Serum Starvation and Stringent Response in H. pylori

German Mejia and Fenfei Leng

Florida International University

Helicobacter pylori is a Gram-negative, spiral shaped bacterium that can be discovered and live on the surface of the human gastric epithelium. This human pathogen infects about 50% of the world’s population. Although most infections are asymptomatic, certain infections can be developed into chronic gastritis, peptic ulcers, and even gastric adenocarcinoma. Current research suggest that the pathogenesis of H. pylori is associated with the expression of several virulent factors such as urease, VacA, and CagA. In this study, we investigate how serum starvation, a condition mimicking its living condition on the surface of the human gastric epithelium, induces the stringent response in H. pylori and leads to a different gene expression pattern using differential RNA seq (dRNA-seq), RT-PCR, and Western blotting. Our preliminary results show a change in the TSS (transcription starting sites) map of H. pylori under serum starvation condition. Interestingly, when H. pylori was starved, expression for some virulence factors and DNA topology related proteins is significantly increased. This led us to hypothesize that DNA supercoiling plays an important role in serum starvation and virulence factor expression. Since previous studies showed that serum starvation induces the stringent response in H. pylori mediated solely by a SpoT mediated pathway, it is likely that the SpoT-mediated pathway also causes a change in DNA supercoiling, thereby leading to a different expression pattern along the whole chromosome.