title: Motility is involved in Silicibacter sp. TM1040 interaction with dinoflagellates.
abstract: 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.
authors.affiliation: Center of Marine Biotechnology, University of Maryland Biotechnology Institute, 701 East Pratt Street, Baltimore, MD 21202, USA.
authors.forename: Todd R
authors.initials: TR
authors.lastname: Miller
authors.forename: Robert
authors.initials: R
authors.lastname: Belas
mesh_terms: D000818:Animals; D005407:Flagella / Q000235:genetics / Q000382:microbiology*; D018613:Microscopy, Confocal; D020045:Pfiesteria piscicida / Q000254:growth & development / Q000382:microbiology*; D041902:Rhodobacteraceae / Q000235:genetics / Q000502:physiology* / Q000648:ultrastructure; D013559:Symbiosis / Q000502:physiology*