scholarly journals Listeria monocytogenes σB Modulates PrfA-Mediated Virulence Factor Expression

2009 ◽  
Vol 77 (5) ◽  
pp. 2113-2124 ◽  
Author(s):  
Juliane Ollinger ◽  
Barbara Bowen ◽  
Martin Wiedmann ◽  
Kathryn J. Boor ◽  
Teresa M. Bergholz
Keyword(s):  
Gene Expression ◽  
Listeria Monocytogenes ◽  
Transcriptional Activation ◽  
Virulence Gene ◽  
Transcript Profiling ◽  
Virulence Gene Expression ◽  
Qrt Pcr ◽  
Genome Wide

ABSTRACT Listeria monocytogenes σB and positive regulatory factor A (PrfA) are pleiotropic transcriptional regulators that coregulate a subset of virulence genes. A positive regulatory role for σB in prfA transcription has been well established; therefore, observations of increased virulence gene expression and hemolytic activity in a ΔsigB strain initially appeared paradoxical. To test the hypothesis that L. monocytogenes σB contributes to a regulatory network critical for appropriate repression as well as induction of virulence gene expression, genome-wide transcript profiling and follow-up quantitative reverse transcriptase PCR (qRT-PCR), reporter fusion, and phenotypic experiments were conducted using L. monocytogenes prfA*, prfA* ΔsigB, ΔprfA, and ΔprfA ΔsigB strains. Genome-wide transcript profiling and qRT-PCR showed that in the presence of active PrfA (PrfA*), σB is responsible for reduced expression of the PrfA regulon. σB-dependent modulation of PrfA regulon expression reduced the cytotoxic effects of a PrfA* strain in HepG2 cells, highlighting the functional importance of regulatory interactions between PrfA and σB. The emerging model of the role of σB in regulating overall PrfA activity includes a switch from transcriptional activation at the P2 prfA promoter (e.g., in extracellular bacteria when PrfA activity is low) to posttranscriptional downregulation of PrfA regulon expression (e.g., in intracellular bacteria when PrfA activity is high).

Studies of the Listeria monocytogenes Cellobiose Transport Components and Their Impact on Virulence Gene Repression

2019 ◽  
Vol 29 (1-6) ◽  
pp. 10-26 ◽  
Author(s):  
Thanh Nguyen Cao ◽  
Philippe Joyet ◽  
Francine Moussan Désirée Aké ◽  
Eliane Milohanic ◽  
Josef Deutscher
Keyword(s):  
Listeria Monocytogenes ◽  
Double Mutant ◽  
Virulence Gene ◽  
Gene Repression ◽  
Phosphotransferase System ◽  
Bacteria Transport ◽  
Virulence Gene Expression ◽  
Transcription Regulator ◽  
Related Phenotype

<b><i>Background:</i></b> Many bacteria transport cellobiose via a phosphoenolpyruvate:carbohydrate phosphotransferase system (PTS). In <i>Listeria monocytogenes</i>, two pairs of soluble PTS components (EIIA<sup>Cel1</sup>/EIIB<sup>Cel1</sup> and EIIA<sup>Cel2</sup>/EIIB<sup>Cel2</sup>) and the permease EIIC<sup>Cel1</sup> were suggested to contribute to cellobiose uptake. Interestingly, utilization of several carbohydrates, including cellobiose, strongly represses virulence gene expression by inhibiting PrfA, the virulence gene activator. <b><i>Results:</i></b> The LevR-like transcription regulator CelR activates expression of the cellobiose-induced PTS operons <i>celB1</i>-<i>celC1</i>-<i>celA1</i>, <i>celB2</i>-<i>celA2</i>, and the EIIC-encoding monocistronic <i>celC2</i>. Phosphorylation by P∼His-HPr at His550 activates CelR, whereas phosphorylation by P∼EIIB<sup>Cel1</sup> or P∼EIIB<sup>Cel2</sup> at His823 inhibits it. Replacement of His823 with Ala or deletion of both <i>celA</i> or <i>celB</i> genes caused constitutive CelR regulon expression. Mutants lacking EIIC<sup>Cel1</sup>, CelR or both EIIA<sup>Cel</sup> exhibited<i></i>slow cellobiose consumption. Deletion of <i>celC1</i> or <i>celR</i> prevented virulence gene repression by the disaccharide, but not by glucose and fructose. Surprisingly, deletion of both <i>celA</i> genes caused virulence gene repression even during growth on non-repressing carbohydrates. No cellobiose-related phenotype was found for the <i>celC2</i> mutant. <b><i>Conclusion:</i></b> The two EIIA/B<sup>Cel</sup> pairs are similarly efficient as phosphoryl donors in EIIC<sup>Cel1</sup>-catalyzed cellobiose transport and CelR regulation. The permanent virulence gene repression in the <i>celA</i> double mutant further supports a role of PTS<sup>Cel</sup> components in PrfA regulation.

scholarly journals Role of the Histone-Like Nucleoid Structuring Protein in Colonization, Motility, and Bile-Dependent Repression of Virulence Gene Expression in Vibrio cholerae

2006 ◽  
Vol 74 (5) ◽  
pp. 3060-3064 ◽  
Author(s):  
Amalendu Ghosh ◽  
Kalidas Paul ◽  
Rukhsana Chowdhury
Keyword(s):  
Gene Expression ◽  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Virulence Gene ◽  
Virulence Gene Expression

ABSTRACT Bile-mediated repression of virulence gene expression is relieved in a Vibrio cholerae hns mutant. The mutant also exhibited reduced motility due to lower flrA expression, higher in vivo production of the virulence factors, and lower colonization efficiency. The colonization defect of the mutant was due to low FlrA production.

scholarly journals The response regulator ResD modulates virulence gene expression in response to carbohydrates in Listeria monocytogenes

2006 ◽  
Vol 61 (6) ◽  
pp. 1622-1635 ◽  
Author(s):  
Marianne H. Larsen ◽  
Birgitte H. Kallipolitis ◽  
Janne K. Christiansen ◽  
John E. Olsen ◽  
Hanne Ingmer
Keyword(s):  
Gene Expression ◽  
Listeria Monocytogenes ◽  
Response Regulator ◽  
Virulence Gene ◽  
Virulence Gene Expression

The role of RNAs in the regulation of virulence-gene expression

2006 ◽  
Vol 9 (2) ◽  
pp. 229-236 ◽  
Author(s):  
Pascale Romby ◽  
François Vandenesch ◽  
E Gerhart H Wagner
Keyword(s):  
Gene Expression ◽  
Virulence Gene ◽  
Virulence Gene Expression

scholarly journals Listeria monocytogenes σB Regulates Stress Response and Virulence Functions

2003 ◽  
Vol 185 (19) ◽  
pp. 5722-5734 ◽  
Author(s):  
Mark J. Kazmierczak ◽  
Sharon C. Mithoe ◽  
Kathryn J. Boor ◽  
Martin Wiedmann
Keyword(s):  
Gene Expression ◽  
Listeria Monocytogenes ◽  
Stress Response ◽  
Consensus Sequence ◽  
Virulence Gene ◽  
Wild Type ◽  
Promoter Regions ◽  
Virulence Gene Expression ◽  
Stress Response Genes ◽  
In The Wild

ABSTRACT While the stress-responsive alternative sigma factor σB has been identified in different species of Bacillus, Listeria, and Staphylococcus, theσ B regulon has been extensively characterized only in B. subtilis. We combined biocomputing and microarray-based strategies to identify σB-dependent genes in the facultative intracellular pathogen Listeria monocytogenes. Hidden Markov model (HMM)-based searches identified 170 candidateσ B-dependent promoter sequences in the strain EGD-e genome sequence. These data were used to develop a specialized, 208-gene microarray, which included 166 genes downstream of HMM-predicted σB-dependent promoters as well as selected virulence and stress response genes. RNA for the microarray experiments was isolated from both wild-type and ΔsigB null mutant L. monocytogenes cells grown to stationary phase or exposed to osmotic stress (0.5 M KCl). Microarray analyses identified a total of 55 genes with statistically significantσ B-dependent expression under the conditions used in these experiments, with at least 1.5-fold-higher expression in the wild type over the sigB mutant under either stress condition (51 genes showed at least 2.0-fold-higher expression in the wild type). Of the 55 genes exhibiting σB-dependent expression, 54 were preceded by a sequence resembling the σB promoter consensus sequence. Rapid amplification of cDNA ends-PCR was used to confirm the σB-dependent nature of a subset of eight selected promoter regions. Notably, theσ B-dependent L. monocytogenes genes identified through this HMM/microarray strategy included both stress response genes (e.g., gadB, ctc, and the glutathione reductase gene lmo1433) and virulence genes (e.g., inlA, inlB, and bsh). Our data demonstrate that, in addition to regulating expression of genes important for survival under environmental stress conditions, σB also contributes to regulation of virulence gene expression in L. monocytogenes. These findings strongly suggest thatσ B contributes to L. monocytogenes gene expression during infection.

scholarly journals Role of Staphylococcus aureus Global Regulators sae and σB in Virulence Gene Expression during Device-Related Infection

2005 ◽  
Vol 73 (6) ◽  
pp. 3415-3421 ◽  
Author(s):  
Christiane Goerke ◽  
Ursula Fluckiger ◽  
Andrea Steinhuber ◽  
Vittoria Bisanzio ◽  
Martina Ulrich ◽  
...  
Keyword(s):  
Gene Expression ◽  
Staphylococcus Aureus ◽  
Virulence Gene ◽  
Northern Analysis ◽  
Virulence Gene Expression ◽  
Global Regulators ◽  
Reverse Transcription Pcr ◽  
Direct Cross

ABSTRACT The ability of Staphylococcus aureus to adapt to different environments is due to a regulatory network comprising several loci. Here we present a detailed study of the interaction between the two global regulators sae and σB of S. aureus and their influence on virulence gene expression in vitro, as well as during device-related infection. The expression of sae, asp23, hla, clfA, coa, and fnbA was determined in strain Newman and its isogenic saeS/R and sigB mutants by Northern analysis and LightCycler reverse transcription-PCR. There was no indication of direct cross talk between the two regulators. sae had a dominant effect on target gene expression during device-related infection. σB seemed to be less active throughout the infection than under induced conditions in vitro.

Sign in / Sign up

Export Citation Format

Share Document