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Quantitative Effect of luxS Gene Inactivation on the Fitness of Helicobacter pylori

Woo-Kon Lee,^1, Keiji Ogura,^1, John T. Loh,² Timothy L. Cover,^2,3,4 and Douglas E. Berg^1*

Departments of Molecular Microbiology, Genetics and Medicine, Washington University Medical School, St. Louis, Missouri 63110,¹ Department of Medicine,² Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232,³ Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee 37212⁴

Received 6 June 2006/ Accepted 15 August 2006

Furanone metabolites called AI-2 (autoinducer 2), used by some bacterial species for signaling and cell density-regulated changes in gene expression, are made while regenerating S-adenosyl methionine (SAM) after its use as a methyl donor. The luxS-encoded enzyme, in particular, participates in this activated methyl cycle by generating both a pentanedione, which is transformed chemically into these AI-2 compounds, and homocysteine, a precursor of methionine and SAM. Helicobacter pylori seems to contain the genes for this activated methyl cycle, including luxS, but not genes for AI-2 uptake and transcriptional regulation. Here we report that deletion of luxS in H. pylori reference strain SS1 diminished its competitive ability in mice and motility in soft agar, whereas no such effect was seen with an equivalent luxS derivative of the unrelated strain X47. These different outcomes are consistent with H. pylori's considerable genetic diversity and are reminiscent of phenotypes seen after deletion of another nonessential metabolic gene, that encoding polyphosphate kinase 1. We suggest that synthesis of AI-2 by H. pylori may be an inadvertent consequence of metabolite flux in its activated methyl cycle and that impairment of this cycle and/or pathways affected by it, rather than loss of quorum sensing, is deleterious for some H. pylori strains. Also tenable is a model in which AI-2 affects other microbes in H. pylori's gastric ecosystem and thereby modulates the gastric environment in ways to which certain H. pylori strains are particularly sensitive.

Published ahead of print on 25 August 2006.

Present address: Department of Microbiology, Gyeongsang National University School of Medicine, Jinju, Republic of Korea.

Present address: Department of Gastroenterology, University of Tokyo, Tokyo, Japan.

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