A single mutation in Escherichia coli connects two essential cell envelope assembly pathways and confers vancomycin resistance by displaying molecular decoys at the cell surface.

Palmitoleic acid not only potentiates vancomycin killing of Gram-positive bacteria, but the insertion of palmitoleic acid into the membrane leads to the unexpected accumulation of membrane-bound cell wall precursors, representing a novel mechanism of action for unsaturated fatty acids.

A large-scale analysis of Staphylococcus aureus within-host evolution based on a comprehensive catalogue of bacterial genetic variation reveals an excess of genome degradation signatures in infecting strains and new genetic loci of clinically relevant adaptation.

Morphological constraints dictate division mode in the human pathogen Staphylococcus aureus.

The ubiquitous second messenger cyclic AMP, produced by Rv3645/MacE, controls long-chain fatty acid metabolism and intrinsic multidrug resistance in M. tuberculosis.

An Acinetobacter baumannii ABC transporter likely facilitates transport of glycerophospholipids from the inner to the outer membrane.

The density of the gut microbiota influences the host immune system and adiposity, and can be therapeutically manipulated.

The envelope stress factor DolP associates with the outer membrane protein assembly machinery and supports proper folding and functioning of BamA contributing to preserve envelope integrity.

Cholestyramine, an FDA-approved bile acid sequestrant, can be repurposed to inactivate the antibiotic daptomycin in the gut, which prevents the emergence of transmissible antibiotic resistance in gastrointestinal Enterococcus faecium populations.

Phenotypic variants that avoid antibiotic accumulation within clonal bacterial populations are a significant contributor to antibiotic treatment failure and can rely on previously unrecognised survival strategies such as fast growth during drug treatment.