Abstract
Summary Serratia sp. strain ATCC 39006 (S39006) can float in aqueous environments due to natural production of gas vesicles (GVs). Expression of genes for GV morphogenesis is stimulated in low oxygen conditions, thereby enabling migration to the air–liquid interface. Quorum sensing (via SmaI and SmaR) and transcriptional and post‐transcriptional regulators, including RbsR and RsmA, respectively, connect the control of cell buoyancy, motility and secondary metabolism. Here, we define a new pleiotropic regulator found in screens of GV mutants. A mutation in the gene trkH , encoding a potassium transporter, caused upregulation of GV formation, flotation, and the prodigiosin antibiotic, and downregulation of flagellar motility. Pressure nephelometry revealed that the mutation in trkH affected cell turgor pressure. Our results show that osmotic change is an important physiological parameter modulating cell buoyancy and antimicrobial production in S39006, in response to environmental potassium levels.