Title | The quorum-sensing molecule autoinducer 2 regulates motility and flagellar morphogenesis in Helicobacter pylori. |
Publication Type | Journal Article |
Year of Publication | 2007 |
Authors | Rader, BA, Campagna, SR, Semmelhack, MF, Bassler, BL, Guillemin, K |
Journal | J Bacteriol |
Volume | 189 |
Issue | 17 |
Pagination | 6109-17 |
Date Published | 2007 Sep |
ISSN | 0021-9193 |
Keywords | Bacterial 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 |
Abstract | <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> |
DOI | 10.1128/JB.00246-07 |
Alternate Journal | J Bacteriol |
PubMed ID | 17586631 |
PubMed Central ID | PMC1951907 |
Grant List | R56 DK075667 / DK / NIDDK NIH HHS / United States R56 DK075667-01 / DK / NIDDK NIH HHS / United States |