Pseudomonas aeruginosa strain:ps1 | isolate:ksa
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ABSTRACT:
PROVIDER: PRJNA1226941 | ENA |
REPOSITORIES: ENA
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Project description:Pseudomonas aeruginosa strain:Ps1 Genome sequencing and assembly
| PRJNA295426 | ENA
Project description:Pseudomonas aeruginosa strain:PS1 Genome sequencing and assembly
| PRJNA498487 | ENA
Project description:Purpose: Pseudomonas aeruginosa is a major cause of morbidity and mortality in patients with cystic fibrosis (CF). We provide an insight to the DNA auxotrophy of P. aeruginosa PASS4 isolate. Better understanding of P. aeruginosa adaptations in the CF lung environment can have a great impact in the development of specialised treatment regimes aimed at the eradications of P. aeruginosa infections. Methods: P. aeruginosa strains PAO1 and PASS4 were grown in minimal medium with either L-Asparagine or DNA as a carbon source, in biological triplicates. RNA was extracted and sequenced on Illumina HiSeq 1000 platform. The sequence reads that passed quality filters were analyzed using EdgePro and DESeq packages, as well as the Rockhopper tool. Results: We mapped > 10 million paired sequence reads per sample to the genome of P. aeruginosa PAO1 and identified a total of 576 genes differentially expressed by PASS4 when grown in DNA (P value < 0.01, log2 fold-change 1< to < -1), with 322 genes upregulated and 254 genes downregulated. There were a total of 423 genes differentially expressed by PAO1 when grown in DNA (P value < 0.01, log2 fold-change 1< to <-1), with 359 genes upregulated and 64 genes downregulated . A total of 129 transcripts displayed similar expression patterns in both organisms, with 112 being upregulated and 17 down-regulated. Conclusions: Our study identified that P. aeruginosa PASS4 was a purine auxotroph. Purine auxotropy may represent a viable microbial strategy for adaptation to DNA rich environments such as the CF lung.
2019-06-16 | GSE100287 | GEO
Project description:Taxonomic outliers of Pseudomonas aeruginosa recently emerged as infectious for humans. Here we present the first analysis of a hyper-virulent isolate that cause hemorrhagic pneumonia. We demonstrated that, in two sequential clones CLJ1 and CLJ3 recovered from a patient with chronic obstructive pulmonary disease undergoing antibiotic therapy, insertion of a mobile genetic element into the P. aeruginosa chromosome affected major virulence-associated phenotypes and led to increased resistance to antibiotics used to treat the patient. Our work reveals insertion sequences as major players in enhancing the pathogenic potential of a P. aeruginosa taxonomic outlier by modulating both the virulence and resistance to antimicrobials. This also explains the ability of this bacterium to adapt to an infected host and cause a serious disease.
2019-03-18 | PXD011105 | Pride
Project description:This study addresses the impact of zinc limitation on the opportunistic human pathogen, Pseudomonas aeruginosa. Zinc limitation was assessed in the P. aeruginosa PAO1 strain using an isogenic deletion mutant lacking the periplasmic, zinc solute-binding protein, znuA (PA5498). ZnuA delivers bound zinc to its cognate ABC transporter, ZnuBC, for import into the cytoplasm. Our transcriptional analyses revealed P. aeruginosa to possess a multitude of zinc acquisition mechanisms, each of which were highly up-regulated in the zinc-deficient znuA mutant strain. P. aeruginosa also utilized zinc-independent paralogues of zinc-dependent genes to maintain cellular function under zinc limitation. Together, these data reveal the complex transcriptional response and versatility of P. aeruginosa to zinc depletion.
2017-01-01 | GSE60177 | GEO
Project description:Pseudomonas aeruginosa is a major cause of morbidity and mortality in patients with cystic fibrosis (CF). The P. aeruginosa CF isolate PASS4 has reduced ability to catabolise various carbon sources however can grow on DNA as a sole carbon source but, with a higher biomass production than P. aeruginosa burns wound, laboratory strain PAO1. Therefore, proteomic profiling of PASS4 and PAO1 was conducted following growth on DNA as a sole carbon source. To compare the protein expression of P. aeruginosa strains PAO1 and PASS4 following growth in DNA, the amino acid, asparagine was used a control condition, as asparagine was one of the amino acids PASS4 could utilise.
2019-06-24 | PXD006742 | Pride
Project description:Pseudomonas aeruginosa isolate:Pseudomonas aeruginosa HN41 Genome sequencing
| PRJNA1180259 | ENA
Project description:Analysis of a SigX knockout mutant of Pseudomonas aeruginosa H103 strain in minimal medium with glucose as carbon source (M9G). SigX, one of the 19 extra-cytoplasmic function sigma factors of P. aeruginosa, was only known to be involved in transcription of the gene encoding the major outer membrane protein OprF in Pseudomonas aeruginosa. Deletion of the ECF sigma factor sigX gene provide insights into the SigX role in several virulence and biofilm- related phenotypes in Pseudomonas aeruginosa.
2014-01-01 | GSE51076 | GEO
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
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