FliT acts as an anti-FlhD2C2 factor in the transcriptional control of the flagellar regulon in Salmonella enterica serovar typhimurium.

Flagellar operons are divided into three classes with respect to their transcriptional hierarchy in Salmonella enterica serovar Typhimurium. The class 1 gene products FlhD and FlhC act together in an FlhD(2)C(2) heterotetramer, which binds upstream of the class 2 promoters to facilitate binding of RNA polymerase. Class 2 expression is known to be enhanced by a disruption mutation in a flagellar gene, fliT. In this study, we purified FliT protein in a His-tagged form and showed that the protein prevented binding of FlhD(2)C(2) to the class 2 promoter and inhibited FlhD(2)C(2)-dependent transcription. Pull-down and far-Western blotting analyses revealed that the FliT protein was capable of binding to FlhD(2)C(2) and FlhC and not to FlhD alone. We conclude that FliT acts as an anti-FlhD(2)C(2) factor, which binds to FlhD(2)C(2) through interaction with the FlhC subunit and inhibits its binding to the class 2 promoter.