Related Experiment Video

Updated: Jul 19, 2025

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection
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Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection

Published on: October 25, 2013

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Molecular Basis of Cell Membrane Adaptation in Daptomycin-Resistant Enterococcus faecalis

April H Nguyen, Truc T Tran, Diana Panesso

    Biorxiv : the Preprint Server for Biology
    |August 14, 2023
    PubMed

    Insights

    Enterococcus faecalis resists the antibiotic daptomycin by altering its cell membrane. Cardiolipin synthase activity is crucial for this resistance mechanism, involving phospholipid redistribution.

    Area of Science:

    • Microbiology
    • Molecular Biology
    • Biochemistry

    Background:

    • Daptomycin is a critical antibiotic for treating Gram-positive bacterial infections.
    • Enterococcus faecalis exhibits resistance to daptomycin through cell membrane (CM) remodeling.
    • The LiaFSR system and cardiolipin synthase (Cls) are implicated in this resistance, but their roles are unclear.

    Approach:

    • Investigated the role of cardiolipin synthase (Cls) in daptomycin resistance.
    • Examined the function of the LiaFSR regulatory system and LiaY protein in CM remodeling.
    • Utilized gene deletion strategies to assess the necessity of Cls activity and LiaY.

    Key Points:

    • Cardiolipin synthase activity is essential for anionic phospholipid redistribution and daptomycin resistance in E. faecalis.
    • Deletion of cardiolipin synthase genes (cls1 and cls2) abrogated CM remodeling.
    • LiaY, a LiaFSR-regulated transmembrane protein, mediates CM remodeling through interaction with Cls1.

    Conclusions:

    • Cardiolipin synthase activity is indispensable for the enterococcal daptomycin resistance mechanism.
    • LiaY acts as a key mediator in the LiaFSR-controlled CM response.
    • This study elucidates a mechanistic framework for enterococcal antibiotic resistance, offering potential therapeutic targets.

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