Figure 7.

The His–FlgM fusion proteins are active in vivo and the His–FlgM* mutants are defective for σ²⁸ inhibition. β-Galactosidase assays demonstrating inhibition of σ²⁸-dependent lacZ expression by the His–FlgM proteins (both wild type and mutant) in vivo. The His–FlgM proteins are being expressed from the arabinose-inducible P_BAD promoter from the S. typhimurium chromosome. The ability of the His–FlgM proteins to inhibit σ²⁸-dependent expression of lacZ was measured in strains grown to mid-log phase in the presence of 1.3 μm arabinose. β-Galactosidase activities are expressed as nmole/min per OD₆₅₀/ml (Davis et al. 1980).