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Journal of Bacteriology, August 2005, p. 5742-5750, Vol. 187, No. 16
0021-9193/05/$08.00+0     doi:10.1128/JB.187.16.5742-5750.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Helicobacter pylori Flagellar Hook-Filament Transition Is Controlled by a FliK Functional Homolog Encoded by the Gene HP0906{dagger}

Kieran A. Ryan,1 Najma Karim,2 Mulugeta Worku,3 Charles W. Penn,4 and Paul W. O'Toole1*

Department of Microbiology and Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland,1 Department of Microbiology, Imperial College School Medicine, St. Mary's Hospital, London, United Kingdom,2 Department of Medicine, Imperial College School Medicine, St. Mary's Hospital, London, United Kingdom,3 School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom4

Received 22 April 2005/ Accepted 24 May 2005

Helicobacter pylori is a human gastric pathogen which is dependent on motility for infection. The H. pylori genome encodes a near-complete complement of flagellar proteins compared to model enteric bacteria. One of the few flagellar genes not annotated in H. pylori is that encoding FliK, a hook length control protein whose absence leads to a polyhook phenotype in Salmonella enterica. We investigated the role of the H. pylori gene HP0906 in flagellar biogenesis because of linkage to other flagellar genes, because of its transcriptional regulation pattern, and because of the properties of an ortholog in Campylobacter jejuni (N. Kamal and C. W. Penn, unpublished data). A nonpolar mutation of HP0906 in strain CCUG 17874 was generated by insertion of a chloramphenicol resistance marker. Cells of the mutant were almost completely nonmotile but produced sheathed, undulating polyhook structures at the cell pole. Expression of HP0906 in a Salmonella fliK mutant restored motility, confirming that HP0906 is the H. pylori fliK gene. Mutation of HP0906 caused a dramatic reduction in H. pylori flagellin protein production and a significant increase in production of the hook protein FlgE. The HP0906 mutant showed increased transcription of the flgE and flaB genes relative to the wild type, down-regulation of flaA transcription, and no significant change in transcription of the flagellar intermediate class genes flgM, fliD, and flhA. We conclude that the H. pylori HP0906 gene product is the hook length control protein FliK and that its function is required for turning off the {sigma}54 regulon during progression of the flagellar gene expression cascade.


* Corresponding author. Mailing address: Department of Microbiology & Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland. Phone: 353 21 490 3997. Fax: 353 21 490 3101. E-mail: pwotoole{at}ucc.ie.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.


Journal of Bacteriology, August 2005, p. 5742-5750, Vol. 187, No. 16
0021-9193/05/$08.00+0     doi:10.1128/JB.187.16.5742-5750.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




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