Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Regulation by growth temperature of Pseudomonas aeruginosa quorum-sensing depedent virulence factors production involves two RNA-thermometers.

ABSTRACT: Several bacterial human pathogens regulate the production of virulence factors by temperature, expressing them only at 37 °C. Accordingly we show that the production of all P. aeruginosa virulence factors that are dependent on the QS transcriptional regulator RhlR, but only a fraction that are activated by LasR, are induced at 37 °C compared to 30 °C or 25 °C. The RhlR-dependent induction at 37 °C is a posttranscriptional effect due to an RNA thermometer of the ROSE family that thermoregulates the expression of rhlAB operon involved in rhamnolipids production, a virulence associated trait. This RNA structure also affects the expression of the downstream rhlR gene. A second thermometer is present upstream lasI and causes a reduced expression of this gene at lower temperatures without causing a significant decrease of the autoinducer 3-oxo-dodecanoyl homoserine lactone. Using transcriptomic analysis and quantitative real time PCR we show that these RNA thermometers are the main mechanism of thermoregulation of P. aeruginosa virulence factor production

ORGANISM(S): Pseudomonas aeruginosa

PROVIDER: GSE45695 | GEO | 2013/04/02

SECONDARY ACCESSION(S): PRJNA195619

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Regulation by growth temperature of Pseudomonas aeruginosa quorum-sensing depedent virulence factors production involves two RNA-thermometers.

Project description:Several bacterial human pathogens regulate the production of virulence factors by temperature, expressing them only at 37 M-BM-0C. Accordingly we show that the production of all P. aeruginosa virulence factors that are dependent on the QS transcriptional regulator RhlR, but only a fraction that are activated by LasR, are induced at 37 M-BM-0C compared to 30 M-BM-0C or 25 M-BM-0C. The RhlR-dependent induction at 37 M-BM-0C is a posttranscriptional effect due to an RNA thermometer of the ROSE family that thermoregulates the expression of rhlAB operon involved in rhamnolipids production, a virulence associated trait. This RNA structure also affects the expression of the downstream rhlR gene. A second thermometer is present upstream lasI and causes a reduced expression of this gene at lower temperatures without causing a significant decrease of the autoinducer 3-oxo-dodecanoyl homoserine lactone. Using transcriptomic analysis and quantitative real time PCR we show that these RNA thermometers are the main mechanism of thermoregulation of P. aeruginosa virulence factor production For the transcriptome analysis, cells were growth in PPGAS media at 25 M-BM-0C and 37 M-BM-0C, respectively. Samples were harvested at O.D600 of 1.5. Three biological replicates of each growth condition was used for RNA extraction and hybridization on Affimetrix microarrays.

2013-04-02 | E-GEOD-45695 | biostudies-arrayexpress

Microarray for suspension cells of PA14 WT with and without NE (50 uM and 500 uM) for 7 h

Project description:It has been proposed that the gastro-intestinal tract environment containing high levels of neuroendocrine hormones is important for gut-derived P. aeruginosa infections. In this study, we report that the hormone norepinephrine increases P. aeruginosa PA14 growth, virulence factor production, invasion of HCT-8 epithelial cells, and swimming motility in a concentration-dependent manner. Transcriptome analysis of P. aeruginosa exposed to 500 µM, but not 50 µM, norepinephrine for 7 h showed that genes involved in the regulation of the virulence determinants pyocyanin, elastase, and Pseudomonas quinolone signal (PQS, 2-heptyl-3-hydroxy-4-quinolone) were up-regulated. The production of rhamnolipids, which are also important in P. aeruginosa infections, was significantly decreased on semi-solid surfaces, but not in planktonic cultures, upon exposure to norepinephrine. Swarming motility, a phenotype that is directly influenced by rhamnolipids, was also decreased upon 500 µM norepinephrine exposure. The increase in the transcriptional activation of lasR, but not that of rhlR, suggest that the effects of norepinephrine are mediated primarily through the las quorum sensing pathway. Together, our data strongly suggests that norepinephrine can play an important role in gut-derived infections by increasing the pathogenicity of P. aeruginosa PA14.

2009-08-27 | GSE13326 | GEO

A Distinct QscR Regulon in the Pseudomonas aeruginosa Quorum Sensing Circuit

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

Genetic and transcriptomic characteristics of RhlR-dependent quorum sensing in cystic fibrosis isolates of Pseudomonas aeruginosa: isolate E167

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

Genetic and transcriptomic characteristics of RhlR-dependent quorum sensing in cystic fibrosis isolates of Pseudomonas aeruginosa: isolate E131

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 E131. In this strain, RhlR positively regulates 105 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 | GSE198718 | GEO

Genetic and transcriptomic characteristics of RhlR-dependent quorum sensing in cystic fibrosis isolates of Pseudomonas aeruginosa: isolate E104

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

Genetic and transcriptomic characteristics of RhlR-dependent quorum sensing in cystic fibrosis isolates of Pseudomonas aeruginosa: isolate E125

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

Genetic and transcriptomic characteristics of RhlR-dependent quorum sensing in cystic fibrosis isolates of Pseudomonas aeruginosa: isolate E113

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

RNA-seq for RpoN

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, RpoN has 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 RpoN in vivo, this study focused on identifying the potential targets of RpoN directly regulating QS system and T6SS. We performed a chromatin immunoprecipitation coupled to high-throughput sequencing (ChIP-seq) assay that identified 1, 068 binding sites of RpoN, including mostly metabolic genes, a group of genes in QS (lasI, rhlI and pqsR) and type VI secretion system (T6SS) (hcpA and hcpB). The direct regulation of these genes by RpoN has been biochemically and genetically verified. Results revealed that, on one hand, the deletion of rpoN resulted in reduced production of pyocyanin, motility and proteolytic activity. On the other hand, the production of rhamnolipids and biofilm formation was higher in the RpoN mutant than in the wild-type. In sum, the results indicated that RpoN had direct and profound effects on QS and T6SS, which provides new cues to better understand the detailed regulatory networks of virulence.

2018-06-30 | GSE110445 | GEO

PqsE expands and differentially modulates the RhlR quorum sensing regulon in Pseudomonas aeruginosa

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data