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

Relocation of BdlA to the cell pole activates DipA, triggering motility gene expression and enabling Pseudomonas aeruginosa biofilm dispersion.

• Why it matters: Understanding how bacteria switch from sessile to motile states is crucial for controlling biofilm-related infections and antibiotic resistance, yet the underlying mechanisms remain unclear.
• What they did: The study investigated the regulatory process by analyzing BdlA and DipA interactions during dispersion, revealing that BdlA relocates to the flagellated cell pole to stimulate DipA activity and promote motility.
• The result: This mechanism links signal sensing to motility reversion, offering insights into biofilm dispersion regulation and extending existing models of bacterial surface attachment to include dispersion processes.