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The Staphylococcus aureus RNA polymerase beta' subunit (RpoC) is a fundamental component of the bacterial transcription machinery, forming the catalytic core of the RNA polymerase (RNAP) enzyme alongside the alpha, beta, and omega subunits [7, 9]. It is primarily responsible for DNA binding and facilitating the elongation of the RNA chain during transcription [8, 11]. In S. aureus, RpoC is a critical therapeutic target for antibiotics such as fidaxomicin, which interacts with the 'switch' region at the interface of the beta and beta' subunits to inhibit transcription initiation [4, 9]. Mutations in the rpoC gene are clinically significant as they are frequently associated with the development of resistance to last-resort antibiotics, including vancomycin (contributing to the 'slow VISA' phenotype) and daptomycin [2, 14]. Because bacterial RNAP subunits are structurally distinct from eukaryotic RNA polymerases, RpoC serves as an important target for the development of selective antimicrobial agents with minimal host toxicity [4, 10].
Inhibition of DNA-directed RNA polymerase activity, blocking of transcription initiation by binding to the switch region, and steric hindrance of RNA chain elongation.
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