Influence of the pqs genes on Pseudomonas quorum sensing
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ABSTRACT:
PROVIDER: PRJNA1086972 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28322076_1.fastq.gz | Fastqsanger.gz | |||
| SRR28322076_2.fastq.gz | Fastqsanger.gz | |||
| SRR28322077_1.fastq.gz | Fastqsanger.gz | |||
| SRR28322077_2.fastq.gz | Fastqsanger.gz | |||
| SRR28322078_1.fastq.gz | Fastqsanger.gz |
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Project description:The opportunistic pathogen Pseudomonas aeruginosa has 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 full RhlR-dependent activation of some genes. We used comparative transcriptomics to examine the influence of a pqsE mutation 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 the P. aeruginosa QS regulon and to the role PqsE plays in RhlR-dependent gene activation.
2024-03-17 | GSE261453 | GEO
Project description:Influence of the pqs genes on Pseudomonas quorum sensing
| PRJNA1063357 | ENA
Project description:Pseudomonas aeruginosa employs quorum sensing (QS) small molecules such as Pseudomonas Quinolone Signal (PQS) to manipulate host cell death. Although PQS triggers several cell death modalities, its role in ferroptosis remains enigmatic. Here, we reported that PQS induces ferroptosis in macrophages through a previously unrecognized carnosine-N-methyltransferase (CNMT)-transferrin receptor 1 (TFR1) methylation pathway. Using thermal proteome profilingscreening, we identified CNMT as the direct intracellular receptor of PQS in macrophage. Mechanistically, PQS binding activates CNMT’s histidine methyltransferase activity, catalyzing H35 methylation on TFR1. This methylation modification increases TFR1 expressions, amplifying iron acquisition and lipid peroxidation for ferroptosis. Crucially, the PQS-CNMT-TFR1 axis is distinct from canonical bacterial pathogens that exploit host cell death pathways, revealing P. aeruginosa’s unique strategy to exploit host epigenetic machinery. Our findings redefine QS molecules as mediators of interkingdom signaling and position CNMT-TFR1 methylation as therapeutic targets aimed at blocking ferroptosis-driven immunopathology to mitigate P. aeruginosa virulence.
2025-02-27 | PXD061292 |
Project description:Pseudomonas aeruginosa (Pa) is a ubiquitous bacterium that uses quorum sensing (QS), a cell-cell communication system that enables it to sense cell density and to alter gene expression. Pa has three complete QS circuits controlled by the transcriptional regulators LasR, RhlR, and PqsR (MvfR), that together control hundreds of genes, including virulence factors. In the well-described strain PAO1, QS is organized hierarchically, with PqsR and RhlR activity dependent on LasR. In PAO1, this hierarchy depends on the non-QS transcription factor MexT; by an unknown mechanism, deletion of mexT allows for RhlR activity in the absence of LasR. We aimed to identify how regulators such as MexT modulate the QS architecture in Pa. We compared the transcriptome of PAO1 to that of PAO1ΔmexT and identified 152 differentially expressed genes. MexT does not appear to regulate rhlR or pqsR directly; however, we identified two MexT-regulated operons that may affect the hierarchy in PAO1. These operons encode the drug efflux pump genes mexEF-oprN and the Pseudomonas quinolone signal (PQS) synthesis genes pqsABCDE. We performed genetic experiments to test whether the products of these genes affected the QS hierarchy. As with the mexT knockout mutant, we found that a PAO1 mexEF knockout mutant exhibited RhlR activity earlier, and to a higher magnitude, than wild-type PAO1. MexEF-OprN is known to export the PQS precursor HHQ, and we found that exogenous addition of PQS to PAO1 partially affects RhlR activity, resulting in earlier timing and higher magnitude compared to wild-type PAO1. We further elucidated that this is likely due to positive regulation by PqsE. These data link both the drug efflux pump MexEF-OprN and PQS QS to the regulation of the QS hierarchy in PAO1. We wondered if the same applied to QS architectures in Pa clinical isolates. We discovered that there are alternate QS architectures in clinical isolates, where RhlR activity is not fully dependent on LasR. In these isolates, surprisingly, MexT does not influence the relationship between LasR and RhlR, and this is indicative of a different QS architecture in the clinical isolates. Overall, we further elucidated the regulation of QS architecture in PAO1 and identified unique QS architectures in clinical isolates. Importantly, our work reveals a new suite of factors that regulate QS in Pa, with implications for a variety of Pa behaviors both in the laboratory and clinical settings.
2025-04-09 | GSE291609 | GEO
Project description:Pseudomonas fluorescens is an important plant growth-promoting rhizobacteria (PGPR) for its biocontrol properties, which are mostly influenced by the quorum sensing (QS) system. Plants produce multiple metabolites like flavonoids to regulate physiology of PGPR. However, it remains under-explored how flavonoids produced by plant roots influence the QS system of PGPR. In this study, we found the TetR-family regulator AefR was capable of binding to flavonoids and could inhibit production of AHLs by suppressing the expression of mexEF-oprN in P. fluorescens 2P24. We further showed that the efflux pump MexEF-OprN could attenuate the quorum sensing system PcoR/PcoI by extruding homoserine lactone (AHLs) molecules, leading to reduced biosynthesis of secondary metabolite mupirocin. Taken together, this study identified a TetR-like regulator responding to plant flavonoids and regulating the quorum sensing, providing insights into the interaction between PGPR and plant roots.
2025-02-15 | PXD052703 | Pride
Project description:Pseudomonas fluorescens is an important plant growth-promoting rhizobacteria (PGPR) for its biocontrol properties, which are mostly influenced by the quorum sensing (QS) system. Plants produce multiple metabolites like flavonoids to regulate physiology of PGPR. However, it remains under-explored how flavonoids produced by plant roots influence the QS system of PGPR. In this study, we found the TetR-family regulator AefR was capable of binding to flavonoids and could inhibit production of AHLs by suppressing the expression of mexEF-oprN in P. fluorescens 2P24. We further showed that the efflux pump MexEF-OprN could attenuate the quorum sensing system PcoR/PcoI by extruding homoserine lactone (AHLs) molecules, leading to reduced biosynthesis of secondary metabolite mupirocin. Taken together, this study identified a TetR-like regulator responding to plant flavonoids and regulating the quorum sensing, providing insights into the interaction between PGPR and plant roots.
2025-02-15 | PXD052702 | Pride
Project description:Pseudomonas aeruginosa pathogenicity mainly relies on its ability to finely control the expression of virulence determinants via multiple quorum sensing (QS) systems. Despite the relevant role of the pqs QS system in controlling the expression of key virulence factors and biofilm formation in P. aeruginosa, our understanding of the molecular mechanisms governing this QS circuit, which employs 2-alkyl-4-quinolones (AQs) as signal molecules, is still preliminary, probably due to its complexity. Multiple genes are required for the synthesis of the primary AQs, 2-heptyl-4-hydroxyquinoline (HHQ), 2-heptyl-3-hydroxy-4-quinolone (PQS), and 2-heptyl-4-hydroxyquinoline N-oxide (HQNO). These include the pqsABCDE operon, required for the synthesis of HHQ, which in turn is oxidized to PQS via the action of the monooxygenase PqsH. The monooxygenase PqsL is required for HQNO synthesis together with the pqsABCD genes. The fifth gene of the pqsABCDE operon, pqsE, is also required for the production of major virulence factors and for biofilm formation, and exerts a homeostatic effect on AQs synthesis by repressing the transcription of the pqsABCDE operon. The pqs system is subject to positive autoregulation, with the PqsR regulator promoting pqsABCDE transcription upon binding to HHQ or PQS. However, the individual contributions and relative importance of HHQ, PQS, HQNO and PqsE to AQ-dependent signalling is not fully apparent, because of the overlapping and interdependent nature of the factors involved in this complex QS network. We used microarrays to detail the global response of a P. aeruginosa mutant strain unable to synthesise or convert AQs, and to express PqsE to exogenously provided AQs or IPTG (to induce pqsE expression).
2020-11-21 | GSE81364 | GEO
Project description:The biocontrol agent Pseudomonas chlororaphis PA23 protects canola (Brassica napus) against infection by the necrotrophic fungus Sclerotinia sclerotiorum. Production of PA23 secondary metabolites is governed by a complex regulatory pathway that includes the GacA/GacS two component system, the PhzI/PhzR quorum-sensing system, and a novel LysR-type transcriptional regulator, called PtrA. Through RNA-sequencing, transcriptomic profiles of PA23-WT, two quorum sensing-deficient strains, PA23-AHL and PA23-phzR, and regulatory mutants PA23-gacA, PA23-gacS and PA23-ptrA were generated allowing elucidation of the PhzRI, Gac and PtrA regulons of P. chlororaphis PA23.
2018-05-26 | GSE114924 | GEO
Project description:Pseudomonas aeruginosa possesses at least three well-defined quorum-sensing (QS) (las, rhl, and pqs) systems. These QS systems control a variety of important functions including virulence. RsaL is a QS repressor that reduces QS signal production and ensures homeostasis by functioning in opposition to LasR. However, its regulatory role in signal homeostasis remains elusive. Here, we conducted a ChIP-seq assay and revealed that RsaL bound to two new targets, the intergenic regions of PA2228/PA2229 and pqsH/cdpR, which are required for PQS synthesis. Deletion of rsaL reduced the transcription of pqsH and cdpR, thus decreasing PQS signal production. The ΔrsaL strain exhibited increased pyocyanin production and reduced biofilm formation, which are dependent on CdpR or PqsH activity. In addition, we solved the structure of the RsaL-DNA complex at a 2.4 Å resolution. Although the overall sequence similarity is quite low, RsaL folds into a HTH-like structure, which is conserved among many transcriptional regulators. Complementation results of the rsaL knockout cells with different rsaL mutants further confirmed the critical role of the DNA-binding residues (including Arg20, Gln27, Gln38, Gly35, Ser37, and Ser42) that are essential for DNA binding. Our findings reveal new targets of RsaL and provide insight into the detailed characterization of the RsaL-DNA interaction.
2016-12-20 | GSE87157 | GEO
Project description:The Pseudomonas aeruginosa quorum-sensing (QS) systems contribute to bacterial homeostasis and pathogenicity. Although many regulators have been characterized to control the production of virulence factors and QS signaling molecules, its detailed regulatory mechanisms still remain elusive. Here, we performed chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-seq) on 10 key QS regulators. The direct regulation of these genes by corresponding regulator has been confirmed by Electrophoretic mobility shift assays (EMSAs) and quantitative real-time polymerase chain reactions (qRT-PCR). Binding motifs are found by using MEME suite and verified by footprint assays in vitro. Collectively, this work provides new cues to better understand the detailed regulatory networks of QS systems. ChIP-seq of 10 QS regulators in Pseudomonas aeruginosa
2015-08-04 | E-GEOD-65356 | biostudies-arrayexpress