Chemotaxis to self-generated AI-2 promotes biofilm formation in .

Responses to the interspecies quorum-sensing signal autoinducer-2 (AI-2) regulate the patterns of gene expression that promote biofilm development. also senses AI-2 as a chemoattractant, a response that requires the periplasmic AI-2-binding protein LsrB and the chemoreceptor Tsr. Here, we confirm, as previously observed, that under static conditions highly motile cells self-aggregate and form surface-adherent structures more readily than cells lacking LsrB and Tsr, or than Δ cells unable to produce AI-2. This difference is observed both at 37 and 30 °C. Cells deleted for the genes encoding the operon repressor (Δ), or the AI-2 kinase (Δ), or an AI-2 uptake channel protein (Δ), or an AI-2 metabolism enzyme (Δ) are also defective in biofilm formation. The Δ and Δ cells are totally defective in AI-2 chemotaxis, whereas the other mutants show normal or near-normal chemotaxis to external gradients of AI-2. These data demonstrate that chemotaxis to external AI-2 is necessary but not sufficient to induce the full range of density-dependent behaviours that are required for optimal biofilm formation. We also demonstrate that, compared to other binding-protein-dependent chemotaxis systems in , low levels (on the order of ~250 molecules of periplasmic LsrB per wild-type cell and as low as ~50 molecules per cell in some mutants) are adequate for a strong chemotaxis response to external gradients of AI-2.