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.

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.

Arabidopsis seed germination can be repressed by a Pseudomonas factor.

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.

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

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

C. elegans utilizes bacterially produced nitric oxide as a sensory cue to elicit avoidance of pathogenic bacteria.

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

RNA degradation is completed through specific intermediates, such as diribonucleotides, which must be removed from the cells by a specific enzyme.