Motility is involved in Silicibacter sp. TM1040 interaction with dinoflagellates

Summary Silicibacter sp. TM1040, originally isolated from a culture of the dinoflagellate Pfiesteria piscicida , senses and responds to the dinoflagellate secondary metabolite dimethylsulfoniopropionate (DMSP) by flagella‐mediated chemotaxis behaviour. In this report we show that swimming motility is important for initiating the interaction between the bacterium and dinoflagellate. Following transposon mutagenesis, three mutants defective in wild‐type swimming motility (Mot – ) were identified. The defects in motility were found to be in homologues of cckA and ctrA , encoding a two‐component regulatory circuit, and in a novel gene, flaA , likely to function in flagellar export or biogenesis . Mutation of flaA or cckA results in the loss of flagella and non‐motile cells (Fla – ), while CtrA – cells possess flagella, but have reduced motility due to increased cell length. All three Mot – mutants were defective in attaching to the dinoflagellate, particularly to regions that colocalized with intracellular organelles. The growth rate of the dinoflagellates was reduced in the presence of the Fla – mutants compared with Fla + cells. These results indicate that bacterial motility is important for the Silicibacter sp. TM1040– P. piscicida interaction.