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Published online ahead of print on 21 April 2009 as doi:10.1099/mic.0.026062-0
Microbiology 2009;155:1901.

Microbiology (2009), DOI 10.1099/mic.0.026062-0
© 2009 Society for General Microbiology

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Microbiology 0 (2009), mic.0.026062; DOI  10.1099/mic.0.026062-0
© 2009 Society for General Microbiology


Effect of FliK mutation on the transcriptional activity of the {sigma}54 sigma factor RpoN in Helicobacter pylori

F. P. Douillard1, K. A. Ryan2, J. Hinds3 and P. W. O'Toole1,4

1 Univ College Cork;
2 NUI Galway;
3 St George's Univ London

ABSTRACT

Helicobacter pylori is a motile gram-negative bacterium that colonises and persists in the human gastric mucosa. The flagellum gene regulatory circuitry of H. pylori is unique in many aspects compared to the Salmonella/E. 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 {sigma}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 feed-back 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.

4 E-mail: pwotoole{at}ucc.ie







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