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A new global repressor (bvlR) of pathogenicity and tight microcolony formation in P. aeruginosa

ABSTRACT: LysR-type transcriptional regulators (LTTRs) are the most common family of transcriptional regulators found in the opportunistic pathogen Pseudomonas aeruginosa. They are known to regulate a wide variety of virulence determinants and have emerged recently as positive global regulators of pathogenicity in a broad spectrum of serious bacterial pathogens. However, in spite of their key role in modulating expression of key virulence determinants underpinning pathogenic traits associated with the process of infection, surprisingly few were found to be transcriptionally altered in co-culture with host cells. bvlR (PA14_26880) an LTTR of previously unknown function, has been shown to be induced in response to host cells, and was therefore investigated for its potential role in virulence. BvlR expression was found to play a pivotal role in regulation of acute virulence determinants such as type III secretion and exotoxin A production. In contrast, loss of bvlR led to an inability to form tight microcolonies, a key step in biofilm formation in the mucoid lung, although surface attachment was increased. bvlR was also seen to a key role in P.aeruginosa pathogenicity within the acute model of infection, Caenorhabditis elegans. Unusually for LTTRs, BvlR was shown to exert its influence exclusively through the transcriptional repression of 307 genes, including the divergently transcribed gene bvlA. This highlights the importance of BvlR as a previously uncharacterized global virulence regulator in P. aeruginosa with a key role in the transcriptional response underlying the host pathogen interaction.

ORGANISM(S): Pseudomonas aeruginosa Pseudomonas aeruginosa PA14

PROVIDER: GSE51491 | GEO | 2014/12/10

SECONDARY ACCESSION(S): PRJNA223304

REPOSITORIES: GEO

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A new global repressor (bvlR) of pathogenicity and tight microcolony formation in P. aeruginosa

Project description:LysR-type transcriptional regulators (LTTRs) are the most common family of transcriptional regulators found in the opportunistic pathogen Pseudomonas aeruginosa. They are known to regulate a wide variety of virulence determinants and have emerged recently as positive global regulators of pathogenicity in a broad spectrum of serious bacterial pathogens. However, in spite of their key role in modulating expression of key virulence determinants underpinning pathogenic traits associated with the process of infection, surprisingly few were found to be transcriptionally altered in co-culture with host cells. bvlR (PA14_26880) an LTTR of previously unknown function, has been shown to be induced in response to host cells, and was therefore investigated for its potential role in virulence. BvlR expression was found to play a pivotal role in regulation of acute virulence determinants such as type III secretion and exotoxin A production. In contrast, loss of bvlR led to an inability to form tight microcolonies, a key step in biofilm formation in the mucoid lung, although surface attachment was increased. bvlR was also seen to a key role in P.aeruginosa pathogenicity within the acute model of infection, Caenorhabditis elegans. Unusually for LTTRs, BvlR was shown to exert its influence exclusively through the transcriptional repression of 307 genes, including the divergently transcribed gene bvlA. This highlights the importance of BvlR as a previously uncharacterized global virulence regulator in P. aeruginosa with a key role in the transcriptional response underlying the host pathogen interaction. Six samples were analysed in total, three biological replicates of the bvlR mutant and bvlR complemented strains.

2014-12-10 | E-GEOD-51491 | biostudies-arrayexpress

The LysR-type transcriptional regulator BsrA (PA2121) is engaged in the control of vital metabolic pathways in Pseudomonas aeruginosa (RNA-seq)

Project description:Pseudomonas aeruginosa, a facultative human pathogen causing nosocomial infections, has complex regulatory systems involving many transcriptional regulators. The LTTR family (LysR-Type Transcriptional Regulators) consists of proteins involved in regulation of various processes including stress response, motility, virulence or amino acid metabolism. The aim of this study was characterization of the LysR-type regulator BsrA (PA2121), identified previously as a negative regulator of biofilm formation in P. aeruginosa. To identify the BsrA binding sites in P. aeruginosa the ChIP-seq analysis was performed. It revealed 765 BsrA binding sites in P. aeruginosa PAO1161 genome, among them 367 was localized in the intergenic regions. Parallel transcriptomic analysis identified altered expression of 157 genes in response to BsrA excess, among them 35 had a BsrA binding site in the corresponding promoter regions, indicating direct influence of BsrA on expression of these genes. BsrA-repressed loci encompass genes encoding proteins engaged in key metabolic pathways including the tricarboxylic acid cycle. A group of directly activated genes by BsrA, consists of several loci encoding proteins involved in pili/fimbriae assembly as well as secretion and transport systems. Results also confirmed that BsrA acts as an autorepressor. Presented data uncover the regulon of BsrA protein with its role as transcriptional regulator of genes engaged in vital cellular processes in P. aeruginosa.

2021-06-17 | GSE163234 | GEO

The LysR-type transcriptional regulator BsrA (PA2121) is engaged in the control of vital metabolic pathways in Pseudomonas aeruginosa (ChIP-seq)

2021-06-17 | GSE163233 | GEO

ChIP-seq analyses of 10 quorum sensing regulators in Pseudomonas aeruginosa

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

ChIP-seq and RNA-seq analyses of genomic regulators in Pseudomonas aeruginosa

Project description:Regulatory networks including virulence-related transcriptional factors (TFs) determine bacterial pathogenicity in response to different environmental cues. Pseudomonas aeruginosa, a Gram-negative opportunistic pathogen of humans, recruits numerous TFs in quorum sensing (QS) system, type III secretion system (T3SS) and Type VI secretion system (T6SS) to mediate the pathogenicity. Although many virulence-related TFs have been illustrated individually, very little is known about their crosstalks and regulatory network. Here, based on chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) and transcriptome profiling (RNA-seq), we primarily focused on understanding the crosstalks of 20 virulence-related TFs, which led to construction of a virulence regulatory network named PAGnet (Pseudomonas aeruginosa Genomic integrated regulatory network), including 82 crosstalk targets. The PAGnet uncovered the intricate mechanism of virulence regulation and revealed master regulators in QS, T3SS and T6SS pathways. In particular, GacA and ExsA showed novel functions in QS and nitrogen metabolism. In addition, an online PAGnet platform was provided to analyze these TFs and more virulence factors. Taken together, the present study revealed the function-specific crosstalks of virulence regulatory network, which might provide new strategies for treating infections in P. aeruginosa in the future.

2019-07-16 | GSE128430 | GEO

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

Hypoxia decreases the pathogenicity of Pseudomonas aeruginosa by reducing expression of multiple virulence factors.

Project description:Hypoxia is a feature of the microenvironment during P. aeruginosa infection in several disease states. We confirm that the pathogenicity of P. aeruginosa derived from sites of acute infection is higher than those derived from sites of chronic infection. Hypoxia attenuated the pathogenicity of acute but not chronic strains implicating a role for hypoxia in controlling virulence. Mass spectrometric analysis revealed reduced expression of multiple virulence factors in hypoxia including exotoxin A, alkaline protease and proteins important in the synthesis of pyoverdine. Inhibition of pyoverdine production by iron supplementation mimicked the effects of hypoxia. Finally, strains of P. aeruginosa which lacks a functional pseudomonas prolyl-hydroxylase domain containing protein (PPHD) do not respond to hypoxia implicating a possible role for PPHD as an oxygen-sensing determinant of pathogenicity. Understanding how hypoxia influences bacterial virulence will identify new targets for anti–infective therapy against P. aeruginosa.

2017-06-06 | PXD004421 | Pride

Glycosylation of the HA protein of H5N1 virus increases its virulence in mice by exacerbating the host immune response

Project description:The highly pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in nature and threaten public health. Although several viral determinants and host factors that influence the virulence of HPAI H5N1 viruses in mammals have been identified, the detailed molecular mechanism remains poorly defined and requires further clarification. In our previous studies, we characterized two naturally isolated HPAI H5N1 viruses that had similar viral genomes but differed substantially in their lethality in mice. Here, we explored the molecular determinants and potential mechanism for this difference in virulence. By using reverse genetics, we found that a single amino acid at position 158 of the hemagglutinin (HA) protein substantially affected the systemic replication and pathogenicity of these H5N1 influenza viruses in mice. We further found that the G158N mutation introduced an N-linked glycosylation at sites 158–160 of the HA protein and that this N-linked glycosylation enhanced viral productivity in infected mammalian cells and induced stronger host immune and inflammatory responses to viral infection. These findings further our understanding of the determinants of pathogenicity of H5N1 viruses in mammals.

2016-12-22 | GSE89246 | GEO

Expression data from Pseudomonas aeruginosa (wild type and lasRrhlR mutant strains) exposed to human neutrophils

Project description:In the present in vitro study, interactions between P. aeruginosa (sessile biofilms as well as planktonic cells) and PMNs were analyzed by means of DNA microarray based transcriptomics. We found that the P. aeruginosa wild type biofilms, in contrast to planktonic cultures and quorum sensing (QS) deficient strains, respond to PMN exposure in a rather aggressive manner. The response does not involve protective mechanisms such as those involved in oxidative stress. Rather it is dominated by QS controlled virulence determinants such as those encoded by pqs, phz, rhlAB, all of which are designed to cripple Eukaryotic cells including PMNs and macrophages. Our comparative analysis supports the view that QS plays a major role in mechanisms by which P. aeruginosa evades host defense systems. Keywords: Stress response

2009-08-04 | GSE6769 | GEO

ChIP-seq analyses of 10 quorum sensing regulators in Pseudomonas aeruginosa

2015-08-04 | GSE65356 | GEO

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