Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26047099_1.fastq.gz | Fastqsanger.gz | |||
| SRR26047099_2.fastq.gz | Fastqsanger.gz |
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Project description:we performed ChIP-seq assays to identify in vivo targets of GltR. The plasmid mini-gltR-flag-lacz was constructed and the resultant plasmid was fused to P. aeruginosa strain PAO1, yielding PAO1/mini-gltR-flag-lacz. We investigated GltR-binding to the chromosome of PAO1 during growth with glucose by ChIP-Seq. Sequence reads obtained from three independent ChIP-Seq experiments using anti-flag antibody and mapped to the P. aeruginosa PAO1 genome.Using the MACS software,we identified 55 enriched loci (q-value < 0.05) harboring GltR-binding peaks, that were enriched > 3-fold, but were absent in control sample conducted without anti-flag antibody.
2021-02-22 | GSE153848 | GEO
Project description:SbrI and SbrR are an extracytoplasmic function sigma factor and its cognate anti-sigma factor, respectively. To identify the SbrIR regulon, we measured gene expression in wild type PAO1 , PAO1 ∆sbrR, and PAO1 ∆sbrIR mutants using microarrays.
2015-12-23 | GSE74917 | GEO
Project description:SbrI and SbrR are an extracytoplasmic function sigma factor and its cognate anti-sigma factor, respectively. To identify the SbrIR regulon, we measured gene expression in wild type PAO1 , PAO1 âsbrR, and PAO1 âsbrIR mutants using microarrays. WT PAO1 pPSV38 (empty vector), PAO1 âsbrR pPSV38, PAO1 âsbrR pSbrR, and PAO1 âsbrIR pPSV38 were grown to mid-log. RNA was extracted and reverse transcribed into cDNA. The cDNA was biotinylated and hybridized to Pseudomonas aeruginosa Affymetrix microarrays.
2015-12-23 | E-GEOD-74917 | biostudies-arrayexpress
Project description:To determined the phosphorylation sites of MvaU purified from MPAO1, PAO1, PAO1/pHERD20T-fpkA, PAO1/pHERD20T-fpkB, PAO1/pHERD20T-fpkA-pfkB and PAO1/pHERD20T-fpkA-pfkB-pfpC
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Project description:Genomic DNA from Pseudomonas aeruginosa strains PAO1 and PA14
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Project description:We identified PhaF as an RNA binding protein in Pseudomonas aeruginosa. In order to identify the different target transcripts of PhaF, we carried out the CLIP (Crosslinking and immunoprecipitation) and CLAP-Seq (Covalent linkage affinity purification) approaches, which utilizes UV irradiation to crosslink PhaF with the transcripts that are in close vicinity to it. For CLIP-Seq experiments, we used the Pseudomonas aeruginosa PAO1 strain along with a derivative of PAO1 that harbors a C-terminal VSVG tag on PhaF. In order to determine the importance of the C-terminal domain (CTD) of PhaF on RNA binding, we used PAO1ΔphaF strains carrying plasmids that express a C-terminal VSVG tagged version of PhaF-CTD (pPhaF-CTD-V), along with a control strain that carries the same plasmid (pPhaF-CTD) but without the VSVG tag. For CLAP-Seq experiments, we used the Pseudomonas aeruginosa PAO1 strain along with a derivative of PAO1 that harbors a C-terminal Halo tag on PhaF. All the strains were subjected to UV irradiation, lysed, immunoprecipitated using either anti-VSVG-antibody coated beads or Magne Halo tagged beads. Following immunoprecipitation, the RNAs were purified. We also purified Total (Tot) RNA (samples collected before immunoprecipitation) from the PAO1 strains harboring the C-terminal VSVG tag on PhaF. The purified RNA samples were converted to cDNA libraries, which were subsequently sequenced using the Illumina NextSeq. The sequences were mapped to the genome to identify the target transcripts. In a separate series of experiments we also carried out RNA-Seq to identify the genes that are differentially regulated using Pseudomonas aeruginosa PAO1 and PAO1ΔphaF strains. The isolated RNA was sent to SeqCenter (Pittsburgh, PA) and the sequences obtained were mapped to the genome and DESeq analysis was performed.
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Project description:We identified PhaF as an RNA binding protein in Pseudomonas aeruginosa. In order to identify the different target transcripts of PhaF, we carried out the CLIP (Crosslinking and immunoprecipitation) and CLAP-Seq (Covalent linkage affinity purification) approaches, which utilizes UV irradiation to crosslink PhaF with the transcripts that are in close vicinity to it. For CLIP-Seq experiments, we used the Pseudomonas aeruginosa PAO1 strain along with a derivative of PAO1 that harbors a C-terminal VSVG tag on PhaF. In order to determine the importance of the C-terminal domain (CTD) of PhaF on RNA binding, we used PAO1ΔphaF strains carrying plasmids that express a C-terminal VSVG tagged version of PhaF-CTD (pPhaF-CTD-V), along with a control strain that carries the same plasmid (pPhaF-CTD) but without the VSVG tag. For CLAP-Seq experiments, we used the Pseudomonas aeruginosa PAO1 strain along with a derivative of PAO1 that harbors a C-terminal Halo tag on PhaF. All the strains were subjected to UV irradiation, lysed, immunoprecipitated using either anti-VSVG-antibody coated beads or Magne Halo tagged beads. Following immunoprecipitation, the RNAs were purified. We also purified Total (Tot) RNA (samples collected before immunoprecipitation) from the PAO1 strains harboring the C-terminal VSVG tag on PhaF. The purified RNA samples were converted to cDNA libraries, which were subsequently sequenced using the Illumina NextSeq. The sequences were mapped to the genome to identify the target transcripts. In a separate series of experiments we also carried out RNA-Seq to identify the genes that are differentially regulated using Pseudomonas aeruginosa PAO1 and PAO1ΔphaF strains. The isolated RNA was sent to SeqCenter (Pittsburgh, PA) and the sequences obtained were mapped to the genome and DESeq analysis was performed.
2026-01-12 | GSE298077 | GEO
Project description:A special immune system exists at distinct respiratory epithelium to combat invasion by Pseudomonas aeruginosa (PAO1). This study aimes to determine if interleukin-17C (IL-17C) is correlated with acute PAO1 infection in human nasal epithelium and to prove the role of IL-17C on iron sequestration during PAO1 infection. IL-17C has antipseudomonal effect by lowering iron sequestration and reducing siderophore activity. IL-17C could be efficient mediator to control PAO1 infection in human nasal epithelium.
2018-01-12 | GSE109118 | GEO