Required for transcription of the fliF gene during vegetative and intracellular growth and for production of the two flagellar components flgE and fliC during vegetative growth. Specifically binds to the fliF promoter region. Could mediate the action of VjbR on flagellar gene expression. Inactivation of the ftcR gene down-regulates the activity of the fliF promoter region and the production of both flgE and fliC proteins during vegetative growth or during macrophage infection. This mutant also lacks the flagellar structures under growth conditions in which the wild-type strain is flagellated. The mutant is not attenuated in cellular infection models but exhibits a marked virulence defect after 4 weeks or more of infection in mice. There is no cognate histidine kinase partner identified so far for FtcR. Lacks the conserved Asp residue in position 50 usually required for phosphorylation. The Glu residue in position 50 may mimic constitutive phosphorylation and allow FtcR to bypass the requirement for phosphorylation.