Pseudomonas salinarum strain:cf-09
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ABSTRACT:
PROVIDER: PRJNA316517 | ENA |
REPOSITORIES: ENA
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Project description:Pseudomonas aeruginosa (P. aeruginosa) lung infection is a significant cause of mortality in patients with cystic fibrosis (CF). Most CF patients acquire unique P. aeruginosa strains from the environment; however clonal strains have been identified in CF communities in several countries. Two clonal strains infect 10% to 40% of patients in three CF clinics in mainland eastern Australia. The expression profiles of four planktonically-grown isolates of one Australian clonal strain (AES-2), and four non–clonal CF P. aeruginosa isolates were compared to each other and to the reference strain PAO1 using the Affymetrix P. aeruginosa PAO1 genome array, to gain insight into properties mediating the enhanced infectivity of AES-1. The isolates were subsequently grown as 3-day old biofilms and similarly extracted for RNA and compared as above. Data analysis was carried out using BIOCONDUCTOR software. Keywords: Comparative strain hybridization
2009-02-05 | GSE10304 | GEO
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2008-12-05 | GSE6122 | GEO
Project description:The opportunistic pathogen Pseudomonas aeruginosa is among the main colonizers of the lungs of cystic fibrosis (CF) patients. We have isolated and sequenced several P. aeruginosa isolates from the sputum of CF patients and used phenotypic, genomic and proteomic analyses to compare these CF derived strains with each other and with the model strain PAO1.
2015-10-14 | PXD002865 | Pride
Project description:Surfing motility is a complex adaptation that is different from swarming motility and requires the stringent stress response in Pseudomonas aeruginosa LESB58 Cystic fibrosis (CF) is a genetic disease that affects mucin-producing body organs such as the lungs. Characteristic of CF is the production of thick and sticky mucus that can lead to progressive airway obstruction. The glycoprotein mucin is the major macromolecular component of mucus. Recently, we identified that the presence of mucin induced a rapid surface adaptation termed surfing motility in motile bacteria. P. aeruginosa, the main colonizing pathogen in CF employs several stress coping mechanisms to survive the highly viscous environment of the CF lung. Here, RNA-Seq was used to study the stringent stress response in the hypervirulent CF isolate LESB58 (Liverpool Epidemic Strain) via transcriptional profiling. As the stringent response is regulated by relA and spoT, we created a double knockout of these genes in LESB58 to study the impact of these stress regulators on surfing motility using RNA-Seq.
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Project description:The biodegradation of lignite (brown coal) by microorganisms has the potential for bioremediation of contaminated mining sites and to generate alternative ways to valorize lignite, such as by producing humic acids or building block chemicals. Previously, a lignite-degrading strain of Trichoderma was isolated, but the genomic and transcriptomic basis of its lignite-degrading ability remained unknown. Here we report that the sequenced genome of the T. cf. simile WF8 strain encoded for enzymes with roles in the degradation of lignite, and potentially tolerance to lignite-breakdown products. There was only a small number of annotated unique genes in the T. cf. simile WF8 genome compared to other fungi, and likely the expression of gene families shared with other fungi is a key factor in lignite biosolubilization by T. cf. simile. The transcriptomes were analyzed of T. cf. simile cultured at two time-points with the lignite-breakdown model compounds 4-phenoxybenzoic acid (which was growth inhibitory), and phenetole and 9-10-dibutoxyanthracene (neither of which inhibited growth), and showed ~20% of genes up-regulated by one or more of these compounds. The analysis highlights candidates for characterization and engineering enzyme over-expressing T. cf. simile strains with potentially improved degradation capacity, e.g., laccases and peroxidases, or tolerance and catabolism of breakdown products, e.g., cytochrome P450s, and ring cleavage dioxygenases.
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Project description:We set out to determine a) if histone in Halobacterium salinarum regulates transcription and b) whether the magnitude and extent of these changes matches those observed in organisms which use histone protein as their primary DNA packaging agent. To this end, gene expression data for a histone knock-out (Δura3ΔhpyA) strain versus parent (Δura3) were collected.
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Project description:Mutations in CFTR have been shown to alter the immune response of macrophages, for example, by reducing the ability of macrophages to phagocytose and kill bacteria. This contributes to chronic bacterial infection and inflammation in the lungs, which leads to significant morbidity and mortality in cystic fibrosis (CF). Extracellular vesicles (EVs) are secreted by a variety of cell types in the lungs and participate in the host immune response to bacterial infection. However, nothing is known about the effect of EVs secreted by CF airway epithelial cells (AEC) on CF macrophages. Therefore, we examined the effect of EVs secreted by primary CF AEC on CF monocyte derived macrophages (MDM) and compared it with the effect of EVs secreted by wild type (WT) AEC on WT MDM. EVs increased pro-inflammatory cytokine secretion and enhanced the expression of numerous innate immune genes in WT MDM. However, the response of CF MDM to EVs was significantly attenuated compared to WT MDM, a difference that was also observed when EVs were isolated from WT and CF AEC exposed to Pseudomonas aeruginosa. Attenuated responses by CF MDM can be attributed to defects in the CF macrophages themselves rather than differences between CF and WT EVs, because EVs secreted by CF AEC or WT AEC elicited similar cytokine secretion by CF MDM. EVs secreted by P. aeruginosa exposed AEC resulted in the upregulation of immune response genes and increased secretion of pro-inflammatory cytokines, chemoattractants and chemokines involved in tissue repair by WT MDM, whereas the response of CF MDM was attenuated by comparison. To our knowledge, this is the first study examining the effect of EVs secreted by CF AEC on CF MDM, and it demonstrates that the Phe508del mutation in CFTR attenuates the innate immune response of MDM to EVs.
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