Expression profile for PA14 lasR rhlR double mutant with H2O2 stress
Ontology highlight
ABSTRACT:
ORGANISM(S): Pseudomonas aeruginosa
PROVIDER: GSE54245 | GEO | 2015/01/09
SECONDARY ACCESSION(S): PRJNA236030
REPOSITORIES: GEO
Similar Datasets
Project description:Quorum sensing controls the expression of multiple virulence factors. PA14 genes lasR and rhlR are necessary for quorum sensing via homoserine lactones. A PA14 lasR rhlR deficient mutant exhibits a reduced oxidative stress response. Here we conducted a microarray to determine oxidative stress response gene regulation mediated by the homoserine lactone quorum sensing circuits. A PA14 lasR rhlR deficient mutant was compared to the wild-type with and without H2O2 stress.
2015-01-09 | E-GEOD-54245 | biostudies-arrayexpress
Project description:To better understand the role of QscR in P. aeruginosa gene regulation and to better understand the relationship between QscR, LasR and RhlR control of gene expression we used transcription profiling to identify a QscR-dependent regulon. Our analysis revealed that QscR activates some genes and represses others. Some of the repressed genes are not regulated by the LasR-I or RhlR-I systems while others are. The LasI-generated 3-oxododecanoyl-homoserine lactone serves as a signal molecule for QscR. Thus QscR appears to be an integral component of the P. aeruginosa quorum sensing circuitry. QscR uses the LasI-generated acyl-homoserine lactone signal and controls a specific regulon that overlaps with the already overlapping LasR and RhlR-dependent regulons. Keywords: Quorum sensing regulon, Direct activation
2006-01-18 | GSE4026 | GEO
Project description:Effect of acyl-HSL signal or ectopic lasR, rhlR, or rpoS expression on the advancement of quorum sensing gene expression during the logarithmic phase of growth
2007-08-10 | E-MEXP-1183 | biostudies-arrayexpress
Project description:Pseudomonas aeruginosa is a troublesome opportunistic pathogen isolated from diverse environmental sources. An arsenal of degrading enzymes and antagonistic factors contribute to P. aeruginosa persistence and damage of a susceptible host. Largely through density-dependent regulation referred to as quorum sensing, the LasR, RhlR, and PqsR transcription factors collectively modulate hundreds of genes, including the expression of several virulence factors, in response to diffusible signals called autoinducers. LasR loss-of-function (LasR-) strains are commonly isolated from clinical samples and produce fewer toxins in monoculture, yet these strains are associated with worse clinical outcomes. We show that in co-culture with P. aeruginosa wild type where LasR loss-of-function strains are often found in vivo, ∆lasR hyperproduces RhlR/I dependent antagonistic factors. Specifically, we present a cyclic model of interaction between wild type and ∆lasR wherein the iron-scavenging siderophore pyochelin produced by the lasR mutant induces citrate release and cross-feeding from the wild type to ∆lasR to stimulate production of antagonistic factors with native functions involved in iron acquisition. Co-culture specific behaviors mediated by altered metabolite secretion and metabolism may explain complications associated with LasR loss-of-function strains. More broadly, this report illustrates how heterogenous behaviors within a mono-species community can promote antagonism associated with carbon and metal assimilation.
2020-04-28 | GSE149385 | GEO
Project description:The PqsE enzyme plays a vital role in quorum sensing and virulence in Pseudomonas aeruginosa, yet its enzymatic function is unknown. Here, we identify the protein interaction network of PqsE as well as that of a catalytically dead variant, PqsE(D73A) in P. aeruginosa PA14. Our analyses identify proteins that interact with PqsE that are independent of and that depend on PqsE catalytic function. One such catalysis-independent interaction is with the quorum-sensing regulator, RhlR, consistent with our previous work. We also characterize the PqsE interaction network in a delta rhlR P. aeruginosa PA14 strain and identify additional proteins as PqsE-interactors.
2022-09-06 | PXD035779 | Pride
Project description:Pseudomonas aeruginosa is a major cause of nosocomial infections and also leads to severe exacerbations in cystic fibrosis or chronic obstructive pulmonary disease. Three intertwined quorum sensing systems control virulence of P. aeruginosa, with the rhl circuit playing the leading role in late and chronic infections. The majority of traits controlled by rhl transcription factor RhlR depend on PqsE, a dispensable thioesterase in Pseudomonas Quinolone Signal (PQS) biosynthesis that interferes with RhlR through an enigmatic mechanism likely involving direct interaction of both proteins. Here we show that PqsE and RhlR form a 2:2 protein complex that, together with RhlR agonist N-butanoyl-L-homoserine lactone (C4-HSL), solubilizes RhlR and thereby renders the otherwise insoluble transcription factor active. We determined crystal structures of the complex and identified residues essential for the interaction. To corroborate the chaperone like activity of PqsE, we designed stability-optimized variants of RhlR that bypass the need for C4-HSL and PqsE in activating PqsE/RhlR-controlled processes of P. aeruginosa. Together, our data provide insight into the unique regulatory role of PqsE and lay groundwork for developing new P. aeruginosa-specific pharmaceuticals.
2023-03-11 | PXD038000 | Pride
Project description:In people with the genetic disease cystic fibrosis (CF), bacterial infections involving the opportunistic pathogen Pseudomonas aeruginosa are a significant cause of morbidity and mortality. P. aeruginosa uses a cell-cell signaling mechanism called quorum sensing (QS) to regulate many virulence functions. One type of QS consists of acyl-homoserine lactone (AHL) signals produced by LuxI-type signal synthases, which bind a cognate LuxR-type transcription factor. In laboratory strains and conditions, P. aeruginosa employs two AHL synthase/receptor pairs arranged in a hierarchy, with the LasI/R system controlling the RhlI/R system and many downstream virulence factors. However, P. aeruginosa isolates with inactivating mutations in lasR are frequently isolated from chronic CF infections. We and others have shown that these isolates frequently use RhlR as the primary QS regulator. RhlR is rarely mutated in CF and environmental settings. We were interested if there were reproducible genetic characteristics of these isolates and if there was a central group of genes regulated by RhlR in all isolates. We examined five isolates and found signatures of adaptation common to CF isolates. Here, we analyzed CF clinial isolate E104. In this strain, RhlR positively regulates 48 genes, including those coding for known virulence factors. These results suggest a key group of QS-regulated factors important for pathogenesis of chronic infection, and position RhlR as a target for anti-QS therapeutics. Our work underscores the need to sample a diversity of isolates to understanding QS beyond what has been described in laboratory strains.
2022-03-18 | GSE198534 | GEO
Project description:In people with the genetic disease cystic fibrosis (CF), bacterial infections involving the opportunistic pathogen Pseudomonas aeruginosa are a significant cause of morbidity and mortality. P. aeruginosa uses a cell-cell signaling mechanism called quorum sensing (QS) to regulate many virulence functions. One type of QS consists of acyl-homoserine lactone (AHL) signals produced by LuxI-type signal synthases, which bind a cognate LuxR-type transcription factor. In laboratory strains and conditions, P. aeruginosa employs two AHL synthase/receptor pairs arranged in a hierarchy, with the LasI/R system controlling the RhlI/R system and many downstream virulence factors. However, P. aeruginosa isolates with inactivating mutations in lasR are frequently isolated from chronic CF infections. We and others have shown that these isolates frequently use RhlR as the primary QS regulator. RhlR is rarely mutated in CF and environmental settings. We were interested if there were reproducible genetic characteristics of these isolates and if there was a central group of genes regulated by RhlR in all isolates. We examined five isolates and found signatures of adaptation common to CF isolates. Here, we analyzed CF clinial isolate E167. In this strain, RhlR positively regulates 78 genes, including those coding for known virulence factors. These results suggest a key group of QS-regulated factors important for pathogenesis of chronic infection, and position RhlR as a target for anti-QS therapeutics. Our work underscores the need to sample a diversity of isolates to understanding QS beyond what has been described in laboratory strains.
2022-03-18 | GSE198719 | GEO
Project description:In people with the genetic disease cystic fibrosis (CF), bacterial infections involving the opportunistic pathogen Pseudomonas aeruginosa are a significant cause of morbidity and mortality. P. aeruginosa uses a cell-cell signaling mechanism called quorum sensing (QS) to regulate many virulence functions. One type of QS consists of acyl-homoserine lactone (AHL) signals produced by LuxI-type signal synthases, which bind a cognate LuxR-type transcription factor. In laboratory strains and conditions, P. aeruginosa employs two AHL synthase/receptor pairs arranged in a hierarchy, with the LasI/R system controlling the RhlI/R system and many downstream virulence factors. However, P. aeruginosa isolates with inactivating mutations in lasR are frequently isolated from chronic CF infections. We and others have shown that these isolates frequently use RhlR as the primary QS regulator. RhlR is rarely mutated in CF and environmental settings. We were interested if there were reproducible genetic characteristics of these isolates and if there was a central group of genes regulated by RhlR in all isolates. We examined five isolates and found signatures of adaptation common to CF isolates. Here, we analyzed CF clinial isolate E125. In this strain, RhlR positively regulates 28 genes, including those coding for known virulence factors. These results suggest a key group of QS-regulated factors important for pathogenesis of chronic infection, and position RhlR as a target for anti-QS therapeutics. Our work underscores the need to sample a diversity of isolates to understanding QS beyond what has been described in laboratory strains.
2022-03-18 | GSE198717 | GEO
Project description:In people with the genetic disease cystic fibrosis (CF), bacterial infections involving the opportunistic pathogen Pseudomonas aeruginosa are a significant cause of morbidity and mortality. P. aeruginosa uses a cell-cell signaling mechanism called quorum sensing (QS) to regulate many virulence functions. One type of QS consists of acyl-homoserine lactone (AHL) signals produced by LuxI-type signal synthases, which bind a cognate LuxR-type transcription factor. In laboratory strains and conditions, P. aeruginosa employs two AHL synthase/receptor pairs arranged in a hierarchy, with the LasI/R system controlling the RhlI/R system and many downstream virulence factors. However, P. aeruginosa isolates with inactivating mutations in lasR are frequently isolated from chronic CF infections. We and others have shown that these isolates frequently use RhlR as the primary QS regulator. RhlR is rarely mutated in CF and environmental settings. We were interested if there were reproducible genetic characteristics of these isolates and if there was a central group of genes regulated by RhlR in all isolates. We examined five isolates and found signatures of adaptation common to CF isolates. Here, we analyzed CF clinial isolate E113. In this strain, RhlR positively regulates 186 genes, including those coding for known virulence factors. These results suggest a key group of QS-regulated factors important for pathogenesis of chronic infection, and position RhlR as a target for anti-QS therapeutics. Our work underscores the need to sample a diversity of isolates to understanding QS beyond what has been described in laboratory strains.
2022-03-18 | GSE198716 | GEO