Control of the flagellation pattern in Helicobacter pylori by FlhF and FlhG.

FlhF and FlhG control the location and number of flagella, respectively, in many polar-flagellated bacteria. The roles of FlhF and FlhG are not well characterized in bacteria that have multiple polar flagella, such as . Deleting in shifted the flagellation pattern where most cells had approximately four flagella to a wider and more even distribution in flagellar number. As reported in other bacteria, deleting in resulted in reduced motility, hypoflagellation, and the improper localization of flagella to nonpolar sites. Motile variants of ∆ mutants that had a higher proportion of flagella localizing correctly to the cell pole were isolated, but we were unable to identify the genetic determinants responsible for the increased localization of flagella to the cell pole. One motile variant though produced more flagella than the Δ parental strain, which apparently resulted from a missense mutation in (encodes the MS ring protein), which changed Asn-255 to aspartate. Recombinant FliF, but not recombinant wild-type FliF, formed ordered ring-like assemblies that were ~50 nm wide and displayed the MS ring architecture. We infer from these findings that the FliF variant forms the MS ring more effectively in the absence of FlhF than wild-type FliF. IMPORTANCE colonizes the human stomach where it can cause a variety of diseases, including peptic ulcer disease and gastric cancer. uses flagella for motility, which is required for host colonization. FlhG and FlhF control the flagellation patterns in many bacteria. We found that in , FlhG ensures that cells have approximately equal number of flagella and FlhF is needed for flagellum assembly and localization. FlhF is proposed to facilitate the assembly of FliF into the MS ring, which is one of the earliest structures formed in flagellum assembly. We identified a FliF variant that assembles the MS ring in the absence of FlhF, which supports the proposed role of FlhF in facilitating MS ring assembly.