Pseudomonas aeruginosa
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA149089 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:XDR-PA from XDR-PA meningitis patient and environment
| PRJDB10735 | ENA
Project description:Pseudomonas aeruginosa (Pa) is a ubiquitous bacterium that uses quorum sensing (QS), a cell-cell communication system that enables it to sense cell density and to alter gene expression. Pa has three complete QS circuits controlled by the transcriptional regulators LasR, RhlR, and PqsR (MvfR), that together control hundreds of genes, including virulence factors. In the well-described strain PAO1, QS is organized hierarchically, with PqsR and RhlR activity dependent on LasR. In PAO1, this hierarchy depends on the non-QS transcription factor MexT; by an unknown mechanism, deletion of mexT allows for RhlR activity in the absence of LasR. We aimed to identify how regulators such as MexT modulate the QS architecture in Pa. We compared the transcriptome of PAO1 to that of PAO1ΔmexT and identified 152 differentially expressed genes. MexT does not appear to regulate rhlR or pqsR directly; however, we identified two MexT-regulated operons that may affect the hierarchy in PAO1. These operons encode the drug efflux pump genes mexEF-oprN and the Pseudomonas quinolone signal (PQS) synthesis genes pqsABCDE. We performed genetic experiments to test whether the products of these genes affected the QS hierarchy. As with the mexT knockout mutant, we found that a PAO1 mexEF knockout mutant exhibited RhlR activity earlier, and to a higher magnitude, than wild-type PAO1. MexEF-OprN is known to export the PQS precursor HHQ, and we found that exogenous addition of PQS to PAO1 partially affects RhlR activity, resulting in earlier timing and higher magnitude compared to wild-type PAO1. We further elucidated that this is likely due to positive regulation by PqsE. These data link both the drug efflux pump MexEF-OprN and PQS QS to the regulation of the QS hierarchy in PAO1. We wondered if the same applied to QS architectures in Pa clinical isolates. We discovered that there are alternate QS architectures in clinical isolates, where RhlR activity is not fully dependent on LasR. In these isolates, surprisingly, MexT does not influence the relationship between LasR and RhlR, and this is indicative of a different QS architecture in the clinical isolates. Overall, we further elucidated the regulation of QS architecture in PAO1 and identified unique QS architectures in clinical isolates. Importantly, our work reveals a new suite of factors that regulate QS in Pa, with implications for a variety of Pa behaviors both in the laboratory and clinical settings.
2025-04-09 | GSE291609 | GEO
Project description:Pseudomonas aeruginosa strain:Pa-R Transcriptome or Gene expression
| PRJNA255834 | ENA
Project description:Our findings have clinical implications. Identification of sputum exosomal miRNA helps explore the important biological pathways underlying the pathogenesis of bronchiectasis, thus unraveling candidate targets for future interventions of PA colonization. Apart from canonical inflammatory pathways, we have unraveled the modulation of longevity regulation pathway which opens a new avenue for exploring how PA colonization interacts with the airway epithelium. The significant correlation between sputum inflammatory biomarkers and miR-92b-5p and miR-223-3p provided further evidence on the unresolved inflammation in the PA-colonized microenvironment. However, causality cannot be inferred based on the current study design.
2022-01-01 | GSE138820 | GEO
Project description:Experimentally evolved PA population
| PRJDB13465 | ENA
Project description:To assess gene expression changes, RNA-sequencing technology was employed to map the temporal shifts in the transcriptional profile of the host lung post-infection. Our findings provide novel insights into the pathogenesis of PA pulmonary infections and offer valuable suggestions for inhalational infection protection and immunotherapy.
2024-08-13 | GSE272417 | GEO
Project description:Chronic airway infection with P. aeruginosa (PA) is a hallmark of cystic fibrosis (CF) disease. The mechanisms producing PA persistence in CF therapies remain poorly understood. To gain insight on PA physiology in patient airways and better understand how in vivo bacterial functioning differs from in vitro conditions, we investigated the in vivo proteomes of PA in 35 sputum samples from 11 CF patients. We developed a novel bacterial-enrichment method enabling improved identification of PA proteome with CF sputum samples. The in vivo PA proteomes were compared with the proteomes of ex vivo-grown PA populations from the same patient sample. We detected 1528 PA proteins (encoded by 1458 core genes and 70 accessory genes) that were expressed in CF airways, of which 1178 proteins were commonly identified with the ex vivo-grown PA populations. Label-free quantitation and proteome comparison revealed the in vivo up-regulation of siderophore TonB-dependent receptors, remodeling in central carbon metabolism including glyoxylate cycle and lactate utilization, and alginate overproduction. Knowledge of these in vivo proteome differences or others derived using the presented methodology could lead to future treatment strategies aimed at altering PA physiology in vivo to compromise infectivity or improve antibiotic efficacy.
2019-05-09 | PXD011792 | Pride
Project description:Chitinases are ubiquitous enzymes involved in biomass degradation and chitin turnover in nature. Pseudomonas aeruginosa (PA), an opportunistic human pathogen, expresses ChiC, a secreted glycoside hydrolase 18 (GH18) family chitinase. Despite speculation about ChiC's role in PA disease pathogenesis, there is scant evidence supporting this hypothesis. Since PA cannot catabolize chitin, we investigated the potential function(s) of ChiC in PA pathophysiology
2024-04-30 | PXD048596 | Pride
Project description:Chitinases are ubiquitous enzymes involved in biomass degradation and chitin turnover in nature. Pseudomonas aeruginosa (PA), an opportunistic human pathogen, expresses ChiC, a secreted glycoside hydrolase 18 (GH18) family chitinase. Despite speculation about ChiC's role in PA disease pathogenesis, there is scant evidence supporting this hypothesis. Since PA cannot catabolize chitin, we investigated the potential function(s) of ChiC in PA pathophysiology
2024-04-30 | PXD048320 | Pride