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54 sigma factor RpoN in Helicobacter pylori
1 Department of Microbiology and Alimentary Pharmabiotic Centre, University College Cork, Western Road, Cork, Ireland
2 Bacterial Microarray Group, Division of Cellular and Molecular Medicine, St George's University of London, Cranmer Terrace, London SW17 0RE, UK
Helicobacter pylori is a motile Gram-negative bacterium that colonizes and persists in the human gastric mucosa. The flagellum gene regulatory circuitry of H. pylori is unique in many aspects compared with the Salmonella/Escherichia coli paradigms, and some regulatory checkpoints remain unclear. FliK controls the hook length during flagellar assembly. Microarray analysis of a fliK-null mutant revealed increased transcription of genes under the control of the
54 sigma factor RpoN. This sigma factor has been shown to be responsible for transcription of the class II flagellar genes, including flgE and flaB. No genes higher in the flagellar hierarchy had altered expression, suggesting specific and localized FliK-dependent feedback on the RpoN regulon. FliK thus appears to be involved in three processes: hook-length control, export substrate specificity and control of RpoN transcriptional activity.
Correspondence
Paul W. O'Toole
pwotoole{at}ucc.ie
The microarray design is available in B µG@Sbase (accession number A-BUGS-18; http://bugs.sgul.ac.uk/A-BUGS-18) and also ArrayExpress (accession number A-BUGS-18). Fully annotated microarray data have been deposited in B µG@Sbase (accession number E-BUGS-78; http://bugs.sgul.ac.uk/E-BUGS-78) and also ArrayExpress (accession number E-BUGS-78).
A supplementary table, listing oligonucleotide primers used in this study, is available with the online version of this paper.
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