Open Access Highly Accessed Research article

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

Feifei Shen126*, Laura Hobley3, Neil Doherty127, John T Loh4, Timothy L Cover4, R Elizabeth Sockett3, Kim R Hardie15 and John C Atherton12

Author Affiliations

1 Centre for Biomolecular Sciences, University of Nottingham, University Park, Nottingham NG7 2RD, UK

2 Nottingham Digestive Diseases Centre NIHR Biomedical Research Unit, School of Clinical Sciences, University of Nottingham and Nottingham University Hospitals NHS Trust, Nottingham NG7 2UH, UK

3 Institute of Genetics, School of Biology, Queen's Medical Centre, University of Nottingham NG7 2UH, UK

4 Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 037232-2605 and Veterans Affairs Tennessee Valley Healthcare System, Nashville, TN 37212, USA

5 School of Molecular Medical Sciences, University of Nottingham, University Park, Nottingham NG7 2RD, UK

6 Current Address: Department of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, UK

7 Current Address: Department of Food Sciences, Sutton Bonington Campus, University of Nottingham, Leicestershire LE12 5RD, UK

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BMC Microbiology 2010, 10:210  doi:10.1186/1471-2180-10-210

Published: 6 August 2010



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.


We report that disruption of luxS renders H. pylori non-motile in soft agar and by microscopy, whereas disruption of mccAHp or mccBHp (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 ΔluxSHp mutant was complemented genetically by luxSHp 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 ΔluxSHp 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 ΔluxSHp mutant. Immunoblotting identified decreased levels of FlaA and FlgE but not FlaB in the ΔluxSHp 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 ΔluxSHp mutant restored flagellar gene transcription, and the number and length of flagella.


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.