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A resistance gene, carB, originally isolated from the carbomycin-producing organism. Streptomyces thermotolerans, confers on Streptomyces lividans high-level resistance to the drug. However, ribosomes from S. lividans expressing carB show only moderate resistance to this macrolide in vitro, although they are highly resistant to the action of lincosamide antibiotics. The carB product monomethylates the amino group of the adenosine residue located at position 2058 in 23S ribosomal RNA. In contrast, ribosomes from S. lividans expressing ermE, in which 23S RNA is dimethylated at this same position, are much more highly resistant to macrolides and insensitive to lincosamides. [ABSTRACT FROM AUTHOR]

A mutant strain of Bacillus megaterium, arising spontaneously and resistant to micrococcin, possesses ribosomes which contain an altered form of protein BM-L11 (the homologue of Escherichia coli protein L11). Reconstitution analysis has revealed that the alteration to protein BM-L11 is the sole cause of resistance in this strain. [ABSTRACT FROM AUTHOR]

Thiostrepton binds with high affinity and with a 1:1 stoichiometry to a complex formed between Escherichia coli 23-S ribosomal RNA and ribosomal protein LI 1 of E. coli or the homologous protein BM-LI 1 of Bacillus megaterium. In the presence of T1 ribonuclease, protein BM-L11 and thiostrepton protect from degradation a fragment of E. coli 23-S RNA estimated to be about 50 nucleotides in length. [ABSTRACT FROM AUTHOR]

1. The novel aminoglycoside antibiotic apramycin is shown to be a potent inhibitor of protein synthesis in bacteria both in vivo and in vitro. 2. In cell-free systems from Escherichia coli programmed with poly(U), apramycin induces translation errors, as assayed by incorporation of leucine, isoleucine and serine, although this effect occurs only to a limited extent. 3. Apramycin inhibits the translocation step of protein synthesis both in vivo, in protoplasts of Bacillus megaterium, and in vitro, in cell-free systems from E. coli. It is proposed that this is the primary inhibitory effect of the drug. [ABSTRACT FROM AUTHOR]