In vivo induced clpB1 gene of Vibrio cholerae is involved in different stress responses and affects in vivo cholera toxin production

2005 ◽  
Vol 331 (4) ◽  
pp. 1365-1373 ◽  
Author(s):  
Sanjay Nag ◽  
Soumita Das ◽  
Keya Chaudhuri
1985 ◽  
Vol 21 (6) ◽  
pp. 884-890 ◽  
Author(s):  
P C Turnbull ◽  
J V Lee ◽  
M D Miliotis ◽  
C S Still ◽  
M Isaäcson ◽  
...  

1998 ◽  
Vol 66 (1) ◽  
pp. 394-397 ◽  
Author(s):  
Sara Lazar ◽  
Matthew K. Waldor

ABSTRACT The ctxAB operon, which encodes cholera toxin, resides in the genome of CTXφ, a filamentous bacteriophage. WithinVibrio cholerae cells, the CTXφ genome can exist either as a replicating plasmid or as a prophage integrated into the chromosome. Previous work established that ToxR is required for chromosomal ctxAB expression. We have learned that strains harboring the CTXφ replicative form produce cholera toxin under all conditions tested, independently of ToxR. During passage of CTXφ lysogens through the infant mouse intestine, transduction of CTXφ to a recipient strain can be detected, indicating that phage excision and replication occur in vivo. These results suggest that phage induction might provide a novel mechanism for the regulation of cholera toxin production.


2016 ◽  
Vol 26 (3) ◽  
pp. 627-636 ◽  
Author(s):  
Young Taek Oh ◽  
Kang-Mu Lee ◽  
Wasimul Bari ◽  
Hwa Young Kim ◽  
Hye Jin Kim ◽  
...  

2004 ◽  
Vol 186 (5) ◽  
pp. 1355-1361 ◽  
Author(s):  
Joaquín Sánchez ◽  
Gerardo Medina ◽  
Thomas Buhse ◽  
Jan Holmgren ◽  
Gloria Soberón-Chavez

ABSTRACT The regulatory systems controlling expression of the ctxAB genes encoding cholera toxin (CT) in the classical and El Tor biotypes of pathogenic Vibrio cholerae have been characterized and found to be almost identical. Notwithstanding this, special in vitro conditions, called AKI conditions, are required for El Tor bacteria to produce CT. The AKI conditions involve biphasic cultures. In phase 1 the organism is grown in a still tube for 4 h. In phase 2 the medium is poured into a flask to continue growth with shaking. Virtually no expression of CT occurs if this protocol is not followed. Here we demonstrated that CT expression takes place in single-phase still cultures if the volume-to-surface-area ratio is decreased, both under air and under an inert atmosphere. The expression of key genes involved in the regulation of CT production was analyzed, and we found that the expression pattern closely resembles the in vivo expression pattern.


1986 ◽  
Vol 53 (3) ◽  
pp. 700-701 ◽  
Author(s):  
T Shimamura ◽  
S Watanabe ◽  
S Sasaki

2006 ◽  
Vol 74 (2) ◽  
pp. 927-930 ◽  
Author(s):  
Mariam Quinones ◽  
Brigid M. Davis ◽  
Matthew K. Waldor

ABSTRACT Cholera toxin, one of the main virulence factors of Vibrio cholerae, is encoded in the genome of CTXφ, a V. cholerae-specific lysogenic filamentous bacteriophage. Although the genes encoding cholera toxin, ctxAB, are known to have their own promoter, the toxin genes can also be transcribed from an upstream CTXφ promoter, PrstA . The V. cholerae SOS response to DNA damage induces the CTX prophage by stimulating gene expression initiating from PrstA . Here, we investigated whether ctxA mRNA levels increase along with the levels of the transcripts for the other CTXφ genes following stimulation of the V. cholerae SOS response. Treatment of V. cholerae with the SOS-inducing agent mitomycin C increased the level of ctxA mRNA approximately sevenfold, apparently by augmenting the activity of PrstA . However, using suckling mice as a model host, we found that intraintestinal ctxA transcription does not depend on PrstA . In fact, the suckling mouse intestine does not appear to be a potent inducer of the V. cholerae SOS response. Furthermore, alleviation of LexA-mediated repression of the V. cholerae SOS regulon was not required for V. cholerae growth in the suckling mouse intestine. Our observations suggest that pathogenicity of V. cholerae does not depend on its SOS response.


1998 ◽  
Vol 37 (4) ◽  
pp. 231-235 ◽  
Author(s):  
Anisia Silva ◽  
Rafael Fando ◽  
Jorge A. Benitez

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