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


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


In Helicobacter pylori auto-inducer-2, but not LuxS-MccAB catalysed reverse transsulphuration, regulates motility through modulation of flagellar gene transcription - Download this document for free, or read online. Document in PDF available to download.

Publication Date: 2010-08-06

Language: English

Type: Article

Metadata: Show full item record

Citation: Shen, F., Hobley, L., Doherty, N., Loh, J. T., Cover, T. L., Sockett, R. E., Hardie, K. R., & et al. (2010). In Helicobacter pylori auto-inducer-2, but not LuxS/MccAB catalysed reverse transsulphuration, regulates motility through modulation of flagellar gene transcription.

Abstract: Abstract 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 ΔluxS 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 ΔluxS 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 ΔluxS Hp mutant. Immunoblotting identified decreased levels of FlaA and FlgE but not FlaB in the ΔluxS 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 ΔluxS 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.

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This record's URL: http://www.dspace.cam.ac.uk/handle/1810/237811http://dx.doi.org/10.1186/1471-2180-10-210

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Rights Holder: Shen et al.; licensee BioMed Central Ltd.





Author: Shen, FeifeiHobley, LauraDoherty, NeilLoh, John T.Cover, Timothy L.Sockett, R. ElizabethHardie, Kim R.Atherton, John C.Show moreSh

Source: https://www.repository.cam.ac.uk/handle/1810/237811



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