Impaired Membrane Energetics Underlies Collateral Sensitivity to Amphenicols During Meropenem Resistance Evolution in Escherichia coli

Collateral sensitivity, an evolutionary trade-off accompanying antibiotic resistance, offers a potential strategy to counteract multidrug resistance. Here, we characterized collateral sensitivity profiles in plasmid-bearing and plasmid-free Escherichia coli (E. coli) lineages evolved under diverse antibiotic selection pressures. Across six independent meropenem (MEM)-evolved lineages derived from two distinct genetic backgrounds, a conserved collateral sensitivity to amphenicols consistently emerged during adaptive laboratory evolution (ALE). Whole genome sequencing identified recurrent mutations in envZ, mrdA and yghB, with yghB as an important genetic determinant associated with amphenicol sensitivity. Functional characterization of yghB disruption revealed that loss of YghB function affected membrane integrity and proton motive force (PMF) homeostasis, accompanied by altered efflux-associated activity, increased intracellular accumulation of amphenicols and altered Mg2+ homeostasis. In the ΔyghB background, these alterations were further associated with disrupted ribosome homeostasis and reduced translational capacity. Restoration of Mg2+ partially recovered ribosome-associated processes and amphenicol resistance in the ΔyghB mutant, suggesting that Mg2+ limitation contributes to yghB-associated amphenicol sensitivity. Furthermore, amphenicol treatment improved infection outcomes against MEM-resistant mutants in both Galleria mellonella and murine septicemia models. Collectively, MEM resistance evolution in E. coli generates robust collateral sensitivity to amphenicols, in which recurrent yghB mutations represent an important genetic basis. Functional analysis of yghB disruption further suggests that altered membrane energetics, efflux-associated processes and Mg2+-dependent ribosome homeostasis may contribute to this collateral sensitivity, revealing a potential therapeutic opportunity based on evolutionary trade-offs.

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Journal
Microorganisms
Published
2026-08-14
DOI
https://doi.org/10.3390/microorganisms14081792
Primary Topic
Antibiotic Resistance in Bacteria
Type
article
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0.00

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article

Impaired Membrane Energetics Underlies Collateral Sensitivity to Amphenicols During Meropenem Resistance Evolution in Escherichia coli

Qi Jiang, Yinshu Li, Yu‐Feng Zhou, Liangxing Fang et al.
Microorganisms
Antibiotic Resistance in Bacteria
article

Impaired Membrane Energetics Underlies Collateral Sensitivity to Amphenicols During Meropenem Resistance Evolution in Escherichia coli

Qi Jiang, Yinshu Li, Yu‐Feng Zhou, Liangxing Fang, Xiaoping Liao, Jian Sun, Hao Ren, Ruanyang Sun, Hongyan Zhang, Tao Zheng
article en

Abstract

Collateral sensitivity, an evolutionary trade-off accompanying antibiotic resistance, offers a potential strategy to counteract multidrug resistance. Here, we characterized collateral sensitivity profiles in plasmid-bearing and plasmid-free Escherichia coli (E. coli) lineages evolved under diverse antibiotic selection pressures. Across six independent meropenem (MEM)-evolved lineages derived from two distinct genetic backgrounds, a conserved collateral sensitivity to amphenicols consistently emerged during adaptive laboratory evolution (ALE). Whole genome sequencing identified recurrent mutations in envZ, mrdA and yghB, with yghB as an important genetic determinant associated with amphenicol sensitivity. Functional characterization of yghB disruption revealed that loss of YghB function affected membrane integrity and proton motive force (PMF) homeostasis, accompanied by altered efflux-associated activity, increased intracellular accumulation of amphenicols and altered Mg2+ homeostasis. In the ΔyghB background, these alterations were further associated with disrupted ribosome homeostasis and reduced translational capacity. Restoration of Mg2+ partially recovered ribosome-associated processes and amphenicol resistance in the ΔyghB mutant, suggesting that Mg2+ limitation contributes to yghB-associated amphenicol sensitivity. Furthermore, amphenicol treatment improved infection outcomes against MEM-resistant mutants in both Galleria mellonella and murine septicemia models. Collectively, MEM resistance evolution in E. coli generates robust collateral sensitivity to amphenicols, in which recurrent yghB mutations represent an important genetic basis. Functional analysis of yghB disruption further suggests that altered membrane energetics, efflux-associated processes and Mg2+-dependent ribosome homeostasis may contribute to this collateral sensitivity, revealing a potential therapeutic opportunity based on evolutionary trade-offs.

MicroorganismsVol. 14(8)
South China Agricultural University (CN)
National Key Research and Development Program of China
Partnerships for the goals
Openalex Percentile: Top 17%
Antibiotic Resistance in Bacteria
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