Transcriptional response of Pseudomonas aeruginosa PAO1r to bacteriophage phiYY infection
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ABSTRACT:
PROVIDER: PRJNA528935 | ENA |
REPOSITORIES: ENA
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Project description:We have isolated and characterized several bacteriophages infecting Pseudomonas aeruginosa distantly related to Felix O1 virus and proposed they form a new subfamily named Felixounavirinae. The infectious cycle of bacteriophages belonging to this subfamily has not been studied yet in terms of gene expression. The present study reports the RNA-Seq analysis of bacteriophage PAK_P3 infecting PAK strain of P. aeruginosa. RNA profile of Host and Phage at 0min, 3.5min and 13 min after infection of Pseudomonas aeruginosa PAK strain with the Pseudomonas phage PAK P3. Three biological replicates for each time point.
2016-07-20 | E-GEOD-76513 | biostudies-arrayexpress
Project description:We have isolated and characterized several bacteriophages infecting Pseudomonas aeruginosa distantly related to Felix O1 virus and proposed they form a new subfamily named Felixounavirinae. The infectious cycle of bacteriophages belonging to this subfamily has not been studied yet in terms of gene expression. The present study reports the RNA-Seq analysis of bacteriophage PAK_P3 infecting PAK strain of P. aeruginosa.
2016-07-20 | GSE76513 | GEO
Project description:We have isolated and characterized several bacteriophages infecting Pseudomonas aeruginosa distantly related to Felix O1 virus and proposed they form a new subfamily named Felixounavirinae. The infectious cycle of bacteriophages belonging to this subfamily has not been studied yet in terms of gene expression. The present study reports the RNA-Seq analysis of bacteriophage PAK_P4 infecting PAK strain of P. aeruginosa.
2017-07-07 | GSE86022 | GEO
Project description:Transcriptional response of Pseudomonas aeruginosa PA3 to bacteriophage PaP3 infection
| PRJNA530399 | ENA
Project description:Biofilms are surface-adhered bacterial communities encased in an extracellular matrix composed of polysaccharides, proteins, and extracelluar (e)DNA, with eDNA being required for the formation and integrity of biofilms. Here we demonstrate that the spatial and temporal release of eDNA is regulated by BfmR, a regulator essential for Pseudomonas aeruginosa biofilm development. The expression of bfmR coincided with localized cell death and DNA release, with high eDNA concentrations localized to the outer part of microcolonies in the form of a ring and as a cap on small clusters. Additionally, eDNA release and cell lysis increased significantly following bfmR inactivation. Genome-wide transcriptional profiling indicated that bfmR was required for repression of genes associated with bacteriophage assembly and bacteriophage-mediated lysis. In order to determine which of these genes were directly regulated by BfmR, we utilized chromatin immunoprecipitation (ChIP) analysis to identify the promoter of PA0691, termed here phdA, encoding a previously undescribed homologue of the prevent-host-death (Phd) family of proteins. Lack of phdA expression coincided with impaired biofilm development, increased cell death and bacteriophage release, a phenotype comparable to ΔbfmR. Expression of phdA in ΔbfmR biofilms restored eDNA release, cell lysis, release of bacteriophages, and biofilm formation to wild type levels. Moreover, overexpression of phdA rendered P. aeruginosa resistant to lysis mediated by superinfective bacteriophage Pf4 which was only detected in biofilms. The expression of bfmR was stimulated by conditions resulting in membrane perturbation and cell lysis. Thus, we propose that BfmR regulates biofilm development by controlling bacteriophage-mediated lysis and thus, cell death and eDNA release, via PhdA. For biofilm growth experiments, three independent replicates of P. aeruginosa strains PAO1 and ΔbfmR were grown as biofilms in a flow-through system using a once-through continuous flow tube reactor system for biofilm sample collection and in flow cells (BioSurface Technologies) for the analysis of biofilm architecture as previously described (Sauer et al., 2002, Sauer et al., 2004, Petrova & Sauer, 2009). Cells were treated with RNAprotect (Qiagen), and total RNA was extracted using an RNeasy mini purification kit (Qiagen) per the manufacturer’s instructions. RNA quality and the presence of residual DNA were checked on an Agilent Bioanalyzer 2100 electrophoretic system pre- and post-DNase treatment. Ten micrograms of total RNA was used for cDNA synthesis, fragmentation, and labeling according to the Affymetrix GeneChip P. aeruginosa genome array expression analysis protocol. Sauer, K., A. K. Camper, G. D. Ehrlich, J. W. Costerton & D. G. Davies, (2002) Pseudomonas aeruginosa displays multiple phenotypes during development as a biofilm. J. Bacteriol. 184: 1140-1154. Sauer, K., M. C. Cullen, A. H. Rickard, L. A. H. Zeef, D. G. Davies & P. Gilbert, (2004) Characterization of nutrient-induced dispersion in Pseudomonas aeruginosa PAO1 biofilm. J. Bacteriol. 186: 7312-7326. Petrova, O. E. & K. Sauer, (2009) A novel signaling network essential for regulating Pseudomonas aeruginosa biofilm development. PLoS Pathogens 5: e1000668.
2011-06-01 | E-GEOD-28953 | biostudies-arrayexpress
Project description:Wound infections are traditionally thought to occur when microbial burden exceeds the innate clearance capacity of host immune system. Here we introduce the idea that the wound environment itself plays a significant contributory role to wound infection. We developed a clinically relevant murine model of soft tissue infection to explore the role of activation of microbial virulence in response to tissue factors as a mechanism by which pathogenic bacteria cause wound infections. Mice underwent abdominal skin incision and light muscle injury with a crushing forceps versus skin incision alone followed by topical inoculation of Pseudomonas aeruginosa. Pseudomonas aeruginosa whole genome transcriptional profiling demonstrated that fascia induced the activation of multiple genes responsible for the synthesis of the iron scavenging protein pyochelin. Ex-vivo murine fascia homogenates were prepared and Pseudomonas aeruginosa MPAO1 was incubated with an inoculum of the fascia homogenate solution. Pseudomonas aeruginosa MPAO1 incubated under the same condtions without the homogenate was used as the control group. Three biological replicates in each group was used.
2014-10-01 | E-GEOD-61925 | biostudies-arrayexpress
Project description:Biofilms are surface-adhered bacterial communities encased in an extracellular matrix composed of polysaccharides, proteins, and extracelluar (e)DNA, with eDNA being required for the formation and integrity of biofilms. Here we demonstrate that the spatial and temporal release of eDNA is regulated by BfmR, a regulator essential for Pseudomonas aeruginosa biofilm development. The expression of bfmR coincided with localized cell death and DNA release, with high eDNA concentrations localized to the outer part of microcolonies in the form of a ring and as a cap on small clusters. Additionally, eDNA release and cell lysis increased significantly following bfmR inactivation. Genome-wide transcriptional profiling indicated that bfmR was required for repression of genes associated with bacteriophage assembly and bacteriophage-mediated lysis. In order to determine which of these genes were directly regulated by BfmR, we utilized chromatin immunoprecipitation (ChIP) analysis to identify the promoter of PA0691, termed here phdA, encoding a previously undescribed homologue of the prevent-host-death (Phd) family of proteins. Lack of phdA expression coincided with impaired biofilm development, increased cell death and bacteriophage release, a phenotype comparable to ΔbfmR. Expression of phdA in ΔbfmR biofilms restored eDNA release, cell lysis, release of bacteriophages, and biofilm formation to wild type levels. Moreover, overexpression of phdA rendered P. aeruginosa resistant to lysis mediated by superinfective bacteriophage Pf4 which was only detected in biofilms. The expression of bfmR was stimulated by conditions resulting in membrane perturbation and cell lysis. Thus, we propose that BfmR regulates biofilm development by controlling bacteriophage-mediated lysis and thus, cell death and eDNA release, via PhdA.
2011-06-01 | GSE28953 | GEO
Project description:Pseudomonas aeruginosa is a common bacteria leading to exacerbations of chronic obstructive pulmonary disease (COPD) patients while this bacteria can be easily eradicated by the immune systems of healthy individuals. Human airway organoids derived from healthy individuals and COPD patients were infected with pseudomonas aeruginosa. This project aims (1) to understand the differences in gene expressions in healthy and COPD airway organoids during stable condition, without infection and (2) to investigate differential pathogenic mechanism (i.e. antimicrobial defense) of pseudomonoas aeruginosa infection in healthy and COPD populations. Three healthy donors and three COPD patients were included in this study and samples were collected with and without pseudomonas aeruginosa infection.
2022-11-10 | GSE201465 | GEO
Project description:Wound infections are traditionally thought to occur when microbial burden exceeds the innate clearance capacity of host immune system. Here we introduce the idea that the wound environment itself plays a significant contributory role to wound infection. We developed a clinically relevant murine model of soft tissue infection to explore the role of activation of microbial virulence in response to tissue factors as a mechanism by which pathogenic bacteria cause wound infections. Mice underwent abdominal skin incision and light muscle injury with a crushing forceps versus skin incision alone followed by topical inoculation of Pseudomonas aeruginosa. Pseudomonas aeruginosa whole genome transcriptional profiling demonstrated that fascia induced the activation of multiple genes responsible for the synthesis of the iron scavenging protein pyochelin.
2014-10-01 | GSE61925 | GEO
Project description:Explore the genome-scale phage–host interactions across different developmental infection stages
2020-07-15 | GSE128811 | GEO