Previous Article | Next Article ![]()
Journal of Bacteriology, December 2008, p. 7975-7984, Vol. 190, No. 24
0021-9193/08/$08.00+0 doi:10.1128/JB.00879-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
,
Department of Microbiology & Alimentary Pharmabiotic Centre, University College Cork, Ireland,1 Bacterial Microarray Group, Division of Cellular and Molecular Medicine, St. George's University of London, Cranmer Terrace, London, United Kingdom2
Received 26 June 2008/ Accepted 7 October 2008
The Helicobacter pylori protein HP0958 is essential for flagellum biogenesis. It has been shown that HP0958 stabilizes the
54 factor RpoN. The aim of this study was to further investigate the role of HP0958 in flagellum production in H. pylori. Global transcript analysis identified a number of flagellar genes that were differentially expressed in an HP0958 mutant strain. Among these, the transcription of the major flagellin gene flaA was upregulated twofold, suggesting that HP0958 was a negative regulator of the flaA gene. However, the production of the FlaA protein was significantly reduced in the HP0958 mutant, and this was not due to the decreased stability of the FlaA protein. RNA stability analysis and binding assays indicated that HP0958 binds and destabilizes flaA mRNA. The HP0958 mutant was successfully complemented, confirming that the mutant phenotype described was due to the lack of HP0958. We conclude that HP0958 is a posttranscriptional regulator that modulates the amount of the flaA message available for translation in H. pylori.
Published ahead of print on 17 October 2008.
Supplemental material for this article may be found at http://jb.asm.org/.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»