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EcoSal Plus

Domain 8:

Pathogenesis

Virulence Gene Regulation in

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  • Author: Charles J. Dorman1
  • Editor: James M. Slauch2
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Department of Microbiology, Moyne Institute of Preventive Medicine, University of Dublin, Trinity College, Dublin 2, Ireland; 2: The Schoold of Molecular and Cellular Biology, University of Illinois at Urbana-Champaign, Urbana, IL
  • Received 30 June 2004 Accepted 02 September 2004 Published 29 December 2004
  • Address correspondence to Charles J. Dorman cjdorman@tcd.ie
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  • Abstract:

    species are the causative agents of bacillary dysentery in humans, an invasive disease in which the bacteria enter the cells of the epithelial layer of the large intestine, causing extensive tissue damage and inflammation. They rely on a plasmid-encoded type III secretion system (TTSS) to cause disease; this system and its regulation have been investigated intensively at the molecular level for decades. The lessons learned have not only deepened our knowledge of biology but also informed in important ways our understanding of the mechanisms used by other pathogenic bacteria to cause disease and to control virulence gene expression. In addition, the story has played a central role in the development of our appreciation of the contribution of horizontal DNA transfer to pathogen evolution.A 30-kilobase-pair "Entry Region" of the 230-kb virulence plasmid lies at the heart of the pathogenesis system. Here are located the and regulatory genes and most of the structural genes involved in the expression of the TTSS and its effector proteins. Expression of the virulence genes occurs in response to an array of environmental signals, including temperature, osmolarity, and pH.At the top of the regulatory hierarchy and lying on the plasmid outside the Entry Region is, encoding an AraC-like transcription factor.Virulence gene expression is also controlled by chromosomal genes,such as those encoding the nucleoid-associated proteins H-NS, IHF, and Fis, the two-component regulators OmpR/EnvZ and CpxR/CpxA, the anaerobic regulator Fnr, the iron-responsive regulator Fur, and the topoisomerases of the cell that modulate DNA supercoiling. Small regulatory RNAs,the RNA chaperone Hfq,and translational modulation also affect the expression of the virulence phenotypetranscriptionally and/orposttranscriptionally.

  • Citation: Dorman C. 2004. Virulence Gene Regulation in , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.9.3

Key Concept Ranking

Transcription Start Site
0.42674312
Type III Secretion System
0.4257954
Bacterial Outer Membrane Proteins
0.41246107
Outer Membrane Proteins
0.34247488
0.42674312

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/content/journal/ecosalplus/10.1128/ecosalplus.8.9.3
2004-12-29
2017-03-24

Abstract:

species are the causative agents of bacillary dysentery in humans, an invasive disease in which the bacteria enter the cells of the epithelial layer of the large intestine, causing extensive tissue damage and inflammation. They rely on a plasmid-encoded type III secretion system (TTSS) to cause disease; this system and its regulation have been investigated intensively at the molecular level for decades. The lessons learned have not only deepened our knowledge of biology but also informed in important ways our understanding of the mechanisms used by other pathogenic bacteria to cause disease and to control virulence gene expression. In addition, the story has played a central role in the development of our appreciation of the contribution of horizontal DNA transfer to pathogen evolution.A 30-kilobase-pair "Entry Region" of the 230-kb virulence plasmid lies at the heart of the pathogenesis system. Here are located the and regulatory genes and most of the structural genes involved in the expression of the TTSS and its effector proteins. Expression of the virulence genes occurs in response to an array of environmental signals, including temperature, osmolarity, and pH.At the top of the regulatory hierarchy and lying on the plasmid outside the Entry Region is, encoding an AraC-like transcription factor.Virulence gene expression is also controlled by chromosomal genes,such as those encoding the nucleoid-associated proteins H-NS, IHF, and Fis, the two-component regulators OmpR/EnvZ and CpxR/CpxA, the anaerobic regulator Fnr, the iron-responsive regulator Fur, and the topoisomerases of the cell that modulate DNA supercoiling. Small regulatory RNAs,the RNA chaperone Hfq,and translational modulation also affect the expression of the virulence phenotypetranscriptionally and/orposttranscriptionally.

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Figures

Image of Figure 1
Figure 1

The entry region is shown in an expanded form below the circular map. Structural genes are yellow, and regulatory genes are red. Within the entry region, the angled arrows show the locations and orientations of major transcriptional promoters. The diagram is not drawn to scale.

Citation: Dorman C. 2004. Virulence Gene Regulation in , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.9.3
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Image of Figure 2
Figure 2

Regulatory genes are red, and the structural genes are yellow. Colored spheres or ovals represent proteins. The horizontal red/gold arrows indicate transcriptional activity. The diagram is not drawn to scale.

Citation: Dorman C. 2004. Virulence Gene Regulation in , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.9.3
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Figure 3

The diagrams represent the domain structures of the positive transcription regulators VirF and VirB and the repressor H-NS. The numbers shown below each protein indicate amino acids at the amino-terminal and carboxyl-terminal boundaries of structural features; the amino-terminal methionine is at position 1 in each case. Abbreviations: HTH, helix-turn-helix DNA-binding motif; LLLLL, a 5-heptad leucine zipper in which every seventh amino acid is -leucine.

Citation: Dorman C. 2004. Virulence Gene Regulation in , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.9.3
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