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Background  LuxS may function as a metabolic enzyme or as the synthase of a quorum sensing signalling molecule, auto-inducer-2 (AI-2); hence, the mechanism underlying phenotypic changes upon  luxS  inactivation is not always clear. In  Helicobacter pylori , we have recently shown that, rather than functioning in recycling methionine as in most bacteria, LuxS (along with newly-characterised MccA and MccB), synthesises cysteine via reverse transsulphuration. In this study, we investigated whether and how LuxS controls motility of  H. pylori , specifically if it has its effects via  luxS -required cysteine metabolism or via AI-2 synthesis only.    Results  We report that disruption of  luxS  renders  H. pylori  non-motile in soft agar and by microscopy, whereas disruption of  mccA  Hp  or  mccB  Hp  (other genes in the cysteine provision pathway) does not, implying that the lost phenotype is not due to disrupted cysteine provision. The motility defect of the Δ luxS  Hp  mutant was complemented genetically by  luxS  Hp  and also by addition of  in vitro  synthesised AI-2 or 4, 5-dihydroxy-2, 3-pentanedione (DPD, the precursor of AI-2). In contrast, exogenously added cysteine could not restore motility to the Δ luxS  Hp  mutant, confirming that AI-2 synthesis, but not the metabolic effect of LuxS was important. Microscopy showed reduced number and length of flagella in the Δ luxS  Hp  mutant. Immunoblotting identified decreased levels of FlaA and FlgE but not FlaB in the Δ luxS  Hp  mutant, and RT-PCR showed that the expression of  flaA, flgE ,  motA ,  motB ,  flhA  and  fliI  but not  flaB  was reduced. Addition of DPD but not cysteine to the Δ luxS  Hp  mutant restored flagellar gene transcription, and the number and length of flagella.    Conclusions  Our data show that as well as being a metabolic enzyme,  H. pylori  LuxS has an alternative role in regulation of motility by modulating flagellar transcripts and flagellar biosynthesis through production of the signalling molecule AI-2.

bmc microbiology

In Helicobacter pylori auto-inducer-2, but not LuxS/MccAB catalysed reverse transsulphuration, regulates motility through modulation of flagellar gene transcription