Pseudomonas aeruginosa PA14, pqsE and PQS
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ABSTRACT:
ORGANISM(S): Pseudomonas aeruginosa
PROVIDER: GSE17116 | GEO | 2009/07/17
SECONDARY ACCESSION(S): PRJNA123657
REPOSITORIES: GEO
Similar Datasets
Project description:The Pseudomonas aeruginosa MvfR-dependent QS regulatory pathway controls the expression of key virulence genes; and is activated via the extracellular signals 4-hydroxy-2-heptylquinoline (HHQ) and 3,4-dihydroxy-2-heptylquinoline (PQS), whose syntheses depend on anthranilic acid (AA), the primary precursor of 4-hydroxy-2-alkylquinolines (HAQs). We identified halogenated AA analogs that specifically inhibited HAQ biosynthesis and disrupted MvfR-dependent gene expression. These compounds restricted P. aeruginosa systemic dissemination and mortality in mice, without perturbing bacterial viability, and inhibited osmoprotection, a widespread bacterial function.
2009-07-17 | GSE17111 | GEO
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 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:The pqs operon of the bacteria P. aeruginosa is responsible for the production of at least 60 secreted compounds mainly hidroxy-quinolones (HAQs). Some of them, like PQS and HHQ, were found to be important signal that control the virulence of the bacteria. We have discover that one of the most abandon molecule produced by the pqs operon, 2 aminoacetophenone (2-AA), a volatile molecule serves as a unique signal. In contrast to the previous described PQS and HHQ, 2-AA is downregulating virulence and acute phase proteins and upregulating chronic phase proteins. In addition we have found that 2-AA promotes the formation of persisters cells that antibiotic tolerant. we have compared the genes profile of wild-type PA14 strain and its derivatives topA which lacks Topoisomerase I and pqsA that do not produces HAQs or 2-AA to cultures that were treated with 3mM of 2-AA. Cell were grown with and without 2-AA (3mM) to OD 2.0.
2011-12-21 | E-GEOD-24036 | biostudies-arrayexpress
Project description:The pqs operon of the bacteria P. aeruginosa is responsible for the production of at least 60 secreted compounds mainly hidroxy-quinolones (HAQs). Some of them, like PQS and HHQ, were found to be important signal that control the virulence of the bacteria. We have discover that one of the most abandon molecule produced by the pqs operon, 2 aminoacetophenone (2-AA), a volatile molecule serves as a unique signal. In contrast to the previous described PQS and HHQ, 2-AA is downregulating virulence and acute phase proteins and upregulating chronic phase proteins. In addition we have found that 2-AA promotes the formation of persisters cells that antibiotic tolerant. we have compared the genes profile of wild-type PA14 strain and its derivatives topA which lacks Topoisomerase I and pqsA that do not produces HAQs or 2-AA to cultures that were treated with 3mM of 2-AA.
2011-12-21 | GSE24036 | GEO
Project description:Pseudomonas aeruginosa PA14 MvfR-dependent QS regulatory pathway
| PRJNA119741 | ENA
Project description:Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen of humans, most notably those with cystic fibrosis or whose immune systems are compromised. As a global regulator, MvfR,RhlR and QscR have been characterized to control a group of virulence-related factors and quorum sensing (QS) genes in P. aeruginosa, but its detailed molecular regulatory mechanism is largely elusive. To further gain insights into the direct targets of MvfR,RhlR and QscR in viv, this study focused on identifying the potential targets of MvfR,RhlR and QscR directly regulating QS system and other vireulence pathways. We performed a chromatin immunoprecipitation coupled to high-throughput sequencing (ChIP-seq) assay that identified 221, 30 and 1 binding sites of MvfR,RhlR and QscR. The direct regulation of these genes by MvfR,RhlR and QscR have been biochemically and genetically verified. The results indicated that MvfR,RhlR and QscR had direct and profound effects on QS, which provides new cues to better understand the detailed regulatory networks of virulence.
2019-07-16 | GSE121243 | GEO
Project description:Pseudomonas aeruginosa PA14, pqsE and PQS
| PRJNA123657 | ENA
Project description:Virulence factor production and the development of biofilms in Pseudomonas aeruginosa have been shown to be regulated by two hierarchically organised quorum sensing (QS) systems via small acyl-homoserine lactone (AHL) signal molecules. Recently, a third bacterial signal molecule, the Pseudomonas quinolone signal (PQS), has been identified, which positively regulates a subset of genes dependent on the QS systems. To further dissect the various independent regulation levels for many QS induced genes and to evaluate the impact of PQS on the QS circuitry, we performed a transcriptome analysis of PAO1 cultures supplemented with PQS. The global transcriptional profile in response to PQS revealed a marked up-regulation of genes belonging to the tightly interdependent functional groups of iron acquisition and oxidative stress response. Remarkably, not only most of the differentially regulated genes but also the induction of a lacZ transcriptional fusion of rhlR could be traced back to a iron chelating effect of PQS. Nevertheless, although iron deficiency per se induced rhlR, there seems to be PQS specific effects that are independent of the PQS effect on P. aeruginosa iron homeostasis Keywords: PQS response
2006-12-12 | GSE3836 | GEO
Project description:While it is known that PqsE can stimulate the ability of RhlR to control some virulence factors, no data are available allowing clear discrimination of the PqsE and RhlR regulons. In this study, a P. aeruginosa PAO1 mutant strain with deletion of multiple QS elements and inducible expression of PqsE and/or RhlR has been generated and validated. RNA-seq performed in this genetic background allowed to unambiguously define the regulons controlled by PqsE and RhlR when produced alone or in combination Data produced in this study demonstrate that PqsE mainly impacts on the P. aeruginosa transcriptome via an RhlR-dependent pathway, and splits the RhlR-regulon in PqsE-dependent and PqsE-independent sub-regulons.
2022-05-17 | GSE200835 | GEO