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. 2004 Oct 4;101(41):14925–14930. doi: 10.1073/pnas.0406410101

Fig. 5.

Fig. 5.

(A) Comparison of the rifampin regions of RNAP β subunits among N. farcinica (RpoB and RpoB2), M. tuberculosis (Mtub), S. avermitilis (Save), B. subtilis (Bsub), and E. coli (Ecol). Boxed regions indicate known positions where mutations lead to rifampin resistance in various bacteria. Substitutions found in the RpoB2 are red-colored. (B) Possible advantage of two types of rpoB genes being present in one genome. 1, Rifampin binds to wild-type RNAP and inhibits its function. 2, Certain mutations (asterisks) on the rpoB gene diminish the binding of rifampin to RNAP, making bacteria resistant in the presence of rifampin. However, rpoB mutants destabilize initiation complexes between RNAP and stringently controlled promoters, for example rrnB P1, even in the absence of rifampin. 3, If both types of rpoB genes are present in one genome, such side effects disappear in the absence of rifampin by the wild-type molecule, and bacteria can survive in the presence of rifampin by the mutant molecule.