The end of the reign of a “master regulator’’? A defect in function of the LasR quorum sensing regulator is a common feature of
            <i>Pseudomonas aeruginosa</i>
            isolates

Trottier, Mylène C.; de Oliveira Pereira, Thays; Groleau, Marie-Christine; Hoffman, Lucas R.; Dandekar, Ajai A.; Déziel, Eric

doi:10.1128/mbio.02376-23

Cited by 2 publications

(1 citation statement)

References 91 publications

(150 reference statements)

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“…A paradox within P. aeruginosa ’s adaptation strategy is the prevalent deficiency in LasR, a critical QS transcriptional regulator. This deficiency is found in approximately 40% of P. aeruginosa isolates from various environments and highlights the need for a functioning rhl system for QS responsiveness [39, 40]. RhlR, an inherently unstable protein, depends on the presence of both its cognate ligand C 4 -HSL and the chaperone-like protein PqsE for its stability and activity.…”

Section: Discussionmentioning

confidence: 99%

Temperature-responsive control ofPseudomonas aeruginosavirulence determinants through the stabilization of quorum sensing transcriptional regulator RhlR

de Oliveira Pereira,

Groleau,

Doucet

et al. 2024

Preprint

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The versatile bacterium Pseudomonas aeruginosa thrives in diverse environments and is notably recognized for its role as an opportunistic pathogen. In line with its adaptability, P. aeruginosa produces various exoproducts crucial for survival and virulence, several of which regulated through quorum sensing (QS). These factors are also regulated in response to environmental cues, such as temperature changes. As a pathogen, P. aeruginosa is generally thought to activate its virulence factors at temperatures akin to warm-blooded hosts rather than environmental temperatures. Recent studies elucidated the functional structure of the QS transcriptional regulator RhlR, which depends on the stabilizing effects of its cognate autoinducing ligand, N‐butanoyl‐L‐homoserine lactone (C4‐HSL), and of the moonlighting chaperone PqsE. Given the influence of temperature on biomolecular dynamics, we investigated how it affects RhlR activity using the RhlR-regulated phzA1 promoter as a proxy. Unexpectedly, we found that RhlR activity is higher at 25°C than at 37°C. This temperature-dependent regulation likely stems from altered RhlR turnover, with the presence of PqsE extending RhlR activity tenfold from its basal level at 37°C to that observed at 25°C. This lower, environmental-like temperature promotes increased affinity between RhlR and C4-HSL, a trait significantly compromised in the absence of PqsE. These results suggest that this response depends on the structural integrity of the complex, indicating that temperature functions as an additional regulating and stabilizing factor of RhlR function. Accordingly, lower growth temperature fails to increase the activity of a structurally stabilized version of RhlR. The thermoregulation aspect of RhlR activity and signalling impacts the virulence profile of a mutant unable to produce C4-HSL, underscoring its significance in bacterial behaviours and potentially conferring an evolutionary advantage.

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Section: Discussionmentioning

confidence: 99%

Temperature-responsive control ofPseudomonas aeruginosavirulence determinants through the stabilization of quorum sensing transcriptional regulator RhlR

de Oliveira Pereira,

Groleau,

Doucet

et al. 2024

Preprint

Self Cite

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The Relationship ofpqsGene Expression to Acylhomoserine Lactone Signaling inPseudomonas aeruginosa

Soto-Aceves,

Smalley,

Schaefer

et al. 2024

Preprint

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The opportunistic pathogenPseudomonas aeruginosahas complex quorum sensing (QS) circuitry, which involves two acylhomoserine lactone (AHL) systems, the LasI AHL synthase and LasR AHL-dependent transcriptional activator system and the RhlI AHL synthase-RhlR AHL-responsive transcriptional activator. There is also a quinoline signaling system (the Pseudomonas quinolone signal, PQS, system). Although there is a core set of genes regulated by the AHL circuits, there is substantial strain-to-strain variation in the non-core QS regulated genes. Reductive evolution of the QS regulon, and variation in specific genes activated by QS, occurs in laboratory evolution experiments with the model strain PAO1. We used a transcriptomics approach to test the hypothesis that reductive evolution in the PAO1 QS regulon can in large part be explained by a simple null mutation in pqsR, the gene encoding the transcriptional activator of the pqs operon. We found that PqsR had very little influence on the AHL QS regulon. This was a surprising finding because the last gene in the PqsR-dependent pqs operon,pqsE, codes for a protein, which physically interacts with RhlR and this interaction is required for RhlR-dependent activation of some genes. We used comparative transcriptomics to examine the influence of apqsEmutation on the QS regulon and identified only three transcripts, which were strictly dependent on PqsE. By using reporter constructs we showed that the PqsE influence on other genes was dependent on experimental conditions and we have gained some insight about those conditions. This work adds to our understanding of the plasticity of theP. aeruginosaQS regulon and to the role PqsE plays in RhlR-dependent gene activation.

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The end of the reign of a “master regulator’’? A defect in function of the LasR quorum sensing regulator is a common feature of Pseudomonas aeruginosa isolates

Cited by 2 publications

References 91 publications

Temperature-responsive control ofPseudomonas aeruginosavirulence determinants through the stabilization of quorum sensing transcriptional regulator RhlR

Temperature-responsive control ofPseudomonas aeruginosavirulence determinants through the stabilization of quorum sensing transcriptional regulator RhlR

The Relationship ofpqsGene Expression to Acylhomoserine Lactone Signaling inPseudomonas aeruginosa

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