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Journal of Bacteriology, December 2008, p. 8025-8032, Vol. 190, No. 24
0021-9193/08/$08.00+0     doi:10.1128/JB.01134-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Regulation of Cell Growth during Serum Starvation and Bacterial Survival in Macrophages by the Bifunctional Enzyme SpoT in Helicobacter pylori{triangledown}

Yan Ning Zhou,1 William G. Coleman Jr.,2 Zhaoxu Yang,1 Yi Yang,1 Nathaniel Hodgson,2 Fuxiang Chen,2 and Ding Jun Jin1*

National Cancer Institute—Frederick, National Institutes of Health, Frederick, Maryland,1 National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland2

Received 12 August 2008/ Accepted 25 September 2008

In Helicobacter pylori the stringent response is mediated solely by spoT. The spoT gene is known to encode (p)ppGpp synthetase activity and is required for H. pylori survival in the stationary phase. However, neither the hydrolase activity of the H. pylori SpoT protein nor the role of SpoT in the regulation of growth during serum starvation and intracellular survival of H. pylori in macrophages has been determined. In this study, we examined the effects of SpoT on these factors. Our results showed that the H. pylori spoT gene encodes a bifunctional enzyme with both a hydrolase activity and the previously described (p)ppGpp synthetase activity, as determined by introducing the gene into Escherichia coli relA and spoT defective strains. Also, we found that SpoT mediates a serum starvation response, which not only restricts the growth but also maintains the helical morphology of H. pylori. Strikingly, a spoT null mutant was able to grow to a higher density in serum-free medium than the wild-type strain, mimicking the "relaxed" growth phenotype of an E. coli relA mutant during amino acid starvation. Finally, SpoT was found to be important for intracellular survival in macrophages during phagocytosis. The unique role of (p)ppGpp in cell growth during serum starvation, in the stress response, and in the persistence of H. pylori is discussed.

* Corresponding author. Mailing address: Transcription Control Section, Gene Regulation and Chromosome Biology Laboratory, National Cancer Institute—Frederick, National Institutes of Health, Frederick, MD 21702. Phone: (301) 846-7684. Fax: (301) 846-1489. E-mail: djjin{at}helix.nih.gov

{triangledown} Published ahead of print on 3 October 2008.

Journal of Bacteriology, December 2008, p. 8025-8032, Vol. 190, No. 24
0021-9193/08/$08.00+0     doi:10.1128/JB.01134-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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