Transcriptome Sequence of Antibiotic-Treated Pseudomonas aeruginosa
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ABSTRACT:
ORGANISM(S): Pseudomonas aeruginosa
PROVIDER: GSE120602 | GEO | 2018/10/31
REPOSITORIES: GEO
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Project description:Transcriptome Sequence of Antibiotic-Treated Pseudomonas aeruginosa
| PRJNA493733 | ENA
Project description:Bacteria in biofilms have higher antibiotic tolerance than their planktonic counterparts. A major outstanding question is the degree to which the biofilm-specific cellular state and its constituent genetic determinants contribute to this hyper-tolerant phenotype. Here, using genome-wide functional profiling of a complex, heterogeneous mutant population of Pseudomonas aeruginosa MPAO1, we identified large sets of mutations that contribute to antibiotic tolerance predominantly in the biofilm or planktonic setting only. Our mixed population-based experimental design recapitulated the complexity of natural biofilms and, unlike previous studies, revealed clinically observed behaviors including the emergence of quorum sensing-deficient mutants. Our study revealed a substantial contribution of the cellular state to the antibiotic tolerance of biofilms, providing a rational foundation for the development of novel therapeutics against P. aeruginosa biofilm-associated infections. This dataset compares the expression of SAH108, a strain with enhanced antibiotic tolerance in the biofilm state, to expression in wild-type strains.
2011-11-21 | GSE26142 | GEO
Project description:Bacteria in biofilms have higher antibiotic tolerance than their planktonic counterparts. A major outstanding question is the degree to which the biofilm-specific cellular state and its constituent genetic determinants contribute to this hyper-tolerant phenotype. Here, using genome-wide functional profiling of a complex, heterogeneous mutant population of Pseudomonas aeruginosa MPAO1, we identified large sets of mutations that contribute to antibiotic tolerance predominantly in the biofilm or planktonic setting only. Our mixed population-based experimental design recapitulated the complexity of natural biofilms and, unlike previous studies, revealed clinically observed behaviors including the emergence of quorum sensing-deficient mutants. Our study revealed a substantial contribution of the cellular state to the antibiotic tolerance of biofilms, providing a rational foundation for the development of novel therapeutics against P. aeruginosa biofilm-associated infections. This dataset compares the expression of SAH108, a strain with enhanced antibiotic tolerance in the biofilm state, to expression in wild-type strains. We compared the expression of two biological replicates from strain SAH108 to samples from three wild-type, reference strains. All samples were collected from exponentially-growing planktonic cultures.
2011-11-21 | E-GEOD-26142 | biostudies-arrayexpress
Project description:Pseudomonas aeruginosa harbors sophisticated transcription factor (TF) networks to coordinately regulate cellular metabolic states for rapidly adapting to changing environments. The superior capacity in fine-tuning the metabolic states enables its success in tolerance to antibiotics and evading host immune defenses. However, the linkage among transcriptional regulation, metabolic states, and antibiotic tolerance in P. aeruginosa remains largely unclear. By screening the P. aeruginosa TF mutant library constructed by CRISPR/Cas12k-guided transposase, we identify that rccR (PA5438) is a major genetic determinant in aminoglycoside antibiotic tolerance, the deletion of which substantially enhances bacterial tolerance. We further reveal the inhibitory roles of RccR in pyruvate metabolism (aceE/F) and glyoxylate shunt pathway (aceA and glcB), and overexpression of aceA or glcB enhances bacterial tolerance. Moreover, we identify that 2-keto-3-deoxy-6-phosphogluconate (KDPG) is a signal molecule that directly binds to RccR. Structural analysis of the RccR/KDPG complex reveals the detailed interactions. Substitution of the key residues R152, K270, or R277 with alanine abolishes KDPG sensing by RccR and impairs bacterial growth with glycerol or glucose as the sole carbon source. Collectively, our study unveils the connection between aminoglycoside antibiotic tolerance and RccR-mediated central carbon metabolism regulation in P. aeruginosa, and elucidates the KDPG sensing mechanism by RccR.
2023-07-20 | GSE237535 | GEO
Project description:Pseudomonas aeruginosa infections can be virtually impossible to eradicate and the evolution of resistance during antibiotic therapy is a significant concern. In this study, we use DNA microarrays to characterize the global transcriptional response of P. aeruginosa to clinical-like doses of the antibiotic ciprofloxacin and also to determine the component that is regulated by LexA cleavage and the SOS response. We find that genes involved in virtually every facet of metabolism are down-regulated in response to ciprofloxacin. The LexA-controlled SOS regulon identified by microarray analysis includes only fifteen genes, but does include several genes that encode proteins involved in recombination and replication, including two inducible polymerases known to play a role in mutation and the evolution of antibiotic resistance in other organisms. The data suggests that the inhibition of LexA cleavage during therapy might help combat this pathogen by decreasing its ability to adapt and evolve resistance. Keywords: Time course of response of P. aeruginosa to the antibiotic ciprofloxacin
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Project description:Gene expression profiles of two Pseudomonas aeruginosa taxonomic outlier clinical isolates, CLJ1 and CLJ3 [CLJ1] Pseudomonas aeruginosa taxonomic outliers emerged recently as infectious for humans, provoking hemorrhagic pneumonia. Those bacteria lack classical type III secretion system, and utilize the pore-forming toxin for infection. Two clones CLJ1 and CLJ3 belonging to these taxonomic outliers have been isolated from the same patient at two different times during hospitalization. P. aeruginosa CLJ3 displays antibiotic resistance phenotype, while CLJ1 is more cytotoxic on epithelial and endothelial cells.
2018-11-30 | GSE123106 | GEO
Project description:Gene expression profiles of two Pseudomonas aeruginosa taxonomic outlier clinical isolates, CLJ1 and CLJ3 [CLJ3] Pseudomonas aeruginosa taxonomic outliers emerged recently as infectious for humans, provoking hemorrhagic pneumonia. Those bacteria lack classical type III secretion system, and utilize the pore-forming toxin for infection. Two clones CLJ1 and CLJ3 belonging to these taxonomic outliers have been isolated from the same patient at two different times during hospitalization. P. aeruginosa CLJ3 displays antibiotic resistance phenotype, while CLJ1 is more cytotoxic on epithelial and endothelial cells.
2018-11-30 | GSE123107 | GEO
Project description:This study aims at investigating the ability of Pseudomonas aeruginosa to detect the presence of siderophore-antibiotic conjugates in an epithelial cell infection assay. We show that the presence of siderophore-antibiotic conjugates induces the transcription and expression of their corresponding transporters, indicating the bacteria are able to sense the chelators in their environment and adapt their phenotype accordingly.
2021-02-18 | PXD020378 | Pride
Project description:The Pseudomonas aeruginosa quorum-sensing (QS) systems contribute to bacterial homeostasis and pathogenicity. Although the AraC family transcription factor VqsM has been characterized to control the production of virulence factors and QS signaling molecules, its detailed regulatory mechanisms still remain elusive. Here, we report that VqsM directly binds to the lasI promoter region, and thus regulates its expression. To identify additional targets of VqsM in P. aeruginosa PAO1, we performed chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-seq) which detected 48 enriched loci harboring VqsM-binding peaks in P. aeruginosa genome. The direct regulation of these genes by VqsM has been confirmed by Electrophoretic mobility shift assays (EMSAs) and quantitative real-time polymerase chain reactions (qRT-PCR). A VqsM-binding motif is found by using MEME suite and verified by footprint assays in vitro. In addition, VqsM directly binds to the promoter regions of antibiotic resistance regulator NfxB and the master type III system regulator ExsA. Notably, the vqsM mutant displayed more resistance to two types of antibiotics and promoted bacterial survival in a mouse model, compared to the wild type PAO1 strain. Collectively, this work provides new cues to better understand the detailed regulatory networks of QS systems, T3SS, and antibiotic resistance. Pseudomonas aeruginosa MAPO1 containing empty pAK1900 or pAK1900-VqsM-VSV
2014-08-04 | E-GEOD-57284 | biostudies-arrayexpress
Project description:The Pseudomonas aeruginosa quorum-sensing (QS) systems contribute to bacterial homeostasis and pathogenicity. Although the AraC family transcription factor VqsM has been characterized to control the production of virulence factors and QS signaling molecules, its detailed regulatory mechanisms still remain elusive. Here, we report that VqsM directly binds to the lasI promoter region, and thus regulates its expression. To identify additional targets of VqsM in P. aeruginosa PAO1, we performed chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-seq) which detected 48 enriched loci harboring VqsM-binding peaks in P. aeruginosa genome. The direct regulation of these genes by VqsM has been confirmed by Electrophoretic mobility shift assays (EMSAs) and quantitative real-time polymerase chain reactions (qRT-PCR). A VqsM-binding motif is found by using MEME suite and verified by footprint assays in vitro. In addition, VqsM directly binds to the promoter regions of antibiotic resistance regulator NfxB and the master type III system regulator ExsA. Notably, the vqsM mutant displayed more resistance to two types of antibiotics and promoted bacterial survival in a mouse model, compared to the wild type PAO1 strain. Collectively, this work provides new cues to better understand the detailed regulatory networks of QS systems, T3SS, and antibiotic resistance.
2014-08-04 | GSE57284 | GEO