1992
DOI: 10.1111/j.1365-2958.1992.tb01489.x
|View full text |Cite
|
Sign up to set email alerts
|

Co‐ordinate expression of virulence genes by ToxR in Vibrio cholerae

Abstract: Evolution of complex regulatory pathways that control virulence factor expression in pathogenic bacteria indicates the importance to these organisms of being able to distinguish time and place. In the human intestinal pathogen Vibrio cholerae, control over many virulence genes identified to date is the responsibility of the ToxR protein. ToxR, in conjunction with a second regulatory protein called ToxS, directly activates the genes encoding the cholera toxin; other ToxR regulated genes are not activated direct… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

2
140
0

Year Published

1992
1992
2008
2008

Publication Types

Select...
7
3

Relationship

1
9

Authors

Journals

citations
Cited by 222 publications
(142 citation statements)
references
References 59 publications
2
140
0
Order By: Relevance
“…Expression of toxT from a constitutive promoter partially corrects a toxR mutant phenotype (except for the expression of OmpU), consistent with a position for ToxT downstream of ToxR in a regulatory cascade . In this cascade, ToxR activates transcription of cholera toxin, OmpU and toxT, and ToxT in turn activates transcription of the other virulence genes of V. cholerae (DiRita, 1992). Since expression of ToxR is not itself regulated by environmental conditions that modulate expression of cholera toxin and Tcp (DiRita, 1992), the mechanism by which these conditions modulate expression of genes in the ToxR regulon is not well understood.…”
Section: Introductionmentioning
confidence: 99%
“…Expression of toxT from a constitutive promoter partially corrects a toxR mutant phenotype (except for the expression of OmpU), consistent with a position for ToxT downstream of ToxR in a regulatory cascade . In this cascade, ToxR activates transcription of cholera toxin, OmpU and toxT, and ToxT in turn activates transcription of the other virulence genes of V. cholerae (DiRita, 1992). Since expression of ToxR is not itself regulated by environmental conditions that modulate expression of cholera toxin and Tcp (DiRita, 1992), the mechanism by which these conditions modulate expression of genes in the ToxR regulon is not well understood.…”
Section: Introductionmentioning
confidence: 99%
“…This and not the opposite direction of evolution is preferred since, on the one hand, Zot and 0RF3 are closely related to gp1 of PfI but only distantly related to gp1 of other bacteriophages, and on the other hand, it appears most likely that all filamentous bacteriophages have a common origin. The zur gene, together with the adjacent CIX operon encoding the two subunits of the classical cholera toxin, belongs to a site-specific transposable element [15]. It is interesting to speculate that this element could have evolved from a filamentous bacteriophage via a plasmid intermediate resembling pKB74CJ.…”
Section: Evolutionary Implicationsmentioning
confidence: 99%
“…Environmental sensing and co-ordinate regulation of gene expression is essential for V. cholerae to persist in drastically different environments and cause disease. Among the increasing number of transcription factors described in the regulation of virulence gene expression in V. cholerae, ToxR is the most extensively characterized (reviewed by DiRita, 1992;Skorupski and Taylor, 1997a).…”
Section: Introductionmentioning
confidence: 99%