ArticleThe Journal of infectious diseases2025
Membrane Lipids Augment Cell Envelope Stress Signaling via the MadRS System to Defend Against Antimicrobial Peptides and Antibiotics in Enterococcus faecalis.
Article in The Journal of infectious diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Genome-based predictions of metabolic preferences and substrate phenotypes in psychrotrophic bacteria from permafrost environments.Microbiology spectrum · 2026Article
- Revealing the Fate of Isomeric Monounsaturated Fatty Acids inACS infectious diseases · 2026Article
- A two-component system signaling hub controls enterococcal membrane remodeling in response to daptomycin.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Therapeutic approach to difficult-to-treat multidrug-resistant enterococcal infections.Antimicrobial agents and chemotherapy · 2025Review
- LiaS-dependent activation of the MadR regulon enables cross-talk betweenbioRxiv : the preprint server for biology · 2025Article
- Insights into ecology, pathogenesis, and biofilm formation ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Guarding the walls: the multifaceted roles of Bce modules in cell envelope stress sensing and antimicrobial resistance.Journal of bacteriology · 2024Review
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16 authors at 5 institutions in 3 countries.
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Abstract
Enterococci have evolved resistance mechanisms to protect their cell envelopes against bacteriocins and host cationic antimicrobial peptides (CAMPs) produced in the gastrointestinal environment. Activation of the membrane stress response has also been tied to resistance to the lipopeptide antibiotic daptomycin. However, the actual effectors mediating resistance have not been elucidated. Here, we show that the MadRS (formerly YxdJK) membrane antimicrobial peptide defense system controls a network of genes, including a previously uncharacterized 3-gene operon (madEFG) that protects the Enterococcus faecalis cell envelope from antimicrobial peptides. Constitutive activation of the system confers protection against CAMPs and daptomycin in the absence of a functional LiaFSR system and leads to persistence of cardiac microlesions in vivo. Moreover, changes in the lipid cell membrane environment alter CAMP susceptibility and expression of the MadRS system. Thus, we provide a framework supporting a multilayered envelope defense mechanism for resistance and survival coupled to virulence.
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