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The pathogenesis of diseases elicited by the gastric pathogenHelicobacter pylori is partially determined by the effectiveness of adaptation to the variably acidic environment of the host stomach. Adaptation includes appropriate adherence to the gastric epithelium via outer membrane protein adhesins such as SabA. The expression ofsabA is subject to regulation via phase variation in the promoter and coding regions as well as repression by the two-component system ArsRS. In this study, we investigated the role of a homopolymeric thymine [poly(T)] tract −50 to −33 relative to thesabA transcriptional start site inH. pylori strain J99. We quantifiedsabA expression inH. pylori J99 by quantitative reverse transcription-PCR (RT-PCR), demonstrating significant changes insabA expression associated with experimental manipulations of poly(T) tract length. Mimicking the length increase of this tract by adding adenines instead of thymines had similar effects, while the addition of other nucleotides failed to affectsabA expression in the same manner. We hypothesize that modification of the poly(T) tract changes DNA topology, affecting regulatory protein interaction(s) or RNA polymerase binding efficiency. Additionally, we characterized the interaction between thesabA promoter region and ArsR, a response regulator affectingsabA expression. Using recombinant ArsR in electrophoretic mobility shift assays (EMSA), we localized binding to a sequence with partial dyad symmetry −20 and +38 relative to thesabA +1 site. The control ofsabA expression by both ArsRS and phase variation at two distinct repeat regions suggests the control ofsabA expression is both complex and vital toH. pylori infection.

Repetitive Sequence Variations in the Promoter Region of the Adhesin-Encoding Gene sabA of Helicobacter pylori Affect Transcription