Escherichia coli
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA381856 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5438180_1.fastq.gz | Fastqsanger.gz | |||
| SRR5438180_2.fastq.gz | Fastqsanger.gz | |||
| SRR5438190_1.fastq.gz | Fastqsanger.gz | |||
| SRR5438190_2.fastq.gz | Fastqsanger.gz | |||
| SRR5438200_1.fastq.gz | Fastqsanger.gz |
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Project description:Adaptive laboratory evolution of antibiotic resistance using different selection regimes
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Project description:Several groups have shown that through evolution experiments, tolerance and resistance evolved rapidly under cyclic antibiotic treatment. In other words, intermittent antibiotic exposure performed in a typical adaptive laboratory evolution (ALE) experiments will “train” the bacteria to become tolerant/resistant to the drug. Using this experimental strategy, we performed in vitro laboratory evolution in MRSA using daptomycin, and mine novel daptomycin tolerance and resistance mutants, which were isolated at specific time points during the evolution experiments. Three daptomycin-tolerant isolates with different tolerance level were generated from our laboratory evolution (TOL2 and TOL5 with a mild-tolerance phenotype, and TOL6 with a high-tolerance phenotype). They all bear mutations at different genes, and have no increase in MIC towards daptomycin. Besides, we also isolated three daptomycin-resistant isolates (RES1, RES2, RES3) that have a single point mutation in the same gene, mprF, but at different locations, leading to an increased MIC towards daptomycin. Through proteomics, we uncovered the differential adaptation strategies of these daptomycin tolerant and resistant MRSA strains, and how they respond differently to antibiotics compared to the ancestral wild-type.
2022-07-14 | PXD026741 | Pride
Project description:Escherichia coli Evolution under Antibiotic Regimes
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Project description:We conducted whole genome sequencing on eight evolved E. coli strains (S1–S8) and the parental wild-type (WT) strain to identify mutations arising from ofloxacin treatments. These strains (S1-S8), generated through fluoroquinolone-mediated adaptive laboratory evolution (ALE), exhibited varying levels of tolerance and resistance. The ALE experiment involved intermittent antibiotic treatments of eight independent cultures over 22 days. The untreated WT strain served as a baseline to pinpoint mutations in the evolved strains.
2024-12-23 | E-MTAB-14682 | biostudies-arrayexpress
Project description:Several groups have shown that through evolution experiments, tolerance and resistance evolved rapidly under cyclic antibiotic treatment. In other words, intermittent antibiotic exposure performed in a typical adaptive laboratory evolution (ALE) experiments will “train” the bacteria to become tolerant/resistant to the drug. Although ALE has added new knowledge regarding the impact of varying treatment conditions on the evolution of tolerance/resistance, the role of some parameters such as population bottlenecks remains poorly understood. In this study, we employed ALE to investigate the evolution of methicillin-resistant S. aureus under repetitive daptomycin treatment using a modified protocol that incorporated population bottleneck following antibiotic exposure. We observed that although tolerance development is slower under bottlenecking conditions, the populations finally attained tolerance mutation in the yycH gene after twelve cycles of treatment. Extending the evolution experiment and changing the treatment scheme to a fast evolution protocol (treatment during exponential phase without bottlenecking) led to the emergence of daptomycin resistance (mutation in mprF gene). Through proteomics, we uncovered the differential adaptation strategies of these daptomycin tolerant and resistant MRSA strains, and how they respond differently to antibiotics compared to the ancestral wild-type.
2022-07-16 | PXD031078 | Pride
Project description:Laboratory adaptive evolution experiments were conducted using serial passage of E. coli in M9 minimal medium supplemented with either 2 g/L of lactate for 60 days or 2 g/L of glycerol for 44 days. 7 parallel evolution strains were generated for growth on lactate and 7 parallel evolution strains were generated for growth on glycerol. Affymetrix arrays were used to study the time-course change in gene expression from unevolved E. coli (day 0) to a midpoint evolved strain (day 20) and evolutionary endpoints Biological replicate arrays were conducted for each of the time points tested for the different evolution strains
2011-10-21 | E-GEOD-33147 | biostudies-arrayexpress
Project description:The evolution of antibiotic resistance is a clear example of adaptation by natural selection. Although a number of mutations contributing to the resistance have been identified, the relationship between the mutations and the related phenotypic changes responsible for the resistance has yet to be fully elucidated. To better characterize phenotype-genotype mapping for drug resistance, we performed parallel laboratory evolution of Escherichia coli under the selection of single antibiotics and after 90 days propagation obtained resistant strains. We find that an acquisition of resistance to one drug drastically changes the resistance and susceptibility to other drugs. Based on transcriptome data of these strains, we demonstrated that the resistances could be quantitatively predicted by the expression changes of a small number of genes. Whole-genome resequencing analysis provided several candidate mutations contributing to the resistances, while phenotype-genotype mapping was suggested to be complex and included various mutations that caused similar phenotypic changes. The integration of transcriptome and genome data enables us to extract essential phenotypic changes for drug resistances. To examine the contribution of the gene expression changes to the antibiotic resistances, transcriptome of the parent strain (duplicated) and 40 resistant strains (4 parallel-evolved resistant strains for 10 antibiotics) were analyzed.
2014-09-17 | E-GEOD-59408 | biostudies-arrayexpress
Project description:Understanding constraints which shape antibiotic resistance is key for predicting and controlling drug resistance. Here, we performed high-throughput laboratory evolution of Actinobacillus pleuropneumoniae and its ciprofloxacin resistance-inducing derivatives.This study aims to explore the mechanism of acquired ciprofloxacin resistance in Actinobacillus pleuropneumoniae.
2021-10-06 | GSE181030 | GEO
Project description:Laboratory adaptive evolution experiments were conducted using serial passage of E. coli in M9 minimal medium supplemented with either 2 g/L of lactate for 60 days or 2 g/L of glycerol for 44 days. 7 parallel evolution strains were generated for growth on lactate and 7 parallel evolution strains were generated for growth on glycerol. Affymetrix arrays were used to study the time-course change in gene expression from unevolved E. coli (day 0) to a midpoint evolved strain (day 20) and evolutionary endpoints
2011-10-22 | GSE33147 | GEO
Project description:Bacterial evolution of antibiotic resistance frequently has deleterious side effects on microbial growth, virulence, and susceptibility to other antimicrobial agents. However, it is unclear how these trade-offs could be utilized for manipulating antibiotic resistance in the clinic, not least because the underlying molecular mechanisms are poorly understood. Using laboratory evolution, we demonstrate that clinically relevant resistance mutations in Escherichia coli constitutively rewire a large fraction of the transcriptome in a repeatable and stereotypic manner. Strikingly, lineages adapted to functionally distinct antibiotics and having no resistance mutations in common show a wide range of parallel gene expression changes that alter oxidative stress response, iron homeostasis, and the composition of the bacterial outer membrane and cell surface. These common physiological alterations are associated with changes in cell morphology and enhanced sensitivity to antimicrobial peptides. Finally, the constitutive transcriptomic changes induced by resistance mutations are largely distinct from those induced by antibiotic stresses in the wild-type. This indicates a limited role for genetic assimilation of the induced antibiotic stress response during resistance evolution. Our work suggests that diverse resistance mutations converge on similar global transcriptomic states that shape genetic susceptibility to antimicrobial compounds.
2023-01-26 | GSE223493 | GEO