Proteomic analysis of the function of sigma factor σ54 in Helicobacter pylori survival with nutrition deficiency stress in vitro.

H. pylori can survive under a nutrition-deficient environment. During infection and transmission, H. pylori is confronted with nutrient limitation and the bacterium requires rapid alteration in gene expression for survival under stress conditions. However, the mechanism underlining this regulation remains unknown. A previous study showed that σ(54) is an important regulation factor for H. pylori survival in the nutrition-deficient environment. Our results show that the expression of σ(54) (rpoN) is significantly induced in the stationary phase (nutrition deficiency) and the rpoN mutant showed a significantly lower viability than wild-type H. pylori in the late stationary phase. Thus, σ(54) is involved in H. pylori survival during nutrient limitation. We used comparative proteomics to analyze the protein differentiation between wild-type and rpoN mutant during the stationary phase. With depleted nutrients, σ(54) can slow the process of proliferation by negatively regulating genes involved in energy metabolism and biosynthesis and enhance stress-resistant ability by positively regulating genes involved in protein fate and redox reaction. Especially, NapA positively regulated by σ(54) plays an important function in H. pylori survival both in the stationary phase and in water, and the latter situation would be beneficial for bacterial in vitro transmission. Our investigations give new light on the adaptive regulation of H. pylori under stress conditions.