The quorum sensing molecule AI-2 regulates motility and flagellar morphogenesis in Helicobacter pylori

Institute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA; Department of Chemistry and Howard Hughes Medical Institute and Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA

^* To whom correspondence should be addressed. Email: guillemin{at}molbio.uoregon.edu.

	Abstract

The genome of the gastric pathogen Helicobacter pylori contains a homologue of the gene luxS, which has been shown to be responsible for production of the quorum sensing signal Autoinducer-2 (AI-2). We report here that deletion of the luxS gene in strain G27 resulted in decreased motility on soft agar plates, a defect that was complemented by a wild type copy of the luxS gene and by the addition of cell free supernatant containing AI-2. The flagella of the luxS mutant appeared normal, however in genetic backgrounds lacking any of three flagellar regulators, the two component sensor kinase flgS, the sigma factor sigma28 (also called fliA), and the anti sigma factor flgM, loss of luxS altered flagellar morphology. In all cases, the double mutant phenotypes were restored to the luxS⁺ phenotype by the addition of synthetic DPD, which cyclizes to form AI-2. Furthermore, in all mutant backgrounds loss of luxS caused a decrease in transcript levels of the flagellar regulator flhA. Addition of DPD to luxS cells induced flhA transcription in a dose dependent manner. Deletion of flhA in a wild type or luxS mutant background resulted in identical loss of motility, flagella, and flagellar gene expression. These data demonstrate that AI-2 functions as a secreted signaling molecule upstream of FlhA that plays a critical role in global regulation of flagellar gene transcription in H. pylori.