Pseudomonas aeruginosa lasR QS network promotes phage infection by regulating the biosynthesis of LPS and type IV pili by regulating the biosynthesis of LPS and type IV pili
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ABSTRACT:
ORGANISM(S): Pseudomonas aeruginosa
PROVIDER: GSE246747 | GEO | 2024/04/08
REPOSITORIES: GEO
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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:Pseudomonas aeruginosa undergoes genetic change during chronic infection of the airways of cystic fibrosis (CF) patients. One common change is mutation of lasR. LasR is a transcriptional regulator that responds to one of the quorum sensing signals in P. aeruginosa, and regulates acute virulence factor expression as well as central metabolic functions. P. aeruginosa mutants in which lasR was inactivated emerged in the airways of CF patients early during chronic infection, and during growth in the laboratory on Luria-Bertani agar. Both environments are rich in amino acids. Inactivation of lasR in these isolates conferred a growth advantage with amino acids, a phenotype that could account for selection of lasR mutants both in vivo and in vitro. P. aeruginosa lasR mutants were identified by their distinctive colony morphology, including autolysis that correlated with an imbalance in 4-hydroxy-2-alkylquinolines (HAQs), and an iridescent metallic sheen likely caused by the accumulation of one such HAQ. The alterations in transcriptional profile due to inactivation of lasR were conserved in isolates from multiple young CF patients. P. aeruginosa lasR mutations may represent surrogate markers to delineate stages in the natural history of CF airway disease, each with different prognostic and therapeutic implications, analogous to the markers used to direct cancer treatment. Similar to cancer cell mutations that promote unrestricted growth, lasR mutations may promote unrestricted growth of P. aeruginosa in the CF airway by enabling more efficient utilization of available amino acids. Analyse the effects of mutation of the lasR gene in Pseudomonas aeruginosa isolates from cystic fibrosis patients by comparing the transcriptional profile of an isolate from a young patient with that of an isogenic engineered lasR mutant.
2010-06-30 | E-GEOD-5560 | biostudies-arrayexpress
Project description:Pseudomonas aeruginosa undergoes genetic change during chronic infection of the airways of cystic fibrosis (CF) patients. One common change is mutation of lasR. LasR is a transcriptional regulator that responds to one of the quorum sensing signals in P. aeruginosa, and regulates acute virulence factor expression as well as central metabolic functions. P. aeruginosa mutants in which lasR was inactivated emerged in the airways of CF patients early during chronic infection, and during growth in the laboratory on Luria-Bertani agar. Both environments are rich in amino acids. Inactivation of lasR in these isolates conferred a growth advantage with amino acids, a phenotype that could account for selection of lasR mutants both in vivo and in vitro. P. aeruginosa lasR mutants were identified by their distinctive colony morphology, including autolysis that correlated with an imbalance in 4-hydroxy-2-alkylquinolines (HAQs), and an iridescent metallic sheen likely caused by the accumulation of one such HAQ. The alterations in transcriptional profile due to inactivation of lasR were conserved in isolates from multiple young CF patients. P. aeruginosa lasR mutations may represent surrogate markers to delineate stages in the natural history of CF airway disease, each with different prognostic and therapeutic implications, analogous to the markers used to direct cancer treatment. Similar to cancer cell mutations that promote unrestricted growth, lasR mutations may promote unrestricted growth of P. aeruginosa in the CF airway by enabling more efficient utilization of available amino acids. Keywords: disease state analysis
2007-12-22 | GSE5560 | GEO
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: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.
2015-01-09 | GSE54245 | GEO
Project description: Not available
| S-EPMC3811610 | biostudies-literature
Project description:Rett syndrome (RTT) is a severe neurological disorder which is mainly caused by mutations found in the X-linked gene encoding MeCP2. Despite extensive studies, the molecular functions of MeCP2 remain elusive. Here, we report that MeCP2 is a new subunit of a higher-order multiunit protein complex Rbfox/LASR and acts as a scaffold for this splicing complex. Deletion or mutation of MeCP2 leads to defects in forming MeCP2/Rbfox/LASR complex and aberrant alternative pre-mRNA splicing. Our data link RTT to an impaired function of MeCP2 in splicing control through its role in nucleating Rbfox/LASR macromolecule assembly.
2021-08-28 | GSE142716 | GEO
Project description:The two adjacent genes encoding the major quorum sensing regulator, LasR, and its opponent, RsaL, overlap in their coding 3´ends and produce mRNA transcripts with long untranslated 3´ends that overlap with the sense transcripts of the gene on the opposing DNA strand. In this study, we evaluated whether the overlapping genes are involved in mutual regulatory events, such as transcriptional interference and interference by natural antisense transcripts. We introduced various gene expression constructs into a P. aeruginosa PA14 lasR/rsaL double deletion mutant, and found that although complementary RNA is produced, this does not interfere with the sense gene expression levels of lasR and rsaL and does not have functional consequences on down-stream gene regulation. Nevertheless, expression of lasR, but not of rsaL, was shown to be further enhanced if transcription was terminated at the end of the respective gene and no overlapping transcription with the gene on the opposite strand was allowed. Our data indicate that the natural organization with a partial overlap at the 3´ends of the lasR/rsaL genes gives rise to a system of checks and balances to prevent dominant and unilateral control by LasR over the RsaL transcriptional regulator of opposing function.
2023-06-12 | GSE152384 | GEO
Project description: Not available
| S-EPMC1913455 | biostudies-literature
Project description: Not available
| S-EPMC6597397 | biostudies-literature