The Quorum-Sensing Molecule Autoinducer 2 Regulates Motility and Flagellar Morphogenesis in Helicobacter pylori

@article{citeulike:2231345, 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 regulatorsthe two-component sensor kinase flgS, the sigma factor {sigma}28 (also called fliA), and the anti-sigma factor flgMloss 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. 10.1128/JB.00246-07}, author = {Rader, Bethany A. and Campagna, Shawn R. and Semmelhack, Martin F. and Bassler, Bonnie L. and Guillemin, Karen }, citeulike-article-id = {2231345}, doi = {10.1128/JB.00246-07}, journal = {J. Bacteriol.}, keywords = {pylori, quorum\_sensing}, month = {September}, number = {17}, pages = {6109--6117}, posted-at = {2008-01-14 18:21:28}, priority = {2}, title = {The Quorum-Sensing Molecule Autoinducer 2 Regulates Motility and Flagellar Morphogenesis in Helicobacter pylori}, url = {http://dx.doi.org/10.1128/JB.00246-07}, volume = {189}, year = {2007} }

TY - JOUR ID - citeulike:2231345 L3 - citeulike-article-id:2231345 TI - The Quorum-Sensing Molecule Autoinducer 2 Regulates Motility and Flagellar Morphogenesis in Helicobacter pylori JF - J. Bacteriol. VL - 189 IS - 17 SP - 6109 EP - 6117 N2 - 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 regulatorsthe two-component sensor kinase flgS, the sigma factor {sigma}28 (also called fliA), and the anti-sigma factor flgMloss 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. 10.1128/JB.00246-07 KW - pylori KW - quorum_sensing AU - Rader, Bethany AU - Campagna, Shawn AU - Semmelhack, Martin AU - Bassler, Bonnie AU - Guillemin, Karen PY - 2007/09/01/ UR - http://dx.doi.org/10.1128/JB.00246-07 ER -