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Metabolic mutations induce antibiotic resistance by pathway specific bottlenecks.

ABSTRACT: Metabolic mutations induce antibiotic resistance by pathway specific bottlenecks.

PROVIDER: PRJEB75679 | ENA |

REPOSITORIES: ENA

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Untargeted metabolomics of " Metabolic mutations induce antibiotic resistance by pathway-specific bottlenecks."

Project description:Untargeted metabolomics dataset for the paper "Metabolic mutations induce antibiotic resistance by pathway-specific bottlenecks " These are the raw files for metabolites of all 41 isolates in Figure 4b of the paper.

2024-05-07 | MSV000094699 | MassIVE

Targeted metabolomics of " Metabolic mutations induce antibiotic resistance by pathway-specific bottlenecks."

Project description:Compilation of the targeted metabolomics data present in the associated paper: Metabolic mutations induce antibiotic resistance by pathway-specific bottlenecks. See "File names association" table in "supplementary files" to link file names with paper figures.

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Metabolic mutations induce antibiotic resistance by pathway-specific mechanisms and tolerance by slow-growth

Project description:Metabolic mutations induce antibiotic resistance

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Metabolic mutations reduce antibiotic susceptibility of E. coli by pathway-specific bottlenecks

Project description:Metabolic variation across pathogenic bacterial strains can impact their susceptibility to antibiotics and promote evolution of antimicrobial resistance (AMR). However, little is known about how metabolic mutations influence metabolism and which pathways contribute to antibiotic susceptibility. Here, we measured antibiotic susceptibility of 15,120 Escherichia coli mutants, each with a single amino acid change in one of 346 essential proteins. Across all mutants, we observed modest increases of the minimal inhibitory concentration (2- to 10-fold) without any cases of major resistance. Most mutants that showed reduced susceptibility to either of the two tested antibiotics carried mutations in metabolic genes. The effect of metabolic mutations on antibiotic susceptibility was antibiotic- and pathway-specific: mutations that reduced susceptibility against the β-lactam antibiotic carbenicillin converged on purine nucleotide biosynthesis, those against the aminoglycoside gentamicin converged on the respiratory chain. Additionally, metabolic mutations conferred tolerance to carbenicillin by reducing growth rates. These results, along with evidence that metabolic bottlenecks are common among clinical E. coli isolates, highlight the contribution of metabolic mutations for AMR.

| S-SCDT-10_1038-S44320-024-00084-Z | biostudies-other

Metabolic mutations reduce antibiotic susceptibility of E. coli by pathway-specific bottlenecks.

Project description:Metabolic variation across pathogenic bacterial strains can impact their susceptibility to antibiotics and promote the evolution of antimicrobial resistance (AMR). However, little is known about how metabolic mutations influence metabolism and which pathways contribute to antibiotic susceptibility. Here, we measured the antibiotic susceptibility of 15,120 Escherichia coli mutants, each with a single amino acid change in one of 346 essential proteins. Across all mutants, we observed modest increases of the minimal inhibitory concentration (twofold to tenfold) without any cases of major resistance. Most mutants that showed reduced susceptibility to either of the two tested antibiotics carried mutations in metabolic genes. The effect of metabolic mutations on antibiotic susceptibility was antibiotic- and pathway-specific: mutations that reduced susceptibility against the β-lactam antibiotic carbenicillin converged on purine nucleotide biosynthesis, those against the aminoglycoside gentamicin converged on the respiratory chain. In addition, metabolic mutations conferred tolerance to carbenicillin by reducing growth rates. These results, along with evidence that metabolic bottlenecks are common among clinical E. coli isolates, highlight the contribution of metabolic mutations for AMR.

| S-EPMC11876631 | biostudies-literature

GNPS - Untargeted metabolomics of

2024-05-07 | MSV000094699 | GNPS

Hotspot mutations induce metabolic reprogramming and vulnerability to serine deprivation

Project description:Hotspot mutations induce metabolic reprogramming and vulnerability to serine deprivation

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GNPS - Targeted metabolomics of

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Mutations in RAS pathway induce synthetic lethality of MEK inhibition with mitochondrial oxidative metabolism in acute myeloid leukemia

Project description:Microarray experiment for pharmacogenomics profilling. Two mutations, an NF1 knockout and NRAS G12D, that induce the RAS signalling pathway were made in TF1 cells. The NRAS G12D mutant was treated with pyrvinium at 250 nM in DMSO (vehicle).

2022-02-22 | E-MTAB-10261 | biostudies-arrayexpress

Metabolic and metagenomic outcomes from early-life pulsed antibiotic treatment

Project description:Mammalian species have co-evolved with intestinal microbial communities that can shape development and adapt to environmental changes, including antibiotic perturbation or nutrient flux. In humans, especially children, microbiota disruption is common, yet the dynamic microbiome recovery from early-life antibiotics is still uncharacterized. Using a mouse model mimicking pediatric antibiotic use, we found that therapeutic-dose pulsed antibiotic treatment (PAT) with a beta-lactam or macrolide altered both host and microbiota development. Early-life PAT accelerated total mass and bone growth, and resulted in progressive changes in gut microbiome diversity, population structure, and metagenomic content, with microbiome effects dependent on the number of courses and class of antibiotic. While control microbiota rapidly adapted to a change in diet, PAT slowed the ecological progression, with delays lasting several months in response to the macrolide. This study identifies key markers of disturbance and recovery, which may help provide therapeutic targets for microbiota restoration following antibiotic treatment. C57BL/6J mice received three antibiotic courses: at days 10-15, 28-31, and 37-40 of life, amoxicillin or tylosin.Livers were collected at age 22 weeks, RNA was extracted, and transcriptional differences were measured by microarray analysis.

2015-05-07 | E-GEOD-68603 | biostudies-arrayexpress

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