Rifampin is an antibiotic that interacts specifically with the β-subunit of DNA-dependent RNA polymerase (RpoB) encoded by therpoB gene (2). Rifampin resistance (Rifr) is usually due to changes in the amino acid sequence of the target site resulting in reduced affinity of RpoB for rifampin. The majority of Escherichia coli Rifr mutations are located in two highly conserved regions of RpoB encompassing amino acid residues 507 to 533 (Rif cluster I) and 563 to 572 (Rif cluster II) (2). Substitutions in these clusters, particularly at “hot spots” such as the residue cognate to E. coli S531, are responsible for acquired Rifr in several species of bacteria. Less common mechanisms of Rifr include mutations in RpoB outside Rif clusters I and II, decreased membrane permeability, efflux, and enzymatic modification of the antibiotic.
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Stamm et al. (2001) studied this question.
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