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

TitleThe quorum-sensing molecule autoinducer 2 regulates motility and flagellar morphogenesis in Helicobacter pylori.
Publication TypeJournal Article
Year of Publication2007
AuthorsRader, BA, Campagna, SR, Semmelhack, MF, Bassler, BL, Guillemin, K
JournalJ Bacteriol
Date Published2007 Sep
KeywordsBacterial Proteins, Carbon-Sulfur Lyases, Flagella, Gene Deletion, Gene Expression Regulation, Bacterial, Genetic Complementation Test, Helicobacter pylori, Homoserine, Lactones, Locomotion, Membrane Proteins, Morphogenesis, Pentanes, Quorum Sensing, RNA, Bacterial, RNA, Messenger, Transcription, Genetic

<p>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 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.</p>

Alternate JournalJ Bacteriol
PubMed ID17586631
PubMed Central IDPMC1951907
Grant ListR56 DK075667 / DK / NIDDK NIH HHS / United States
R56 DK075667-01 / DK / NIDDK NIH HHS / United States