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J. Bacteriol. doi:10.1128/JB.01134-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Regulation of cell growth during serum starvation and bacterial survival in macrophages by the bifunctional enzyme SpoT in Helicobacter pylori

National Cancer Institute and National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Maryland

^* To whom correspondence should be addressed. Email: djjin{at}helix.nih.gov.

	Abstract

In Helicobacter pylori the stringent response is solely mediated by spoT. The spoT gene is known to encode (p)ppGpp synthetase activity, and is required for H. pylori survival of 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 within macrophages has been demonstrated. In this report, we studied the effects of SpoT on these functions. Our results showed that the H. pylori spoT gene encodes a bifunctional enzyme with both a hydrolase activity and its known (p)ppGpp synthetase activity by introducing the gene into E. 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 compared to wild-type, mimicking a "relaxed" phenotype of growth 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, stress response and persistence of H. pylori is discussed.