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.

The transcription factor (TF)-binding specificities of Pseudomonas aeruginosa allow us to predict virulence-associated TFs and their target genes, which will facilitate to find effective treatment and prevention for its associated diseases.

The diguanylate cyclase activity of SiaD is activated by its binding partner SiaC thourgh a dynamic mechanism of promoting the formation of active SiaD dimers.

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

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

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.

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