Abstract
Resistance to the macrolide-lincosamide-streptogramin B (MLS) group of antibiotics, often mediated by plasmids, is widespread among clinically isolated strains of Staphylococcus and Strepto-coccus (1–5). The mechanism of resistance to these inhibitors of protein synthesis has been elucidated by B. Weisblum and his colleagues (6–8). MLS-resistance is associated with the presence of 1additional methyl groups (as N6, N6-dimethyl adenine) on 23S rRNA. This modification reduces the ribosomal affinity for the MLS antibiotics. In many cases exposure to a subinhibitory concentration of erythromycin (Em), results in induction of resistance to elevated levels of antibiotic. Although only Em and a few closely related macrolides like oleandomycin (Om) act as inducers, cultures exposed to these drugs acquire resistance to the entire range of MLS antibiotics. We will deal in this report with the MLS resistance specified by the 3.5 kb plasmid pE194. This entity was isolated from Staphylococcus aureus (9) and then transferred to Bacillus subtilis (10). All of our work has been carried out in the latter organism.
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Dubnau, D. et al. (1981). Regulation of Plasmid Specified MLS-Resistance in Bacillus subtilis by Conformational Alteration of RNA Structure. In: Levy, S.B., Clowes, R.C., Koenig, E.L. (eds) Molecular Biology, Pathogenicity, and Ecology of Bacterial Plasmids. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3983-0_16
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DOI: https://doi.org/10.1007/978-1-4684-3983-0_16
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