Biofilm dispersion by Pseudomonas aeruginosa requires relocation of BdlA to drive a switch in motility by dispersed cells

Biofilm dispersion is a regulated process that enables bacteria to escape as free-living cells. This response coincides with matrix degradation, reduced cyclic di-GMP levels, heightened antibiotic susceptibility, and restored flagellar motility. While dispersed cells have been reported to be motile, the mechanisms enabling motility upon induction of dispersion remain unclear. Here, we explored the regulatory mechanism of how Pseudomonas aeruginosa biofilm cells switch their motility phenotype to disperse from biofilms. Our findings reveal that changes in motility gene expression are initiated at the periphery of biofilms during induced dispersion, in which increased expression of the flagellar gene fliC is controlled by the phosphodiesterase (PDE) DipA and the chemosensory protein BdlA. In response to the dispersion signal, BdlA forms dynamic clusters and relocates to the flagellated cell pole, where it interacts with and stimulates the PDE activity of DipA, ultimately leading to elevated fliC expression. These findings establish a mechanistic link between signal sensing and motility reversion, demonstrating that the spatiotemporal coordination of BdlA and DipA governs the motility switch during P. aeruginosa biofilm dispersion.