PqsE Functions Independently of PqsR-<i>Pseudomonas</i>Quinolone Signal and Enhances the<i>rhl</i>Quorum-Sensing System

Farrow, John M.; Sund, Zoë; Ellison, Matthew L.; Wade, Dana S.; Coleman, James P.; Pesci, Everett C.

doi:10.1128/jb.00753-08

Cited by 156 publications

(200 citation statements)

References 57 publications

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“…Random amplified polymorphic DNA (RAPD) typing of longitudinal isolates was performed as previously described using primer 272 (AGCGGGCCAA) (59). The pqsA mutant was generated in our laboratory's PAO1 strain by allelic exchange (60) using the previously described ⌬pqsA deletion construct (61). Brain heart infusion (BHI) media were used for routine culture of P. aeruginosa.…”

Section: Methodsmentioning

confidence: 99%

Adaptation of Iron Homeostasis Pathways by a Pseudomonas aeruginosa Pyoverdine Mutant in the Cystic Fibrosis Lung

et al. 2014

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c Cystic fibrosis (CF) patients suffer from chronic bacterial lung infections, most notably by Pseudomonas aeruginosa, which persists for decades in the lungs and undergoes extensive evolution. P. aeruginosa requires iron for virulence and uses the fluorescent siderophore pyoverdine to scavenge and solubilize ferric iron during acute infections. Pyoverdine mutants accumulate in the lungs of some CF patients, however, suggesting that the heme and ferrous iron acquisition pathways of P. aeruginosa are more important in this environment. Here, we sought to determine how evolution of P. aeruginosa in the CF lung affects iron acquisition and regulatory pathways through the use of longitudinal CF isolates. These analyses demonstrated a significant reduction of siderophore production during the course of CF lung infection in nearly all strains tested. Mass spectrometry analysis of one of these strains showed that the later CF isolate has streamlined the metabolic flux of extracellular heme through the HemO heme oxygenase, resulting in more-efficient heme utilization. Moreover, gene expression analysis shows that iron regulation via the PrrF small RNAs (sRNAs) is enhanced in the later CF isolate. Finally, analysis of P. aeruginosa gene expression in the lungs of various CF patients demonstrates that both PrrF and HemO are consistently expressed in the CF lung environment. Combined, these results suggest that heme is a critical source of iron during prolonged infection of the CF lung and that changes in iron and heme regulatory pathways play a crucial role in adaptation of P. aeruginosa to this ever-changing host environment.

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Section: Methodsmentioning

confidence: 99%

Adaptation of Iron Homeostasis Pathways by a Pseudomonas aeruginosa Pyoverdine Mutant in the Cystic Fibrosis Lung

et al. 2014

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“…The 4-quinolone signaling system is linked in a hierarchical manner to the AHL signaling systems of P. aeruginosa, as LasR (positively) and RhlR (negatively) control the levels of PQS by binding to the promoter region of the PqsR regulator (202). Additionally, PqsE alone is sufficient to regulate its virulence target genes via the rhl QS system intrinsically linked to RhlR (62). Mutations in either pqsA or pqsE significantly reduce P. aeruginosa virulence in plant and animal infection models (46,164).…”

Section: Pqsmentioning

confidence: 99%

The Multiple Signaling Systems Regulating Virulence in Pseudomonas aeruginosa

Nadal‐Jimenez

Koch

Thompson

et al. 2012

Microbiol Mol Biol Rev

627

626

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SUMMARY Cell-to-cell communication is a major process that allows bacteria to sense and coordinately react to the fluctuating conditions of the surrounding environment. In several pathogens, this process triggers the production of virulence factors and/or a switch in bacterial lifestyle that is a major determining factor in the outcome and severity of the infection. Understanding how bacteria control these signaling systems is crucial to the development of novel antimicrobial agents capable of reducing virulence while allowing the immune system of the host to clear bacterial infection, an approach likely to reduce the selective pressures for development of resistance. We provide here an up-to-date overview of the molecular basis and physiological implications of cell-to-cell signaling systems in Gram-negative bacteria, focusing on the well-studied bacterium Pseudomonas aeruginosa . All of the known cell-to-cell signaling systems in this bacterium are described, from the most-studied systems, i.e., N -acyl homoserine lactones (AHLs), the 4-quinolones, the global activator of antibiotic and cyanide synthesis (GAC), the cyclic di-GMP (c-di-GMP) and cyclic AMP (cAMP) systems, and the alarmones guanosine tetraphosphate (ppGpp) and guanosine pentaphosphate (pppGpp), to less-well-studied signaling molecules, including diketopiperazines, fatty acids (diffusible signal factor [DSF]-like factors), pyoverdine, and pyocyanin. This overview clearly illustrates that bacterial communication is far more complex than initially thought and delivers a clear distinction between signals that are quorum sensing dependent and those relying on alternative factors for their production.

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“…The exact mechanism of action of this protein is still unknown. However, it has been shown recently that PqsE can activate the transcription of PQS-controlled genes in the absence of PqsR and PQS by enhancing the rhl system (Farrow et al, 2008). PqsR is a LysR transcriptional factor that is activated by HHQ and PQS, leading to the positive activation of many virulence factors, which include a large number of genes also controlled by las and rhl.…”

Section: C M Antunes and Othersmentioning

confidence: 99%

Quorum sensing in bacterial virulence

et al. 2010

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Bacteria communicate through the production of diffusible signal molecules termed autoinducers. The molecules are produced at basal levels and accumulate during growth. Once a critical concentration has been reached, autoinducers can activate or repress a number of target genes. Because the control of gene expression by autoinducers is cell-density-dependent, this phenomenon has been called quorum sensing. Quorum sensing controls virulence gene expression in numerous micro-organisms. In some cases, this phenomenon has proven relevant for bacterial virulence in vivo. In this article, we provide a few examples to illustrate how quorum sensing can act to control bacterial virulence in a multitude of ways. Several classes of autoinducers have been described to date and we present examples of how each of the major types of autoinducer can be involved in bacterial virulence. As quorum sensing controls virulence, it has been considered an attractive target for the development of new therapeutic strategies. We discuss some of the new strategies to combat bacterial virulence based on the inhibition of bacterial quorum sensing systems.

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PqsE Functions Independently of PqsR-PseudomonasQuinolone Signal and Enhances therhlQuorum-Sensing System

Cited by 156 publications

References 57 publications

Adaptation of Iron Homeostasis Pathways by a Pseudomonas aeruginosa Pyoverdine Mutant in the Cystic Fibrosis Lung

Adaptation of Iron Homeostasis Pathways by a Pseudomonas aeruginosa Pyoverdine Mutant in the Cystic Fibrosis Lung

The Multiple Signaling Systems Regulating Virulence in Pseudomonas aeruginosa

Quorum sensing in bacterial virulence

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