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

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.

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

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.

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

A correlation between the periplasmic embellishment of the flagellar motor and its stator system type is described, motors with dual H+-dependent stator systems have one periplasmic ring formed by MotY.

Real time measurements of c-di-GMP in individual cells reveal an unexpected mechanism by which the chemotaxis machinery controls c-di-GMP heterogeneity, thereby regulating flagellar-based motility.