Pseudomonas aeruginosa PAO1
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ABSTRACT:
PROVIDER: PRJNA309644 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of Pseudomonas aeruginosa PA01 (ATCC 15692) Psl polysaccharide deficient mutant. Psl polysaccharide deficient mutant is evaluated with microarray to understand the genes affected by this polysaccharide. Our results provide new vision on the roles played by Psl polysaccharide in P. aeruginosa. Exopolysaccharide Psl is a critical biofilm matrix component in Pseudomonas aeruginosa, which forms a fiber-like matrix to enmesh bacteria communities. Iron has been shown to serve as a signal in P. aeruginosa biofilm development, yet how iron controls biofilm formation is not clear. Here we perform a transcriptomic analysis to compare Psl negative strain versus its isogenic wild-type strain PAO1. The results indicate that the expression of genes involved in iron homeostasis and oxidative stress response increased drastically at transcriptional level in Psl negative strain, suggesting Psl deficiency induces iron limitation. Subsequent studies confirm that Psl can efficiently bind iron in vitro and Psl fibers functions as an iron storage channel in P. aeruginosa biofilms. We used two wild type (WT) replicates and two mutant (MT) replicates to compare the differential gene expression.
2016-01-26 | E-GEOD-77163 | biostudies-arrayexpress
Project description:Analysis of Pseudomonas aeruginosa PA01 (ATCC 15692) Psl polysaccharide deficient mutant. Psl polysaccharide deficient mutant is evaluated with microarray to understand the genes affected by this polysaccharide. Our results provide new vision on the roles played by Psl polysaccharide in P. aeruginosa. Exopolysaccharide Psl is a critical biofilm matrix component in Pseudomonas aeruginosa, which forms a fiber-like matrix to enmesh bacteria communities. Iron has been shown to serve as a signal in P. aeruginosa biofilm development, yet how iron controls biofilm formation is not clear. Here we perform a transcriptomic analysis to compare Psl negative strain versus its isogenic wild-type strain PAO1. The results indicate that the expression of genes involved in iron homeostasis and oxidative stress response increased drastically at transcriptional level in Psl negative strain, suggesting Psl deficiency induces iron limitation. Subsequent studies confirm that Psl can efficiently bind iron in vitro and Psl fibers functions as an iron storage channel in P. aeruginosa biofilms.
2016-01-26 | GSE77163 | GEO
Project description:Transcriptional profiles of Pseudomonas aeruginosa PA01 wide type and cysB mutant
| PRJNA436889 | ENA
Project description:Transcriptome analysis of Pseudomonas aeruginosa PAO1 WT, ΔpauA2 mutant, and ΔpauA2 suppressor
| PRJNA344977 | ENA
Project description:Pseudomonas aeruginosa PAO1 is the most commonly used strain for research on this ubiquitous and metabolically versatile opportunistic pathogen. Strain PAO1, a derivative of the original Australian PAO isolate, has been distributed worldwide to laboratories and strain collections. Over decades discordant phenotypes of PAO1 sublines have emerged. Taking the existing PAO1-UW genome sequence (named after the University of Washington, which led the sequencing project) as a blueprint, the genome sequences of reference strains MPAO1 and PAO1-DSM (stored at the German Collection for Microorganisms and Cell Cultures [DSMZ]) were resolved by physical mapping and deep short read sequencing-by-synthesis. MPAO1 has been the source of near-saturation libraries of transposon insertion mutants, and PAO1-DSM is identical in its SpeI-DpnI restriction map with the original isolate. The major genomic differences of MPAO1 and PAO1-DSM in comparison to PAO1-UW are the lack of a large inversion, a duplication of a mobile 12-kb prophage region carrying a distinct integrase and protein phosphatases or kinases, deletions of 3 to 1,006 bp in size, and at least 39 single-nucleotide substitutions, 17 of which affect protein sequences. The PAO1 sublines differed in their ability to cope with nutrient limitation and their virulence in an acute murine airway infection model. Subline PAO1-DSM outnumbered the two other sublines in late stationary growth phase. In conclusion, P. aeruginosa PAO1 shows an ongoing microevolution of genotype and phenotype that jeopardizes the reproducibility of research. High-throughput genome resequencing will resolve more cases and could become a proper quality control for strain collections.
| S-EPMC2812968 | biostudies-literature
Project description:Changes of transcript abundance in clpX deletion mutant compared to wild-type PAO1
| PRJNA629422 | ENA
Project description:Application of transposon inserted mutant sequencing analysis in identifying genetic determinants of bacterial biofilms
| PRJNA701135 | ENA
Project description:The TyrR-like enhancer-binding protein GcsR (or PA2449) was shown to regulate the expression of genes required for glycine metabolism. In order to define the regulon of GcsR we compared the transcriptome of a gcsR deletion mutant of P. aeruginosa PAO1 with that of the wild-type using RNA-Seq.
2016-01-08 | GSE76522 | GEO
Project description:Pseudomonas aeruginosa is ubiquitously present in the environment and acts as an opportunistic pathogen on humans, animals and plants. We report here the effects of the prebiotic polysaccharide inulin and its hydrolysed form FOS on this bacterium. FOS was found to inhibit bacterial growth of strain PAO1, while inulin did not affect growth rate or yield in a significant manner. Inulin stimulated biofilm formation, whereas a dramatic reduction of the biofilm formation was observed in the presence of FOS. Similar opposing effects were observed for bacterial motility, where FOS inhibited the swarming and twitching behaviour whereas inulin caused its stimulation. In co-cultures with eukaryotic cells (macrophages) FOS and, to a lesser extent, inulin reduced the secretion of the inflammatory cytokines IL-6, IL-10 and TNF-?. Western blot experiments indicated that the effects mediated by FOS in macrophages are associated with a decreased activation of the NF-?B pathway. Since FOS and inulin stimulate pathway activation in the absence of bacteria, the FOS mediated effect is likely to be of indirect nature, such as via a reduction of bacterial virulence. Further, this modulatory effect is observed also with the highly virulent ptxS mutated strain. Co-culture experiments of P. aeruginosa with IEC18 eukaryotic cells showed that FOS reduces the concentration of the major virulence factor, exotoxin A, suggesting that this is a possible mechanism for the reduction of pathogenicity. The potential of these compounds as components of antibacterial and anti-inflammatory cocktails is discussed.
| S-EPMC3899050 | biostudies-literature
Project description:Quorum sensing (QS) is used to coordinate social behaviors, such as virulence and biofilm formation, across bacterial populations. However, the role of QS in regulating phage-bacterium interactions remains unclear. Preventing phage recognition and adsorption are the first steps of bacterial defense against phages; however, both phage recognition and adsorption are a prerequisite for the successful application of phage therapy. In the present study, we report that QS upregulated the expression of phage receptors, thus increasing phage adsorption and infection rates in Pseudomonas aeruginosa. In P. aeruginosa PAO1, we found that las QS, instead of rhl QS, upregulated the expression of galU for lipopolysaccharide synthesis. Lipopolysaccharides act as the receptor of the phage vB_Pae_QDWS. This las QS-mediated phage susceptibility is a dynamic process, depending on host cell density. Our data suggest that inhibiting QS may reduce the therapeutic efficacy of phages. IMPORTANCE Phage resistance is a major limitation of phage therapy, and understanding the mechanisms by which bacteria block phage infection is critical for the successful application of phage therapy. In the present study, we found that Pseudomonas aeruginosa PAO1 uses las QS to promote phage infection by upregulating the expression of galU, which is necessary for the synthesis of phage receptor lipopolysaccharides. In contrast to the results of previous reports, we showed that QS increases the efficacy of phage-mediated bacterial killing. Since QS upregulates the expression of virulence factors and promotes biofilm development, which are positively correlated with lipopolysaccharide production in P. aeruginosa, increased phage susceptibility is a novel QS-mediated trade-off. QS inhibition may increase the efficacy of antibiotic treatment, but it will reduce the effectiveness of phage therapy.
| S-EPMC8764535 | biostudies-literature