Upon host cell contact, motile but not non-motile Pseudomonas aeruginosa exhibit a change in their gene expression program that includes the expression of spermidine, which triggers motility-dependent phagocytosis.

During growth in biofilms and host infection, the opportunistic pathogen Pseudomonas aeruginosa employs respiratory heterocomplexes that support extracellular electron shuttling and pathogenicity.

Subpopulations of polysaccharide producer and surface explorer cells play specialized roles in early Pseudomonas aeruginosa biofilm formation.

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

Pseudomonas aeruginosa coordinates invasion and destruction of Staphylococcus aureus communities by modulating single-cell and collective motility.

Arabidopsis seed germination can be repressed by a Pseudomonas factor.

The feedback between hydrodynamic flow conditions and biofilm spatial architecture drives competition in P. aeruginosa biofilms, and can explain variation in biofilm production observed among bacteria in natural environments.

A population of pathogenic bacteria is found to respond to the loss of cooperation by privatising an essential function.

The first high-resolution structure of a bacterial flagellar cap protein, FliD, reveals new insights into the assembly of bacterial flagella.

A bacteriophage remodels the RNA metabolism machinery of a bacterial host to sequentially clear host transcripts and then stabilize the viral RNA.