Quorum sensing and environmental adaptation in Pseudomonas aeruginosa: a tale of regulatory networks and multifunctional signal molecules

Williams, Paul; Cámara, Miguel

doi:10.1016/j.mib.2009.01.005

Cited by 673 publications

(623 citation statements)

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“…For example, in the opportunistic pathogen Pseudomonas aeruginosa , QS systems regulate the expression of 6%–10% of P. aeruginosa genes, including those encoding virulence factors such as hydrogen cyanide, the galactophilic lectin LecA, elastase, rhamnolipids, and others involved in protein secretion and chemotaxis (Schuster, Lostroh, Ogi, & Greenberg, 2003; Schuster, Sexton, Diggle, & Greenberg, 2013; Williams & Camara, 2009). In P .…”

Section: Introductionmentioning

confidence: 99%

“…In P . aeruginosa , QS involves three major QS‐signaling pathways: the las and rhl systems that utilize N ‐acylhomoserine lactones (AHLs) and a Pseudomonas Quinolone Signal (PQS) system that uses 2‐alkyl‐4‐quinolones (AQs) as QS signal molecules (Williams & Camara, 2009). The las and rhl systems are linked such that LasR drives the expression of lasI as well as rhlR and rhlI (Latifi, Foglino, Tanaka, Williams, & Lazdunski, 1996), and PQS and the las and rhl systems have also been found to interact (Diggle et al., 2003; McKnight, Iglewski, & Pesci, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…As a result, P . aeruginosa QS‐signaling pathways are inter‐linked and activation of several systems can be required for full expression of certain “traits” such as bacterial virulence factors (Williams & Camara, 2009). …”

Section: Introductionmentioning

confidence: 99%

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Bacterial cell‐to‐cell signaling promotes the evolution of resistance to parasitic bacteriophages

Moreau

Diggle

Friman

2017

Ecology and Evolution

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The evolution of host–parasite interactions could be affected by intraspecies variation between different host and parasite genotypes. Here we studied how bacterial host cell‐to‐cell signaling affects the interaction with parasites using two bacteria‐specific viruses (bacteriophages) and the host bacterium Pseudomonas aeruginosa that communicates by secreting and responding to quorum sensing (QS) signal molecules. We found that a QS‐signaling proficient strain was able to evolve higher levels of resistance to phages during a short‐term selection experiment. This was unlikely driven by demographic effects (mutation supply and encounter rates), as nonsignaling strains reached higher population densities in the absence of phages in our selective environment. Instead, the evolved nonsignaling strains suffered relatively higher growth reduction in the absence of the phage, which could have constrained the phage resistance evolution. Complementation experiments with synthetic signal molecules showed that the Pseudomonas quinolone signal (PQS) improved the growth of nonsignaling bacteria in the presence of a phage, while the activation of las and rhl quorum sensing systems had no effect. Together, these results suggest that QS‐signaling can promote the evolution of phage resistance and that the loss of QS‐signaling could be costly in the presence of phages. Phage–bacteria interactions could therefore indirectly shape the evolution of intraspecies social interactions and PQS‐mediated virulence in P. aeruginosa.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Bacterial cell‐to‐cell signaling promotes the evolution of resistance to parasitic bacteriophages

Moreau

Diggle

Friman

2017

Ecology and Evolution

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“…In Gram-negative proteobacteria, QS generally comprises a LuxI-type signal synthase that produces a diffusible acyl-homoserine lactone (acyl-HSL) signal, and a cognate LuxR-type receptor that binds the signal and regulates transcription of target genes (Waters and Bassler, 2005;Williams et al, 2007;Schuster et al, 2013). The opportunistic pathogen Pseudomonas aeruginosa, a particularly well-understood example, employs two acyl-HSL signaling systems, LasI/R and RhlI/R, arranged in a hierarchical manner with LasR sitting atop the hierarchy (Schuster and Greenberg, 2006;Williams and Camara, 2009;Jimenez et al, 2012). Together, both systems regulate over 300 genes, many of which encode secreted public goods such as extracellular enzymes or secondary metabolites that have a role in virulence (Hentzer et al, 2003;Schuster et al, 2003;Wagner et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Non-social adaptation defers a tragedy of the commons in Pseudomonas aeruginosa quorum sensing

et al. 2015

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In a process termed quorum sensing (QS), the opportunistic bacterial pathogen Pseudomonas aeruginosa uses diffusible signaling molecules to regulate the expression of numerous secreted factors or public goods that are shared within the population. But not all cells respond to QS signals. These social cheaters typically harbor a mutation in the QS receptor gene lasR and exploit the public goods produced by cooperators. Here we show that non-social adaptation under growth conditions that require QS-dependent public goods increases tolerance to cheating and defers a tragedy of the commons. The underlying mutation is in the transcriptional repressor gene psdR. This mutation has no effect on public goods expression but instead increases individual fitness by derepressing growth-limiting intracellular metabolism. Even though psdR mutant populations remain susceptible to invasion by isogenic psdR lasR cheaters, they bear a lower cheater load than do wild-type populations, and they are completely resistant to invasion by lasR cheaters with functional psdR. Mutations in psdR also sustain growth near wild-type levels when paired with certain partial loss-offunction lasR mutations. Targeted sequencing of multiple evolved isolates revealed that mutations in psdR arise before mutations in lasR, and rapidly sweep through the population. Our results indicate that a QS-favoring environment can lead to adaptations in non-social, intracellular traits that increase the fitness of cooperating individuals and thereby contribute to population-wide maintenance of QS and associated cooperative behaviors.

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“…Three QS systems operate in P. aeruginosa, las, rhl and pqs which function in an interconnecting network, facilitating co-operation and cheating within P. aeruginosa populations [42 ]. The virulence gene regulation of P. aeruginosa is well studied and many virulence determinants including motility and biofilm formation are QS dependent as reviewed recently [43,44]. QS signaling molecules also appear to have direct effects on host cells via calcium signaling.…”

Section: Quorum Sensing Facilitates Adaptationmentioning

confidence: 99%

Bacterial host interactions in cystic fibrosis

Callaghan

McClean

2012

Current Opinion in Microbiology

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This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues.Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited.In most cases authors are permitted to post their version of the article (e.g. in Word or Tex form) to their personal website or institutional repository. Authors requiring further information regarding Elsevier's archiving and manuscript policies are encouraged to visit:http://www.elsevier.com/copyrightAuthor's personal copy Bacterial host interactions in cystic fibrosis Má ire Callaghan and Siobhá n McCleanChronic infection is a hallmark of cystic fibrosis (CF) and the main contributor to morbidity. Microbial infection in CF is complex, due to the number of different species that colonise the CF lung. Their colonisation is facilitated by a host response that is impaired or compromised by highly viscous mucous, zones of hypoxia and the lack of the cystic fibrosis transmembrane regulator (CFTR). Successful dominant CF pathogens combine an effective arsenal to establish infection and counter-attack the host response, together with an ability to adapt readily to an unfavourable environment. Hypermutability is common among CF pathogens facilitating adaptation and as the host response persists, progressive destruction of the normal architecture of lung tissue ensues with catastrophic consequences for the host. Limited information exists on the host-microbial interactions of many of these organisms and this review will focus only on the current understanding of the more clearly defined CF pathogens (Box 1). Role of CFTR in CF lung colonisationA direct role of the CFTR mutation in CF pathogenesis has been attributed to normal CFTR acting as a pathogen receptor involved in the internalisation and subsequent clearance of P. aeruginosa [9], but this mechanism is pathogen-specific. Mutated CFTR has also been attributed to be the cause of reduced internalisation of one Bcc species, Burkholderia dolosa, but not the more virulent Burkholderia cenocepacia in respiratory epithelial cells [10]. Furthermore, in contrast to P. aeruginosa, S. aureus was more invasive of CF cells compared to non-CF cells [11], indicating that CFTR is not the only route of bacterial uptake and invasion into the epithelium.Alterations in the phenotype of CF airway epithelial cells also provide receptors for pathogens to adhere to. For example, CF airways show alterations in membrane glycoproteins and glycolipids which are directly linked to the CFTR defect (reviewed by [12]). The ratio of asialylated to sialylated glycolipids is higher in CF cells compared to non-CF cells, providing additional receptors for P. aeruginosa and Bcc. This is significant as invasion of lung epithelial cells by Bcc depends on asialylated glycolipids [13]. In addition, alteration...

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Quorum sensing and environmental adaptation in Pseudomonas aeruginosa: a tale of regulatory networks and multifunctional signal molecules

Cited by 673 publications

References 58 publications

Bacterial cell‐to‐cell signaling promotes the evolution of resistance to parasitic bacteriophages

Bacterial cell‐to‐cell signaling promotes the evolution of resistance to parasitic bacteriophages

Non-social adaptation defers a tragedy of the commons in Pseudomonas aeruginosa quorum sensing

Bacterial host interactions in cystic fibrosis

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