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Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes
Published on: September 19, 2013
Listeria monocytogenes sigmaB modulates PrfA-mediated virulence factor expression
Juliane Ollinger1, Barbara Bowen, Martin Wiedmann
1Department of Food Science, Cornell University, 405 Stocking Hall, Ithaca, NY 14853, USA. tmb224@cornell.edu
Infection and Immunity
|March 4, 2009
Summary
Listeria monocytogenes sigma(B) surprisingly represses virulence gene expression when the positive regulatory factor A (PrfA) is active. This sigma(B)-mediated downregulation impacts bacterial cytotoxicity, revealing a complex regulatory switch.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Gene Regulation
Background:
- Listeria monocytogenes sigma(B) and positive regulatory factor A (PrfA) are key regulators of virulence genes.
- Sigma(B) was previously thought to only activate prfA transcription, making its role in reduced virulence paradoxical.
Purpose of the Study:
- To investigate the complex regulatory role of sigma(B) in Listeria monocytogenes virulence gene expression.
- To test the hypothesis that sigma(B) is involved in both the induction and repression of virulence genes.
Main Methods:
- Genome-wide transcript profiling (RNA-Seq).
- Quantitative reverse transcriptase PCR (qRT-PCR).
- Reporter fusion assays and phenotypic experiments using various L. monocytogenes mutant strains (prfA*, prfA* DeltasigB, DeltaprfA, DeltaprfA DeltasigB).
Main Results:
- Sigma(B) actively reduces the expression of the PrfA regulon when PrfA is active (PrfA*).
- This sigma(B)-dependent downregulation decreased the cytotoxic effects of L. monocytogenes in HepG2 cells.
- Evidence suggests sigma(B) switches from activating prfA transcription to posttranscriptionally downregulating the PrfA regulon.
Conclusions:
- Sigma(B) plays a critical role in repressing virulence gene expression in L. monocytogenes, particularly when PrfA activity is high.
- The interaction between sigma(B) and PrfA represents a sophisticated regulatory mechanism controlling bacterial pathogenesis.
- A regulatory switch in sigma(B) function is proposed, impacting PrfA activity based on bacterial environment.
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