Effect of Escherichia coli B2 on gene expression before and after citric acid-induced antibiotic tolerance
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA937605 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23582282_1.fastq.gz | Fastqsanger.gz | |||
| SRR23582282_2.fastq.gz | Fastqsanger.gz | |||
| SRR23582283_1.fastq.gz | Fastqsanger.gz | |||
| SRR23582283_2.fastq.gz | Fastqsanger.gz | |||
| SRR23582284_1.fastq.gz | Fastqsanger.gz |
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Project description:In order to explore the differentially expressed genes of E. coli B2 after citric acid induced antibiotic tolerance, we artificially induced the antibiotic tolerance of E. coli O157: H7 and verified its phenotype.
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Project description:In order to explore the differentially expressed genes of E. coli O157: H7 after citric acid induced antibiotic tolerance, we artificially induced the antibiotic tolerance of E. coli O157: H7 and verified its phenotype.
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Project description:Effect of Escherichia coli O157: H7 on gene expression before and after citric acid-induced antibiotic tolerance
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Project description:Staphylococcus aureus is responsible for a substantial number of invasive infections globally each year. These infections are problematic because they are frequently recalcitrant to antibiotic treatment. Antibiotic tolerance, the ability of bacteria to persist despite normally lethal doses of antibiotics, contributes to antibiotic treatment failure in S. aureus infections. To understand how antibiotic tolerance is induced, S. aureus biofilms exposed to multiple anti-staphylococcal antibiotics were examined using both quantitative proteomics and transposon sequencing. These screens indicated that arginine metabolism is involved in antibiotic tolerance within a biofilm and led to the hypothesis that depletion of arginine within S. aureus communities can induce antibiotic tolerance. Consistent with this hypothesis, inactivation of argH, the final gene in the arginine synthesis pathway, induces antibiotic tolerance. Arginine restriction was found to induce antibiotic tolerance via inhibition of protein synthesis. In a mouse skin infection model, an argH mutant has enhanced ability to survive antibiotic treatment with vancomycin, highlighting the relationship between arginine metabolism and antibiotic tolerance during S. aureus infection. Uncovering this link between arginine metabolism and antibiotic tolerance has the potential to open new therapeutic avenues targeting previously recalcitrant S. aureus infections.
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Project description:Antibiotics are a triumph of modern medicine, but their power to cure infections is being eroded through the evolution and dissemination of resistance. Evolution of genetic resistance is in part facilitated by non-genetic resistance mechanisms that increase antibiotic tolerance buying time for evolutionary innovation. Using live cell imaging, we discovered that Escherichia coli treated with aminoglycosides permanently lose the ability to divide within 4 hours, yet a majority of cells maintain membrane integrity and metabolic 2 days post treatment, and some continuing activity for up to > 4 days post treatment – a bacterial senescent-like state. These cells, which we term zombies, exhibit dynamic gene expression and metabolomic profiles even after exiting the cell cycle. Gene expression data revealed upregulated the phage shock protein response maintained membrane integrity. Remarkably, these zombie cells, though unable to form new colonies, increase antibiotic tolerance of treatment-naïve cells, implying chemical communication. Chemical supplementation and genetic knockouts showed that zombies communicate to treatment-naïve cells by secreting indole. In summary, our study revealed a bacterial senescent-like state, induced by aminoglycosides, that modifies the antibiotic tolerance of multiple bacterial species.
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