H-082. The Role of HP1042 in Helicobacter pylori Motility

T. G. Smith, T. R. Hoover;
The Univ. of Georgia, Athens, GA.

The Gram-negative, ε-Proteobacteria Helicobacter pylori is a significant human pathogen infecting a large percentage of the worldwide population and causing acute gastritis, peptic ulcers, gastric carcinoma and B-cell mucosa-associated lymphoid tissue lymphoma in some infected individuals. Many essential colonization factors have been identified in H. pylori including flagellar motility. Flagellum assembly requires over 40 proteins and all three sigma factors (RpoD, RpoN and FliA) within the cell. Transcription of the H. pylori RpoN regulon is controlled by a two-component regulatory system. Previous studies in H. pylori showed that flagellar gene expression is influenced by the flagellar protein export apparatus. Specifically FlhA, a component of the flagellar protein export apparatus, was identified as having a potential regulatory role in transcription of RpoN-dependent flagellar genes. In the present study we found that some insertion mutations in flhA resulted in decreased expression of RpoN-dependent reporter genes, while other insertions resulted in enhanced expression of these reporter genes. These differences may reflect distinct consequences of flhA disruption due to the predicted size of a resulting truncated FlhA protein. Alternatively, the differences could be caused by polar effects on the gene or genes downstream of flhA. The gene immediately downstream of flhA (HP1042) encodes a predicted phosphohydrolase and appears to form an operon with flhA. This synteny is conserved in other genera of the ε-Proteobacteria including Campylobacter, Wolinella and Thiomicrospira. The association of hp1042 with flhA suggested a possible role for HP1042 in flagellar biosynthesis or function. However, deletion of hp1042 in H. pylori 43504 did not affect motility. Experiments are currently underway to determine if disruption of hp1042 influences expression of RpoN-dependent reporter genes.