ArticlebioRxiv : the preprint server for biology2026
Outer membrane remodeling via lipid-peptidoglycan crosstalk enables lipooligosaccharide-deficient colistin resistance.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Gram-negative bacteria rely on an asymmetric outer membrane (OM) for barrier integrity, with phospholipids confined to the inner leaflet and glycolipids such as lipopolysaccharide (LPS) or lipooligosaccharide (LOS) forming the outer leaflet. Although LPS/LOS was long considered essential, recent findings challenge this view, leaving the mechanistic basis and evolutionary flexibility unclear. Here, we identify lipid asymmetry as a structural checkpoint that governs access to LOS-independent survival. Using Significance: Colistin is a last-resort antibiotic targeting lipopolysaccharide (LPS) or lipooligosaccharide (LOS) in Gram-negative pathogens, and many emerging antimicrobials aim to inhibit LPS/LOS biosynthesis and transport. Resistance usually arises via lipid A modification, which preserves LPS/LOS while reducing colistin binding. Resistance to colistin can also arise via complete loss of LOS, which occurs in some
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