Abstract
Antibiotics and other agents that perturb the synthesis or integrity of the bacterial cell envelope trigger compensatory stress responses. Focusing on Bacillus subtilis as a model system, this mini-review summarizes current views of membrane structure and insights into how cell envelope stress responses remodel and protect the membrane. Altering the composition and properties of the membrane and its associated proteome can protect cells against detergents, antimicrobial peptides, and pore-forming compounds while also, indirectly, contributing to resistance against compounds that affect cell wall synthesis. Many of these regulatory responses are broadly conserved, even where the details of regulation may differ, and can be important in the emergence of antibiotic resistance in clinical settings.
Highlights
MEMBRANE HOMEOSTASIS AND ITS MODULATION IN RESPONSE TO STRESSThe cell envelope is a multilayered outer barrier that protects the cell from a changing environment
We focus on Bacillus subtilis as a Gram-positive model for the role of Cell envelope stress responses (CESRs) in membrane homeostasis
We suggest that ACCdependent depletion of acetyl-CoA may contribute to wall stress by negatively affecting synthesis of UDP-N-acetylglucosamine needed for peptidoglycan synthesis
Summary
MEMBRANE HOMEOSTASIS AND ITS MODULATION IN RESPONSE TO STRESSThe cell envelope is a multilayered outer barrier that protects the cell from a changing environment. Focusing on Bacillus subtilis as a model system, this mini-review summarizes current views of membrane structure and insights into how cell envelope stress responses remodel and protect the membrane. Membrane stress responses can modify the cell membrane, by (i) modulating the length, branching, and saturation of the fatty acid (FA) acyl chains, (ii) altering membrane lipid composition, or (iii) synthesizing proteins that modify or protect the membrane (Table 1).
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