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Staphylococcus aureus NAD kinase promotes infection by protecting bacteria from host antimicrobial defenses and by supporting production of major virulence factors.

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

Disruption of disulfide bond formation sensitizes resistant Gram-negative bacteria expressing β-lactamases and mobile colistin resistance enzymes to currently available antibiotics.

Environmental specialization of bacterial cell wall synthases influences intrinsic resistance to cell wall active antibiotics.

Aminoglycoside tolerance in tricarboxylic acid cycle and electron transport chain mutants does not result from impaired proton motive force and altered drug uptake, but rather from the downregulation of ribosomal proteins, which are primary targets of this drug class.

In the ancestor of mammals, a multifunctional innate immune protein evolved when a mutation enhanced the protein’s pro-inflammatory activity and proteolytic regulation without disrupting the protein’s antimicrobial activity.

Evolutionary trade-offs enhance efficacy of antibiotic therapy by constraining bacterial adaptation in dependence of drug order and trade-off effect size.

Bacterial gut pathogens that invade into host tissues during infection can boost the spread and accumulation of plasmids over time by forming reservoirs containing these plasmids within host tissues.

A quorum-sensing-controlled program of multicellularity, aggregation, is identified in Vibrio cholerae, which may be important for transitions between the marine niche and the human host.