Membrane Lipids Augment Cell Envelope Stress Signaling and Resistance to Antibiotics and Antimicrobial Peptides in Enterococcus faecalis
Miller, W. R.; Nguyen, A.; Singh, K. V.; Rizvi, S.; Khan, A.; Erickson, S. G.; Egge, S. L.; Cruz, M.; Dinh, A. Q.; Diaz, L.; Zhang, R.; Xu, L.; Garsin, D. A.; Shamoo, Y.; Arias, C. A.
Show 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 three gene operon (madEFG) that protects the E. 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.
Matching journals
The top 4 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- C-di-AMP levels modulate Staphylococcus aureus cell wall thickness as well as virulence and contribute to antibiotic resistance and tolerance 95%
- Gallocin A, an atypical two-peptide bacteriocin with intramolecular disulfide bonds required for activity 95%
- Mutations in ampD cause hyperproduction of AmpC and CphA beta-lactamases and high resistance to beta-lactam antibiotics in Chromobacterium violaceum 95%
Similar papers in this journal
- Growth arrest of Staphylococcus aureus induces daptomycin tolerance via cell wall remodelling 95%
- Identification of two glycosyltransferases required for synthesis of membrane glycolipids in Clostridioides difficile 94%
- Identification of a novel LysR-type transcriptional regulator in Staphylococcus aureus that is crucial for secondary tissue colonization during metastatic bloodstream infection 94%
Similar papers in this journal
- Klebsiella pneumoniae type VI secretion system-mediated microbial competition is PhoPQ controlled and reactive oxygen species dependent 95%
- Prevalence and mechanisms of high-level carbapenem antibiotic tolerance in clinical isolates of Klebsiella pneumoniae 94%
- Enterococcal cell wall remodelling underpins pathogenesis via the release of the Enteroccocal Polysaccharide Antigen (EPA) 94%
Similar papers in this journal
- Enterococcus faecium sagA mutants have cell envelope defects influencing antibiotic resistance and bacteriophage susceptibility 95%
- Resisting the resistance: The antimicrobial peptide DGL13K selects for small colony variants of Staphylococcus aureus that show increased resistance to its stereoisomer LGL13K, but not to DGL13K. 95%
- The selenophosphate synthetase, selD, is important for Clostridioides difficile physiology 95%
Similar papers in this journal
- Loss of β-ketoacyl acyl carrier protein synthase III activity restores multidrug-resistant Escherichia coli sensitivity to previously ineffective antibiotics 95%
- Regulation of Klebsiella pneumoniae mucoidy by the bacterial tyrosine kinase Wzc 94%
- c-di-GMP inhibits early sporulation in Clostridioides difficile 94%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.