Ontology highlight
ABSTRACT:
PROVIDER: PRJNA995330 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25296206_1.fastq.gz | Fastqsanger.gz | |||
| SRR25296206_2.fastq.gz | Fastqsanger.gz | |||
| SRR25296207_1.fastq.gz | Fastqsanger.gz | |||
| SRR25296207_2.fastq.gz | Fastqsanger.gz |
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Project description:Escherichia coli Outer Membrane Vesicles RNA studies
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Project description:Sepsis causes millions of deaths per year worldwide and is a current global health priority declared by the WHO. Sepsis-related deaths are a result of dysregulated inflammatory immune responses indicating the need to develop strategies to target inflammation. An important mediator of inflammation is extracellular adenosine triphosphate (ATP) that is secreted by inflamed host cells and tissues, and also by bacteria in a strain-specific and growth phase-dependent manner. Here, we investigated the mechanisms by which bacteria release ATP. Using genetic mutant strains of Escherichia coli (E. coli), we demonstrate that ATP release is dependent on ATP synthase within the inner bacterial membrane. In addition, impaired integrity of the outer bacterial membrane and bacterial death notably contribute to ATP release. In a mouse model of abdominal sepsis, local effects of bacterial ATP were analysed using a transformed E. coli bearing an arabinose-inducible periplasmic apyrase hydrolyzing ATP to be released. Abrogating bacterial ATP release shows that bacterial ATP suppresses local immune responses, resulting in reduced neutrophil counts and impaired survival. In addition, bacterial ATP has systemic effects via its transport in outer membrane vesicles (OMV). ATP-loaded OMV are quickly distributed throughout the body and upregulated expression of genes activating degranulation in neutrophils, potentially contributing to the exacerbation of sepsis severity. This study reveals mechanisms of bacterial ATP release and its local and systemic roles in sepsis pathogenesis.
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Project description:The mass spectrometry proteomics data of outer membrane vesicles of wide-type Escherichia coli Nissle 1917 and engineered Escherichia coli Nissle 1917
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Project description:Large-scale production of bacterial extracellular vesicles is a hurdle for their development as novel cancer immunotherapeutic agents. Here, we developed manufacturing processes for mass production of Escherichia coli EVs known as outer membrane vesicles (OMVs). We present a comprehensive proteome of mass-produced E. coli OMVs.
2023-10-24 | PXD043119 | Pride
Project description:RNA sequencing (RNA-seq) is the gold standard for the discovery of small non-coding RNAs. Following a long-standing approach, reads shorter than 16 nucleotides (nt) are removed from the small RNA sequencing libraries or datasets. The serendipitous discovery of a 12 nt-long RNA species capable of modulating the microRNA from which they derive prompted us to challenge this dogma, and by expanding the window of RNA sizes down to 8 nt, to confirm the existence of functional very small RNAs (vsRNAs <16nt). Here we report the profiling of vsRNAs in Escherichia coli (with different experimental conditions), E. coli-derived outer membrane vesicles (OMVs) and five other bacterial strains (Pseudomonas aeruginosa PA7, P. aeruginosa PAO1, Salmonella Typhimurium 14028S, Legionella pneumophila JR32 Philadelphia-1 and Staphylococcus aureus HG001).
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Project description:We performed comparative transcriptomic analysis of the outer membrane vesicles (OMVs) released from B. burgdorferi. We identified a total of ~1200 unique transcripts with at least one mapped read from the bacterial cell and its OMVs.
2018-06-21 | GSE114368 | GEO
Project description:We have investigated the genomic and epigenetic consequences of co-culturing colorectal carcinoma cells with membrane vesicles from pathogenic bacteria Vibrio cholerae and non-pathogenic commensal bacteria Escherichia coli. Our study has revealed that membrane vesicles from pathogenic and commensal bacteria have a global impact on the gene expression of coloncarcinoma cells. The changes in gene expression correlated positively with both epigenetic changes and chromatin accessibility of promoters at transcription start sites of genes induced by both types of membrane vesicles. Moreover, we have demonstrated that membrane vesicles obtained only from V. cholerae induced the expression of genes associated with tumour differentiation. Altogether, our study suggests that the observed genomic changes in host cells might be due to specific components of membrane vesicles and does not require communication by direct contact with the bacteria.
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Project description:Being a ferroxidase and a structural factor of the Escherichia coli nucleoid, Dps protein was recently encountered in the outer membrane and attracted attention as a potential partner for bacterial RNAs. Here, we show the first images visualizing Dps on the surface of bacteria and demonstrate that Dps produced by E. coli K-12 MG1655 or BL21(DE3) cells can cross bacteria-impermeable membrane and attach to the cell surface of a dps-null mutant. Using RNAseq and pull-down assays, we identified RNAs with specifically reduced secretion in the mutant and witnessed preferential interaction of Dps with tRNA and sRNA fragments. Upon analysis of their deviations from the genomic sequences, we selected one circular and six linear oligonucleotides with different folding as model RNAs and showed their ability to affect the growth of bacteria via Dps-dependent internalization by cells. This assumes Dps involvement in intercellular signal transduction within a bacterial population through participation in RNA secretion
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Project description:As nascent polypeptides exit ribosomes, they are engaged by a series of processing, targeting and folding factors. Here we present a selective ribosome profiling strategy that enables global monitoring of when these factors engage polypeptides in the complex cellular environment. Studies of the Escherichia coli chaperone Trigger Factor (TF) reveal that, while TF can interact with many polypeptides, β-barrel outer membrane proteins are the most prominent substrates. Loss of TF leads to broad outer membrane defects and premature, cotranslational protein translocation. While in vitro studies suggested that TF is prebound to ribosomes waiting for polypeptides to emerge from the exit channel, we find that in vivo TF engages ribosomes only after ~100 amino acids are translated. Moreover, excess TF interferes with cotranslational removal of the N-terminal formyl methionine. Our studies support a triaging model in which proper protein biogenesis relies on the fine-tuned, sequential engagement of processing, targeting ad folding factors. Examination of translation in the Gram-negative bacterium Escherichia coli, as well as an analysis of the interactions between nascent chains and the molecular chaperone Trigger Factor.
2011-12-09 | E-GEOD-33671 | biostudies-arrayexpress
Project description:Gram-negative bacteria possess stress responses to maintain the integrity of the cell envelope. Stress sensors monitor outer membrane permeability, envelope protein folding, and energization of the inner membrane. The systems used by Gram-negative bacteria to sense and combat stress resulting from disruption of the peptidoglycan layer are not well characterized. The peptidoglycan layer is a single molecule that completely surrounds the cell and ensures its structural integrity. During cell growth new peptidoglcyan subunits are incorporated into the peptidoglycan layer by a series of enzymes called the penicillin-binding proteins (PBPs). To explore how Gram-negative bacteria respond to peptidoglycan stress, global gene expression analysis was used to identify Escherichia coli stress responses activated following inhibition of specific PBPs by the β-lactam antibiotics mecillinam and cefsulodin. Inhibition of PBPs with different roles in peptidoglycan synthesis has different consequences for cell morphology and viability, suggesting that not all perturbations to the peptidoglycan layer generate equivalent stresses. We demonstrate that inhibition of different PBPs resulted in both shared and unique stress responses. The regulation of capsular synthesis (Rcs) phosphorelay was activated by inhibition of all of the PBPs tested. Furthermore, we show that activation of the Rcs phosphorelay increased survival in the presence of these antibiotics, independently of capsule synthesis. Both activation of the phosphorelay and survival required signal transduction via the outer membrane lipoprotein RcsF and the response regulator RcsB. We propose that the Rcs pathway responds to peptidoglycan damage and contributes to the intrinsic resistance of E. coli to β-lactam antibiotics. We used microarrays to identify changes in gene expression resulting from treatment of Escherichia coli with the β-lactam antibiotics cefsulodin, mecillinam, or the combination. This SuperSeries is composed of the following subset Series:; GSE10158: Expression of Escherichia coli treated with cefsulodin and mecillinam, alone and in combination; GSE10159: Expression of Escherichia coli treated with cefsulodin and mecillinam, alone at the minimum inhibitory concentration Experiment Overall Design: Refer to individual Series
2008-10-20 | E-GEOD-10160 | biostudies-arrayexpress