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

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.

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.

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

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.

The death of bacterial kin cells releases a danger signal that activates a posttranscriptional response in surviving cells, resulting in the rapid elaboration of interbacterial competition factors.

Structural insights show how RNA chaperones cooperate to recognise defined target transcripts and suppress gene expression.