Outer membrane remodeling via lipid-peptidoglycan crosstalk enables lipooligosaccharide-deficient colistin resistance
Outer membrane remodeling via lipid-peptidoglycan crosstalk enables lipooligosaccharide-deficient colistin resistance
Olea-Ozuna et al. show that outer membrane lipid asymmetry acts as a checkpoint controlling lipooligosaccharide-independent survival in Acinetobacter baumannii. Disrupting phospholipid homeostasis creates a permissive state enabling LOS loss under colistin selection, while reduced PBP1A activity stabilizes this transition, defining a three-state model of envelope remodeling and resistance.
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