This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rader, B. A. Articles by Guillemin, K. Search for Related Content PubMed PubMed Citation Articles by Rader, B. A. Articles by Guillemin, K.

 Previous Article  |  Next Article 

Journal of Bacteriology, September 2007, p. 6109-6117, Vol. 189, No. 17
0021-9193/07/$08.00+0     doi:10.1128/JB.00246-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

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

Bethany A. Rader,¹ Shawn R. Campagna,² Martin F. Semmelhack,² Bonnie L. Bassler,³ and Karen Guillemin^1*

Institute of Molecular Biology, University of Oregon, Eugene, Oregon 97403,¹ Department of Chemistry,² Howard Hughes Medical Institute and Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544³

Received 14 February 2007/ Accepted 18 June 2007

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 ²⁸ (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.

---

* Corresponding author. Mailing address: Institute of Molecular Biology, University of Oregon, Eugene, OR 97403. Phone: (541) 346-5360. Fax: (541) 346-5891. E-mail: guillemin{at}molbio.uoregon.edu

Published ahead of print on 22 June 2007.

---

Journal of Bacteriology, September 2007, p. 6109-6117, Vol. 189, No. 17
0021-9193/07/$08.00+0     doi:10.1128/JB.00246-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

This article has been cited by other articles:

• Pereira, C. S., de Regt, A. K., Brito, P. H., Miller, S. T., Xavier, K. B. (2009). Identification of Functional LsrB-Like Autoinducer-2 Receptors. J. Bacteriol. 191: 6975-6987 [Abstract] [Full Text]  
• Kaakoush, N. O., Asencio, C., Megraud, F., Mendz, G. L. (2009). A Redox Basis for Metronidazole Resistance in Helicobacter pylori. Antimicrob. Agents Chemother. 53: 1884-1891 [Abstract] [Full Text]  
• Tsao, M.-Y., Lin, T.-L., Hsieh, P.-F., Wang, J.-T. (2009). The 3'-to-5' Exoribonuclease (Encoded by HP1248) of Helicobacter pylori Regulates Motility and Apoptosis-Inducing Genes. J. Bacteriol. 191: 2691-2702 [Abstract] [Full Text]  
• Smith, T. G., Pereira, L., Hoover, T. R. (2009). Helicobacter pylori FlhB processing-deficient variants affect flagellar assembly but not flagellar gene expression. Microbiology 155: 1170-1180 [Abstract] [Full Text]