Helicobacter pylori is an Epsilonproteobacteria capable of causing gastritis, ulcers, and gastric cancer when it colonizes the human stomach epithelium. Functional flagella are required for the migration of the bacterium though the gastric mucus lining to the gastric epithelial cells. Flagellar biogenesis requires over fifty genes that are transcribed as their products are needed. The sequential expression of flagellar genes is regulated by all three sigma factors found in H. pylori (RpoD, RpoN, and FliA). Genes needed early in assembly are dependent on RpoD, genes needed in the middle stage of assembly are dependent on RpoN, and genes needed late in assembly are dependent on FliA. Transcription of the RpoN-dependent genes is activated by a two-component system consisting of the sensor kinase FlgS and the response regulator FlgR. The cellular cue sensed by the FlgS/FlgR two-component system is currently unknown though several studies have linked the expression of RpoN-dependent genes to the presence of the flagellar protein export apparatus. FliO is a membrane-bound component of the export apparatus and is required for optimal expression of the RpoN regulon. The effect of FliO on transcription of the RpoN regulon may be indirect as FliO is required to support wild-type levels of FlhA, another membrane-bound component of the export apparatus. A deletion analysis revealed that the first 24 residues of FlhA (FlhANT) are needed for the transcription of RpoN-dependent genes. Interaction between FlhANT and FlgS was demonstrated using biolayer interferometry, although FlhANT alone was unable to stimulate autophosphorylation of FlgS. Loss of other structures such as the C ring and FliH, both which facilitate the shuttling of flagellar substrates to the export apparatus, inhibited expression of RpoN-dependent flagellar genes suggesting that these proteins may be important for regulating FlgS activity. Loss of FliE and FlgBC, the first substrates secreted by the export apparatus, increased expression of RpoN-dependent genes. These results support a model where FlgS is brought to the export apparatus via interactions with FliH and the C ring where it can sense the status of flagellar assembly to initiate a signal transduction response resulting in the expression of the RpoN regulon.