Quantitative effect of luxS gene inactivation on the fitness of Helicobacter pylori.

ABSTRACT: 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

SUBMITTER: Lee WK 

PROVIDER: S-EPMC1610275 | biostudies-literature | 2006 Oct

REPOSITORIES: biostudies-literature