Structural mechanism for rifampicin inhibition of bacterial rna polymerase.

By E. Campbell, N. Korzheva, A. Mustaev, K. Murakami, S. Nair, A. Goldfarb, S. Darst. Cell, 2001

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Coagulase-Negative Staphylococci (2014, background): “Rifampin resistance in staphylococci is most frequently based on point mutations in the highly conserved regions of the rpoB gene, which encodes the beta subunit of the bacterial RNA polymerase, resulting in amino acid substitutions at or near the binding site for the drug (591, 592).”
Antibiotic resistance in Staphylococcus aureus. Current status and future prospects (2017, background): “does not prevent RNA polymerase from binding to the promoter and initiating transcription (Campbell et al. 2001).”
How antibiotics kill bacteria: from targets to networks (2010, background): “Rifamycins inhibit DNA-dependent transcription by stably binding with high affinity to the β-subunit (encoded by rpoB ) of a DNA-bound and actively transcribing RNA polymeras”
Mechanisms of Antibiotic Resistance (2016, background): “Thus, bacteria have evolved a sophisticated mRNA-based control mechanism to tightly regulate the expression of these methyl-ases, ensuring a high ef ﬁ ciency of action in the presence of the antibiotic while minimizing the ﬁ tness costs for the bacterial population.”