ArticleScientific reports2024
Genome-wide identification of fitness-genes in aminoglycoside-resistant Escherichia coli during antibiotic stress.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
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- Integrated genomic and phenotypic characterization of antimicrobial resistance in Shiga toxin-producing Escherichia coli from asymptomatic carriers in Japan.Scientific reports · 2026Article
- Prevalence and Differential Plasmid Versus Chromosomal Distribution of Ribosome-Targeting Antibiotic Resistance Genes inAntibiotics (Basel, Switzerland) · 2026Article
- Whole-Genome Sequencing and Antimicrobial Resistance Analysis of EnterotoxigenicAnimals : an open access journal from MDPI · 2026Article
- Identification of a novel gene associated with group B Streptococcus persister cell formation and biofilm production.Scientific reports · 2025Article
- Deletion of pcnB affects antibiotic susceptibility in resistant Escherichia coli by reducing copy number of ColE1-family plasmids.Scientific reports · 2025Article
- ScreeningOpen research Europe · 2025Article
- Recent advances in understanding of enterobacterial common antigen synthesis and regulation.Open biology · 2025Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Resistance against aminoglycosides is widespread in bacteria. This study aimed to identify genes that are important for growth of E. coli during aminoglycoside exposure, since such genes may be targeted to re-sensitize resistant E. coli to treatment. We constructed three transposon mutant libraries each containing > 230.000 mutants in E. coli MG1655 strains harboring streptomycin (aph(3″)-Ib/aph(6)-Id), gentamicin (aac(3)-IV), or neomycin (aph(3″)-Ia) resistance gene(s). Transposon Directed Insertion-site Sequencing (TraDIS), a combination of transposon mutagenesis and high-throughput sequencing, identified 56 genes which were deemed important for growth during streptomycin, 39 during gentamicin and 32 during neomycin exposure. Most of these fitness-genes were membrane-located (n = 55) and involved in either cell division, ATP-synthesis or stress response in the streptomycin and gentamicin exposed libraries, and enterobacterial common antigen biosynthesis or magnesium sensing/transport in the neomycin exposed library. For validation, eight selected fitness-genes/gene-clusters were deleted (minCDE, hflCK, clsA and cpxR associated with streptomycin and gentamicin resistance, and phoPQ, wecA, lpp and pal associated with neomycin resistance), and all mutants were shown to be growth attenuated upon exposure to the corresponding antibiotics. In summary, we identified genes that are advantageous in aminoglycoside-resistant E. coli during antibiotic stress. In addition, we increased the understanding of how aminoglycoside-resistant E. coli respond to antibiotic exposure.
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