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Journal of Bacteriology, November 2005, p. 7687-7695, Vol. 187, No. 22
0021-9193/05/$08.00+0     doi:10.1128/JB.187.22.7687-7695.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Diverse Phenotypes Resulting from Polyphosphate Kinase Gene (ppk1) Inactivation in Different Strains of Helicobacter pylori{dagger}

Shumin Tan,1,§ Cresson D. Fraley,2 Maojun Zhang,1,2,{ddagger} Daiva Dailidiene,1 Arthur Kornberg,2 and Douglas E. Berg1*

Department of Molecular Microbiology, Washington University Medical School, St. Louis, Missouri 63110,1 Department of Biochemistry, Stanford University Medical School, Stanford, California 943052

Received 18 April 2005/ Accepted 29 August 2005

Connections among biochemical pathways should help buffer organisms against environmental stress and affect the pace and trajectory of genome evolution. To explore these ideas, we studied consequences of inactivating the gene for polyphosphate kinase 1 (ppk1) in strains of Helicobacter pylori, a genetically diverse gastric pathogen. The PPK1 enzyme catalyzes synthesis of inorganic polyphosphate (poly P), a reservoir of high-energy phosphate bonds with multiple roles. Prior analyses in less-fastidious microbes had implicated poly P in stress resistance, motility, and virulence. In our studies, ppk1 inactivation caused the expected near-complete absence of poly P (>250-fold decrease) but had phenotypic effects that differed markedly among unrelated strains: (i) poor initial growth on standard brain heart infusion agar (five of six strains tested); (ii) weakened colonization of mice (4 of 5 strains); (iii) reduced growth on Ham's F-12 agar, a nutritionally limiting medium (8 of 11 strains); (iv) heightened susceptibility to metronidazole (6 of 17 strains); and (v) decreased motility in soft agar (1 of 13 strains). Complementation tests confirmed that the lack of growth of one {Delta}ppk1 strain on F-12 agar and the inability to colonize mice of another were each due to ppk1 inactivation. Thus, the importance of ppk1 to H. pylori differed among strains and the phenotypes monitored. We suggest that quantitative interactions, as seen here, are common among genes that affect metabolic pathways and that H. pylori's high genetic diversity makes it well suited for studies of such interactions, their underlying mechanisms, and their evolutionary consequences.

* Corresponding author. Mailing address: Department of Molecular Microbiology, Campus Box 8230, Washington University Medical School, 4940 Parkview Place, St. Louis, MO 63110. Phone: (314) 362-2772. Fax: (314) 362-1232. E-mail: berg{at}borcim.wustl.edu.

{dagger} This report is dedicated to the memory of Robert Kadner, with gratitude for his efforts and insights as a Journal of Bacteriology editor and for his encouragement and friendship.

§ Present address: Department of Microbiology and Immunology, Stanford University Medical School, Stanford, CA 94305.

{ddagger} Present address: Institute for Communicable Disease Control and Prevention, Beijing, China.

Journal of Bacteriology, November 2005, p. 7687-7695, Vol. 187, No. 22
0021-9193/05/$08.00+0     doi:10.1128/JB.187.22.7687-7695.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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