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Journal of Bacteriology, October 2008, p. 6398-6408, Vol. 190, No. 19
0021-9193/08/$08.00+0     doi:10.1128/JB.00626-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Role of the Helicobacter hepaticus Flagellar Sigma Factor FliA in Gene Regulation and Murine Colonization {triangledown}

Torsten Sterzenbach,1 Lucie Bartonickova,1 Wiebke Behrens,1 Birgit Brenneke,1 Jessika Schulze,1 Friederike Kops,1 Elaine Y. Chin,3,{dagger} Elena Katzowitsch,1 David B. Schauer,3 James G. Fox,2,3 Sebastian Suerbaum,1 and Christine Josenhans1*

Hannover Medical School, Institute for Medical Microbiology and Hospital Epidemiology, 30625 Hannover, Germany,1 MIT Division of Comparative Medicine, Cambridge, Massachusetts,2 MIT Division of Biological Engineering, Cambridge, Massachusetts3

Received 6 May 2008/ Accepted 29 July 2008

The enterohepatic Helicobacter species Helicobacter hepaticus colonizes the murine intestinal and hepatobiliary tract and is associated with chronic intestinal inflammation, gall stone formation, hepatitis, and hepatocellular carcinoma. Thus far, the role of H. hepaticus motility and flagella in intestinal colonization is unknown. In other, closely related bacteria, late flagellar genes are mainly regulated by the sigma factor FliA ({sigma}28). We investigated the function of the H. hepaticus FliA in gene regulation, flagellar biosynthesis, motility, and murine colonization. Competitive microarray analysis of the wild type versus an isogenic fliA mutant revealed that 11 genes were significantly more highly expressed in wild-type bacteria and 2 genes were significantly more highly expressed in the fliA mutant. Most of these were flagellar genes, but four novel FliA-regulated genes of unknown function were identified. H. hepaticus possesses two identical copies of the gene encoding the FliA-dependent major flagellin subunit FlaA (open reading frames HH1364 and HH1653). We characterized the phenotypes of mutants in which fliA or one or both copies of the flaA gene were knocked out. flaA_1 flaA_2 double mutants and fliA mutants did not synthesize detectable amounts of FlaA and possessed severely truncated flagella. Also, both mutants were nonmotile and unable to colonize mice. Mutants with either flaA gene knocked out produced flagella morphologically similar to those of wild-type bacteria and expressed FlaA and FlaB. flaA_1 mutants which had flagella but displayed reduced motility did not colonize mice, indicating that motility is required for intestinal colonization by H. hepaticus and that the presence of flagella alone is not sufficient.

* Corresponding author. Mailing address: Hannover Medical School, Institute for Medical Microbiology and Hospital Epidemiology, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. Phone: 495115324348. Fax: 495115324355. E-mail: josenhans.christine{at}mh-hannover.de

{triangledown} Published ahead of print on 8 August 2008.

{dagger} Present address: Vertex Pharmaceuticals, Cambridge, MA 02139.

Journal of Bacteriology, October 2008, p. 6398-6408, Vol. 190, No. 19
0021-9193/08/$08.00+0     doi:10.1128/JB.00626-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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