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EcoSal Plus

Domain 8:

Pathogenesis

Regulation of Pathogenesis by Alternative Sigma Factor N

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  • Authors: James T. Riordan1, and Avishek Mitra2
  • Editor: Michael S. Donnenberg3
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Department of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL 33620; 2: Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294; 3: Virginia Commonwealth University School of Medicine, Richmond, VA
  • Received 12 December 2016 Accepted 27 March 2017 Published 20 June 2017
  • Address correspondence to James T. Riordan, jtriordan@usf.edu
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  • Abstract:

    σ (also σ) is an alternative sigma factor subunit of the RNA polymerase complex that regulates the expression of genes from many different ontological groups. It is broadly conserved in the Eubacteria with major roles in nitrogen metabolism, membrane biogenesis, and motility. σ is encoded as the first gene of a five-gene operon including ), , , , and that has been genetically retained among species of , , and . In an increasing number of bacteria, σ has been implicated in the control of genes essential to pathogenic behavior, including those involved in adherence, secretion, immune subversion, biofilm formation, toxin production, and resistance to both antimicrobials and biological stressors. For most pathogens how this is achieved is unknown. In enterohemorrhagic (EHEC) O157, , and , regulation of virulence by σ requires another alternative sigma factor, σ, yet the model by which σ virulence regulation is predicted to occur is varied in each of these pathogens. In this review, the importance of σ to bacterial pathogenesis is introduced, and common features of σ-dependent virulence regulation discussed. Emphasis is placed on the molecular mechanisms underlying σ virulence regulation in O157. This includes a review of the structure and function of regulatory pathways connecting σ to virulence expression, predicted input signals for pathway stimulation, and the role for cognate σ activators in initiation of gene systems determining pathogenic behavior.

  • Citation: Riordan J, Mitra A. 2017. Regulation of Pathogenesis by Alternative Sigma Factor N, EcoSal Plus 2017; doi:10.1128/ecosalplus.ESP-0016-2016

Key Concept Ranking

Two-Component Signal Transduction Systems
0.45316696
Type III Secretion System
0.42887476
Bacterial Pathogenesis
0.40108797
0.45316696

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/content/journal/ecosalplus/10.1128/ecosalplus.ESP-0016-2016
2017-06-20
2017-09-25

Abstract:

σ (also σ) is an alternative sigma factor subunit of the RNA polymerase complex that regulates the expression of genes from many different ontological groups. It is broadly conserved in the Eubacteria with major roles in nitrogen metabolism, membrane biogenesis, and motility. σ is encoded as the first gene of a five-gene operon including ), , , , and that has been genetically retained among species of , , and . In an increasing number of bacteria, σ has been implicated in the control of genes essential to pathogenic behavior, including those involved in adherence, secretion, immune subversion, biofilm formation, toxin production, and resistance to both antimicrobials and biological stressors. For most pathogens how this is achieved is unknown. In enterohemorrhagic (EHEC) O157, , and , regulation of virulence by σ requires another alternative sigma factor, σ, yet the model by which σ virulence regulation is predicted to occur is varied in each of these pathogens. In this review, the importance of σ to bacterial pathogenesis is introduced, and common features of σ-dependent virulence regulation discussed. Emphasis is placed on the molecular mechanisms underlying σ virulence regulation in O157. This includes a review of the structure and function of regulatory pathways connecting σ to virulence expression, predicted input signals for pathway stimulation, and the role for cognate σ activators in initiation of gene systems determining pathogenic behavior.

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Figures

Image of Figure 1
Figure 1

The operon is controlled by a single σ promoter and consists of 5 genes (nucleotide length is given below each). See the text for a discussion of each product and its function. Percent nucleotide identity for each gene (entire ORF) is given for species of , , and relative to K-12 MG1655; the gene is absent in .

Citation: Riordan J, Mitra A. 2017. Regulation of Pathogenesis by Alternative Sigma Factor N, EcoSal Plus 2017; doi:10.1128/ecosalplus.ESP-0016-2016
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Figure 2

In , σ directly activates (encoding σ) transcription requiring the σ EBP Rrp2. In , σ indirectly reduces σ activity in a manner requiring σ antagonist FliZ, FlhDC, and σ EBP NtrC. In , σ indirectly activates (encoding σ) transcription, requiring an unknown regulator(s). See the text for further details.

Citation: Riordan J, Mitra A. 2017. Regulation of Pathogenesis by Alternative Sigma Factor N, EcoSal Plus 2017; doi:10.1128/ecosalplus.ESP-0016-2016
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Figure 3

σ and cognate EBP NtrC initiate transcription of motility regulator . FlhD activates transcription of σ antagonist, . FliZ repression of σ activity leads to downregulation of GDAR central regulator and concomitant upregulation of the LEE. Increased LEE expression is predicted to occur through increased or decreased transcription. GadE activates transcription of GDAR system glutamate (Glu) decarboxylases (/) for catalytic acid detoxification, converting Glu to γ-aminobutyric acid (GABA).

Citation: Riordan J, Mitra A. 2017. Regulation of Pathogenesis by Alternative Sigma Factor N, EcoSal Plus 2017; doi:10.1128/ecosalplus.ESP-0016-2016
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Figure 4

The σ EBPs QseF and NtrC activate σ-dependent virulence gene regulation in O157 in response to discrete input signals. The QseF-dependent pathway is sensitive to norepinephrine/epinephrine (NEPI/EPI) and autoinducer 3 (AI-3), whereas NtrC responds to nitrogen (N) and acetyl phosphate (AcP). Both QseF and NtrC positively regulate attaching and effacing (AE) lesion formation through different regulatory pathways (see text for details). QseF enhances AE formation by activation of (also known as ), whereas NtrC enhances AE formation by decreasing σ activity. Pathways may intersect at . QseF can activate transcription, the product of which (PII) interferes with phosphorylation of NtrC by sensor kinase NtrB. NtrC can also be activated by AcP. QseF is activated by sensor kinase QseE, as well as several noncognate sensor kinases. See the text for further details. P, Phosphate; LEE, locus of enterocyte effacement; GDAR, glutamate-dependent acid resistance.

Citation: Riordan J, Mitra A. 2017. Regulation of Pathogenesis by Alternative Sigma Factor N, EcoSal Plus 2017; doi:10.1128/ecosalplus.ESP-0016-2016
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Tables

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Table 1

Phenotypes and genetic determinants underlying σ-dependent regulation of pathogenesis in bacteria

Citation: Riordan J, Mitra A. 2017. Regulation of Pathogenesis by Alternative Sigma Factor N, EcoSal Plus 2017; doi:10.1128/ecosalplus.ESP-0016-2016

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