Pseudomonas aeruginosa PA14, mvfR and anthranilic acid analogs
Ontology highlight
ABSTRACT:
ORGANISM(S): Pseudomonas aeruginosa
PROVIDER: GSE17111 | GEO | 2009/07/17
SECONDARY ACCESSION(S): PRJNA123453
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). Our findings reveal a multi-layered homeostatic regulation of PQS and HHQ and the MvfR regulon component PqsE which is a key mediator in orchestrating this homeostatic regulation.
2009-07-17 | GSE17116 | GEO
Project description:Pseudomonas aeruginosa PA14, mvfR and anthranilic acid analogs
| PRJNA123453 | ENA
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 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: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:The interaction of clinically relevant microorganisms is the focus of various studies, e.g. the interaction between the pathogenic yeast, Candida albicans, and the bacterium, Pseudomonas aeruginosa and these interactions can alter the outcome of infection, growth dynamics of each species and antimicrobial resistance of pathogens. During infection, both C. albicans and P. aeruginosa can elicit the release arachidonic acid (AA) from host cells membranes through the action of phospholipases. This polyunsaturated fatty acid can be transformed into immune-modulating compounds, termed eicosanoids, by both host-derived and microbial-derived enzymatic reactions. In its free form, AA can affect the growth of both C. albicans and P. aeruginosa, inhibiting the morphogenesis of C. albicans as well as reducing resistance towards antifungal agents. However, the mechanism of this is unknown. Previous studies on the effect of polyunsaturated fatty acids have indicated a possible alteration in plasma membrane organisation and permeability. Our group aimed to address how AA affects C. albicans in both single species biofilms, as well as in polymicrobial biofilms with P. aeruginosa. RNAseq was performed on single and polymicrobial biofilms in the presence and absence of a sub-inhibitory (100 µM) concentration of AA. Differential expression was determined between C. albicans single species biofilms in the presence and absence of AA. Secondly, the influence of co-incubation of C. albicans with P. aeruginosa in the absence of AA was evaluated to identify novel facets of interaction not previously identified, and to establish a baseline to determine the effect of AA on C. albicans in polymicrobial biofilms. Lastly, the effect of AA on C. albicans in polymicrobial biofilms was determined through comparison with polymicrobial biofilms in the absence of AA. This study provides a comprehensive analysis of the effect of AA and both co-incubation of C. albicans with P. aeruginosa focused on the transcriptome.
2021-01-31 | GSE136726 | GEO
Project description:Phage therapy is a promising adjunct therapeutic approach against bacterial multidrug-resistant infections, including Pseudomonas aeruginosa-derived infections. Nevertheless, the current knowledge about the phage-bacteria interaction within a human environment is limited. In this work, we performed a transcriptome analysis of phage-infected P. aeruginosa adhered to a human epithelium (Nuli-1 ATCC® CRL-4011™). To this end, we performed RNA-sequencing from a complex mixture comprising phage–bacteria–human cells at early, middle, and late infection and compared it to uninfected adhered bacteria. Overall, we demonstrated that phage genome transcription is unaltered by bacterial growth and phage employs a core strategy of predation through upregulation of prophage-associated genes, a shutdown of bacterial surface receptors, and motility inhibition. In addition, specific responses were captured under lung-simulating conditions, with the expression of genes related to spermidine syntheses, sulfate acquisition, spermidine syntheses, biofilm formation (both alginate and polysaccharide syntheses), lipopolysaccharide (LPS) modification, pyochelin expression, and downregulation of virulence regulators. These responses should be carefully studied in detail to better discern phage-induced changes from bacterial responses against phage. Our results establish the relevance of using complex settings that mimics in vivo conditions to study phage-bacteria interplay, being obvious the phage versatility on bacterial cell invasion.
2023-05-31 | GSE213159 | GEO
Project description:Pseudomonas aeruginosa PA14 MvfR-dependent QS regulatory pathway
| PRJNA119741 | ENA