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

Bethany A. Rader, Shawn R. Campagna, Martin F. Semmelhack, Bonnie Lynn Bassler, Karen Guillemin

Research output: Contribution to journalArticle

64 Scopus citations

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 σ28 (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 4,5-dihydroxy-2,3-pentanedione (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 and plays a critical role in global regulation of flagellar gene transcription in H. pylori.

Original languageEnglish (US)
Pages (from-to)6109-6117
Number of pages9
JournalJournal of bacteriology
Volume189
Issue number17
DOIs
StatePublished - Sep 2007

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Molecular Biology

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