scholarly journals High intracellular c-di-GMP levels antagonize quorum sensing and virulence gene expression in Burkholderia cenocepacia H111

Microbiology ◽  
2017 ◽  
Vol 163 (5) ◽  
pp. 754-764 ◽  
Author(s):  
Nadine Schmid ◽  
Angela Suppiger ◽  
Elisabeth Steiner ◽  
Gabriella Pessi ◽  
Volkhard Kaever ◽  
...  
Keyword(s):  
Gene Expression ◽  
Quorum Sensing ◽  
Virulence Gene ◽  
Burkholderia Cenocepacia ◽  
Virulence Gene Expression

scholarly journals Differential Modulation of Burkholderia cenocepacia Virulence and Energy Metabolism by the Quorum-Sensing Signal BDSF and Its Synthase

2009 ◽  
Vol 191 (23) ◽  
pp. 7270-7278 ◽  
Author(s):  
Yinyue Deng ◽  
Calvin Boon ◽  
Leo Eberl ◽  
Lian-Hui Zhang
Keyword(s):  
Gene Expression ◽  
Quorum Sensing ◽  
Minimal Medium ◽  
Virulence Gene ◽  
Burkholderia Cenocepacia ◽  
Signal Interference ◽  
Growth Defect ◽  
Infection Model ◽  
Dependent Manner ◽  
Virulence Gene Expression

ABSTRACT Burkholderia cenocepacia produces the molecule cis-2-dodecenoic acid (BDSF), which was previously shown to play a role in antagonism against the fungal pathogen Candida albicans by interfering with its morphological transition. In this study, we show that production of BDSF is under stringent transcriptional control and the molecule accumulates in a cell density-dependent manner, typically found with quorum-sensing (QS) signals. B. cenocepacia mutant strain J2315 with a deleted Bcam0581 gene, which encodes an enzyme essential for BDSF production, exhibited a growth defect in minimal medium but not in rich medium, decreased virulence gene expression, and attenuated virulence in a zebrafish infection model. Exogenous addition of BDSF to the mutant rescues virulence gene expression but fails to restore its growth defect in minimal medium. We show that Bcam0581, but not BDSF, is associated with B. cenocepacia ATP biogenesis. We also provide evidence that some of the BDSF-regulated genes are also controlled by the acyl-homoserine-lactone-dependent QS system and are thus coregulated by two cell-to-cell signaling systems. These data demonstrate that in addition to the role in cross-kingdom signal interference, BDSF and its synthase are also important for the virulence and physiology of B. cenocepacia.

Glucose Decreases Virulence Gene Expression of Escherichia coli O157:H7

2012 ◽  
Vol 75 (4) ◽  
pp. 748-752 ◽  
Author(s):  
V. DELCENSERIE ◽  
G. LaPOINTE ◽  
T. CHARASLERTRANGSI ◽  
A. RABALSKI ◽  
M. W. GRIFFITHS
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Quorum Sensing ◽  
Shiga Toxin ◽  
Virulence Gene ◽  
Escherichia Coli O157 ◽  
Virulence Gene Expression ◽  
E Coli ◽  
Reverse Transcription Pcr ◽  
Enterocyte Effacement

Escherichia coli O157:H7 is responsible for a human toxico-infection that can lead to severe complications such as hemolytic uremic syndrome. Inside the intestine, E. coli O157:H7 forms typical attaching-effacing lesions and produces Shiga toxins. The genes that are responsible for these lesions are located in a pathogenicity island called the locus of enterocyte effacement (LEE). LEE gene expression is influenced by quorum sensing through the luxS system. In this study, the effect of glucose on the expression of several genes from LEE, on the expression of Shiga toxin genes, and on the expression of luxS was assessed with real-time, reverse transcription PCR. All concentrations of glucose (from 0.1 to 1%) were able to down-regulate genes from the LEE operon. A slight down-regulation of genes implicated in Shiga toxin expression was also observed but was significant for low doses of glucose (0.1 to 0.5%) only. A slight but significant increase in luxS expression was observed with 1% glucose. This confirms that in addition to quorum sensing, the presence or absence of nutrients such as glucose has an impact on the down- or upregulation of LEE-encoded virulence genes by the bacterium. The influence of glucose on the virulence of E. coli O157:H7 has received little attention, and these results suggest that glucose can have an important effect on the virulence of E. coli O157:H7.

scholarly journals Advancing the Quorum in Pseudomonas aeruginosa: MvaT and the Regulation of N-Acylhomoserine Lactone Production and Virulence Gene Expression

2002 ◽  
Vol 184 (10) ◽  
pp. 2576-2586 ◽  
Author(s):  
Stephen P. Diggle ◽  
Klaus Winzer ◽  
Andrée Lazdunski ◽  
Paul Williams ◽  
Miguel Cámara
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Growth Phase ◽  
Virulence Gene ◽  
Homoserine Lactone ◽  
Logarithmic Phase ◽  
Signal Molecules ◽  
Virulence Gene Expression ◽  
Acylhomoserine Lactone

ABSTRACT Pseudomonas aeruginosa regulates the production of many exoproteins and secondary metabolites via a hierarchical quorum-sensing cascade through LasR and RhlR and their cognate signal molecules N-(3-oxododecanoyl)-l-homoserine lactone (3O-C12-HSL) and N-(butanoyl)-l-homoserine lactone (C4-HSL). In this study, we found that transcription of the quorum sensing-regulated genes lecA (coding for PA-IL lectin), lasB (coding for elastase), and rpoS appeared to be growth phase dependent and their expression could not be advanced to the logarithmic phase in cells growing in batch culture by the addition of exogenous C4-HSL and 3O-C12-HSL. To identify novel regulators responsible for this growth phase dependency, a P. aeruginosa lecA::lux reporter strain was subjected to random transposon mutagenesis. A number of mutants affected in lecA expression were found that exhibited altered production of multiple quorum sensing-dependent phenotypes. While some mutations were mapped to new loci such as clpA and mvaT and a putative efflux system, a number of mutations were also mapped to known regulators such as lasR, rhlR, and rpoS. MvaT was identified as a novel global regulator of virulence gene expression, as a mutation in mvaT resulted in enhanced lecA expression and pyocyanin production. This mutant also showed altered swarming ability and production of the LasB and LasA proteases, 3O-C12-HSL, and C4-HSL. Furthermore, addition of exogenous 3O-C12-HSL and C4-HSL to the mvaT mutant significantly advanced lecA expression, suggesting that MvaT is involved in the growth phase-dependent regulation of the lecA gene.

scholarly journals Crystal Structure of the Vibrio cholerae Quorum-Sensing Regulatory Protein HapR

2007 ◽  
Vol 189 (15) ◽  
pp. 5683-5691 ◽  
Author(s):  
Rukman S. De Silva ◽  
Gabriela Kovacikova ◽  
Wei Lin ◽  
Ronald K. Taylor ◽  
Karen Skorupski ◽  
...  
Keyword(s):  
Gene Expression ◽  
Crystal Structure ◽  
Dna Binding ◽  
Quorum Sensing ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Regulatory Protein ◽  
Virulence Gene ◽  
Binding Motif ◽  
Virulence Gene Expression

ABSTRACT Quorum sensing in Vibrio cholerae involves signaling between two-component sensor protein kinases and the response regulator LuxO to control the expression of the master regulator HapR. HapR, in turn, plays a central role in regulating a number of important processes, such as virulence gene expression and biofilm formation. We have determined the crystal structure of HapR to 2.2-Å resolution. Its structure reveals a dimeric, two-domain molecule with an all-helical structure that is strongly conserved with members of the TetR family of transcriptional regulators. The N-terminal DNA-binding domain contains a helix-turn-helix DNA-binding motif and alteration of certain residues in this domain completely abolishes the ability of HapR to bind to DNA, alleviating repression of both virulence gene expression and biofilm formation. The C-terminal dimerization domain contains a unique solvent accessible tunnel connected to an amphipathic cavity, which by analogy with other TetR regulators, may serve as a binding pocket for an as-yet-unidentified ligand.

scholarly journals Quorum-sensing regulators control virulence gene expression in Vibrio cholerae

2002 ◽  
Vol 99 (5) ◽  
pp. 3129-3134 ◽  
Author(s):  
J. Zhu ◽  
M. B. Miller ◽  
R. E. Vance ◽  
M. Dziejman ◽  
B. L. Bassler ◽  
...  
Keyword(s):  
Gene Expression ◽  
Quorum Sensing ◽  
Vibrio Cholerae ◽  
Virulence Gene ◽  
Virulence Gene Expression
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