Vibrio cholerae non-O1, non-O139 strain PL-21 is the etiologic agent of cholera-like syndrome. Hemagglutinin protease (HAP) is one of the major secretory proteins of PL-21. The mature 45-kDa and processed 35-kDa forms of HAP were purified in the presence and absence of EDTA from culture supernatants of PL-21. Enterotoxigenicities of both forms of HAP were tested in rabbit ileal loop (RIL), Ussing chamber, and tissue culture assays. The 35-kDa HAP showed hemorrhagic fluid response in a dose-dependent manner in the RIL assay. Histopathological examination of 20 μg of purified protease-treated rabbit ileum showed the presence of erythrocytes and neutrophils in the upper part of the villous lamina propria. Treatment with 40 μg of protease resulted in gross damage of the villous epithelium with inflammation, hemorrhage, and necrosis. The 35-kDa form of HAP, when added to the lumenal surface of rat ileum loaded in an Ussing chamber, showed a decrease in the intestinal short-circuit current and a cell rounding effect on HeLa cells. The mature 45-kDa form of HAP showed an increase in intestinal short-circuit current in an Ussing chamber and a cell distending effect on HeLa cells. These results show that HAP may play a role in the pathogenesis of PL-21.

scholarly journals Characterization of PmfR, the Transcriptional Activator of the pAO1-Borne purU-mabO-folD Operon of Arthrobacter nicotinovorans

2005 ◽  
Vol 187 (9) ◽  
pp. 3062-3070 ◽  
Author(s):  
Calin B. Chiribau ◽  
Cristinel Sandu ◽  
Gabor L. Igloi ◽  
Roderich Brandsch
Keyword(s):  
Binding Site ◽  
Transcriptional Start Site ◽  
Transcriptional Activator ◽  
Open Reading Frames ◽  
Start Site ◽  
Gene Encoding ◽  
Chloramphenicol Resistance ◽  
Nuclease Digestion ◽  
Arthrobacter Nicotinovorans

ABSTRACT Nicotine catabolism by Arthrobacter nicotinovorans is linked to the presence of the megaplasmid pAO1. Genes involved in this catabolic pathway are arranged on the plasmid into gene modules according to function. During nicotine degradation γ-N-methylaminobutyrate is formed from the pyrrolidine ring of nicotine. Analysis of the pAO1 open reading frames (ORF) resulted in identification of the gene encoding a demethylating γ-N-methylaminobutyrate oxidase (mabO). This gene was shown to form an operon with purU- and folD-like genes. Only in bacteria grown in the presence of nicotine could transcripts of the purU-mabO-folD operon be detected, demonstrating that this operon constitutes part of the pAO1 nicotine regulon. Its transcriptional start site was determined by primer extension analysis. Transcription of the operon was shown to be controlled by a new transcriptional regulator, PmfR, the product of a gene that is transcribed divergently from the purU, mabO, and folD genes. PmfR was purified, and electromobility shift assays and DNase I-nuclease digestion experiments were used to determine that its DNA binding site is located between −48 and −88 nucleotides upstream of the transcriptional start site of the operon. Disruption of pmfR by homologous recombination with a chloramphenicol resistance cassette demonstrated that PmfR acts in vivo as a transcriptional activator. Mutagenesis of the PmfR target DNA suggested that the sequence GTTT-14 bp-AAAC is the core binding site of the regulator upstream of the −35 promoter region of the purU-mabO-folD operon.

scholarly journals Posttranslational Regulation of IL-23 Production Distinguishes the Innate Immune Responses to Live Toxigenic versus Heat-Inactivated Vibrio cholerae

mSphere ◽  
2019 ◽  
Vol 4 (4) ◽  
Author(s):  
Ana A. Weil ◽  
Crystal N. Ellis ◽  
Meti D. Debela ◽  
Taufiqur R. Bhuiyan ◽  
Rasheduzzaman Rashu ◽  
...  
Keyword(s):  
Immune Responses ◽  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Protective Immunity ◽  
Innate Immune ◽  
Posttranslational Regulation ◽  
Content Type ◽  
In Cells ◽  
Cholera Vaccines

ABSTRACT Vibrio cholerae infection provides long-lasting protective immunity, while oral, inactivated cholera vaccines (OCV) result in more-limited protection. To identify characteristics of the innate immune response that may distinguish natural V. cholerae infection from OCV, we stimulated differentiated, macrophage-like THP-1 cells with live versus heat-inactivated V. cholerae with and without endogenous or exogenous cholera holotoxin (CT). Interleukin 23A gene (IL23A) expression was higher in cells exposed to live V. cholerae than in cells exposed to inactivated organisms (mean change, 38-fold; 95% confidence interval [95% CI], 4.0 to 42; P < 0.01). IL-23 secretion was also higher in cells exposed to live V. cholerae than in cells exposed to inactivated V. cholerae (mean change, 5.6-fold; 95% CI, 4.4 to 11; P < 0.001). This increase in IL-23 secretion was more marked than for other key innate immune cytokines (e.g., IL-1β and IL-6) and dependent on exposure to the combination of both live V. cholerae and CT. While IL-23 secretion was reduced following stimulation with either heat-inactivated wild-type V. cholerae or a live isogenic ctxAB mutant of V. cholerae, the addition of exogenous CT restored IL-23 secretion in combination with the live isogenic ctxAB mutant V. cholerae, but not when it was paired with stimulation by heat-inactivated V. cholerae. The posttranslational regulation of IL-23 under these conditions was dependent on the activity of the cysteine protease cathepsin B. In humans, IL-23 promotes the differentiation of Th17 cells to T follicular helper cells, which maintain and support long-term memory B cell generation after infection. Based on these findings, the stimulation of IL-23 production may be a determinant of protective immunity following V. cholerae infection. IMPORTANCE An episode of cholera provides better protection against reinfection than oral cholera vaccines, and the reasons for this are still under study. To better understand this, we compared the immune responses of human cells exposed to live Vibrio cholerae with those of cells exposed to heat-killed V. cholerae (similar to the contents of oral cholera vaccines). We also compared the effects of active cholera toxin and the inactive cholera toxin B subunit (which is included in some cholera vaccines). One key immune signaling molecule, IL-23, was uniquely produced in response to the combination of live bacteria and active cholera holotoxin. Stimulation with V. cholerae that did not produce the active toxin or was killed did not produce an IL-23 response. The stimulation of IL-23 production by cholera toxin-producing V. cholerae may be important in conferring long-term immunity after cholera.

scholarly journals Cholera toxin is synthesized in precursor form on free polysomes in Vibrio cholerae 569B.

1980 ◽  
Vol 144 (2) ◽  
pp. 518-523 ◽  
Author(s):  
J C Nichols ◽  
P C Tai ◽  
J R Murphy
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae

scholarly journals A Cytotoxin-Producing Strain of Vibrio choleraeNon-O1, Non-O139 as a Cause of Cholera and Bacteremia after Consumption of Raw Clams

2000 ◽  
Vol 38 (9) ◽  
pp. 3518-3519 ◽  
Author(s):  
Hassan Namdari ◽  
Christine R. Klaips ◽  
Joan L. Hughes
Keyword(s):  
Blood Culture ◽  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Stool Culture ◽  
Healthy Man

We report a case of a cholera-like gastroenteritis subsequent with bacteremia in a healthy man following consumption of raw clams. Although we failed to recover the organism from the patient's stool culture, his blood culture was positive for a non-cholera toxin-producing yet cytotoxin-producing non-O1 and non-O139Vibrio cholerae.

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