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Pseudomonas aeruginosa strain:NICED-PA-01

ABSTRACT: Pseudomonas aeruginosa strain:NICED-PA-01 Genome sequencing and assembly

PROVIDER: PRJNA602579 | ENA |

REPOSITORIES: ENA

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The Pseudomonas aeruginosa lectins PA-IL and PA-IIL are controlled by quorum sensing and by RpoS.

Project description:In Pseudomonas aeruginosa, many exoproduct virulence determinants are regulated via a hierarchical quorum-sensing cascade involving the transcriptional regulators LasR and RhlR and their cognate activators, N-(3-oxododecanoyl)-L-homoserine lactone (3O-C12-HSL) and N-butanoyl-L-homoserine lactone (C4-HSL). In this paper, we demonstrate that the cytotoxic lectins PA-IL and PA-IIL are regulated via quorum sensing. Using immunoblot analysis, the production of both lectins was found to be directly dependent on the rhl locus while, in a lasR mutant, the onset of lectin synthesis was delayed but not abolished. The PA-IL structural gene, lecA, was cloned and sequenced. Transcript analysis indicated a monocistronic organization with a transcriptional start site 70 bp upstream of the lecA translational start codon. A lux box-type element together with RpoS (sigma(S)) consensus sequences was identified upstream of the putative promoter region. In Escherichia coli, expression of a lecA::lux reporter fusion was activated by RhlR/C4-HSL, but not by LasR/3O-C12-HSL, confirming direct regulation by RhlR/C4-HSL. Similarly, in P. aeruginosa PAO1, the expression of a chromosomal lecA::lux fusion was enhanced but not advanced by the addition of exogenous C4-HSL but not 3O-C12-HSL. Furthermore, mutation of rpoS abolished lectin synthesis in P. aeruginosa, demonstrating that both RpoS and RhlR/C4-HSL are required. Although the C4-HSL-dependent expression of the lecA::lux reporter in E. coli could be inhibited by the presence of 3O-C12-HSL, this did not occur in P. aeruginosa. This suggests that, in the homologous genetic background, 3O-C12-HSL does not function as a posttranslational regulator of the RhlR/C4-HSL-dependent activation of lecA expression.

2000-01-01 | S-EPMC94786 | BioStudies

Pseudomonas aeruginosa strain:Pa-3

Project description:Pseudomonas aeruginosa strain:Pa-3 Genome sequencing and assembly

| PRJNA615643 | ENA

Pseudomonas aeruginosa strain:PA-50010278

Project description:Pseudomonas aeruginosa strain:PA-50010278 Genome sequencing and assembly

| PRJNA595618 | ENA

Pseudomonas aeruginosa strain:PA-81

Project description:Pseudomonas aeruginosa strain:PA-81 Genome sequencing and assembly

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Pseudomonas aeruginosa strain:PA-3

Project description:Pseudomonas aeruginosa strain:PA-3 Genome sequencing

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Genome Sequence of the Nonpathogenic Pseudomonas aeruginosa Strain ATCC 15442.

Project description:Pseudomonas aeruginosa ATCC 15442 is an environmental strain of the Pseudomonas genus. Here, we present a 6.77-Mb assembly of its genome sequence. Besides giving insights into characteristics associated with the pathogenicity of P. aeruginosa, such as virulence, drug resistance, and biofilm formation, the genome sequence may provide some information related to biotechnological utilization of the strain.

2014-01-01 | S-EPMC4007996 | BioStudies

Complete genome sequence of the bacteriophage YMC01/01/P52 PAE BP, which causes lysis of verona integron-encoded metallo-?-lactamase-producing, carbapenem-resistant Pseudomonas aeruginosa.

Project description:Multidrug-resistant Pseudomonas aeruginosa commonly causes serious nosocomial infections. In this study, a novel lytic bacteriophage belonging to a member of the family Podoviridae, YMC01/01/P52 PAE BP, which infects carbapenem-resistant Pseudomonas aeruginosa, was isolated and characterized. YMC01/01/P52 PAE BP genome was analyzed by whole-genome sequencing and putative function identification. The bacteriophage genome consists of a double-stranded linear DNA genome of 49,381 bp with a GC content of 62.16%.

2012-01-01 | S-EPMC3503104 | BioStudies

Effect of efflux pump inhibition on Pseudomonas aeruginosa transcriptome and virulence.

Project description:Efflux pumps of the resistance-nodulation-cell-division (RND) family increase antibiotic resistance in many bacterial pathogens, representing candidate targets for the development of antibiotic adjuvants. RND pumps have also been proposed to contribute to bacterial infection, implying that efflux pump inhibitors (EPIs) could also act as anti-virulence drugs. Nevertheless, EPIs are usually investigated only for their properties as antibiotic adjuvants, while their potential anti-virulence activity is seldom taken into account. In this study it is shown that RND efflux pumps contribute to Pseudomonas aeruginosa PAO1 pathogenicity in an insect model of infection, and that the well-characterized EPI Phe-Arg-?-naphthylamide (PA?N) is able to reduce in vivo virulence of the P. aeruginosa PAO1 laboratory strain, as well as of clinical isolates. The production of quorum sensing (QS) molecules and of QS-dependent virulence phenotypes is differentially affected by PA?N, depending on the strain. Transcriptomic and phenotypic analyses showed that the protection exerted by PA?N from P. aeruginosa PAO1 infection in vivo correlates with the down-regulation of key virulence genes (e.g. genes involved in iron and phosphate starvation). Since PA?N impacts P. aeruginosa virulence, anti-virulence properties of EPIs are worthy to be explored, taking into account possible strain-specificity of their activity.

2017-01-01 | S-EPMC5596013 | BioStudies

Pseudomonas aeruginosa strain:Pa-R

Project description:Pseudomonas aeruginosa strain:Pa-R Transcriptome or Gene expression

| PRJNA255834 | ENA

Genome Sequence of Clinical Strain Pseudomonas aeruginosa NRD619.

Project description:Here, we report the complete genome sequence of the multidrug-resistant (MDR) strain Pseudomonas aeruginosa NRD619, assembled via long- and short-read hybrid assembly. P. aeruginosa is a Gram-negative bacterial pathogen that is a significant public health burden. NRD619 was isolated from a left ventricular assist device (LVAD) draining sinus tract.

2020-01-01 | S-EPMC7595950 | BioStudies

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