@article{2348, keywords = {Gene Expression Regulation, Bacterial, Quorum Sensing, Morphogenesis, Locomotion, Transcription, Genetic, Bacterial Proteins, RNA, Bacterial, RNA, Messenger, Membrane Proteins, Lactones, Gene Deletion, Genetic Complementation Test, Homoserine, Carbon-Sulfur Lyases, Flagella, Helicobacter pylori, Pentanes}, author = {Bethany Rader and Shawn Campagna and Martin Semmelhack and Bonnie Bassler and Karen Guillemin}, title = {The quorum-sensing molecule autoinducer 2 regulates motility and flagellar morphogenesis in Helicobacter pylori.}, 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 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.
}, year = {2007}, journal = {J Bacteriol}, volume = {189}, pages = {6109-17}, month = {2007 Sep}, issn = {0021-9193}, doi = {10.1128/JB.00246-07}, language = {eng}, }