Abstract

Antibiotics of the neomycin, kanamycin and gentamicin, but not streptomycin, groups stabilize the GDP·elongation factor (EF) G·50S subunit·fusidic acid complex. Treatment of 30S subunits, but not of 50S subunits, with neomycin B or kanamycin B, followed by removal of excess unbound antibiotic and supplementation with untreated complementary subunits, promotes poly(U)-dependent binding of Tyr-tRNA to the reassociated ribosomes (misreading). A similar treatment of either ribosomal subunit with neomycin B inhibits the EF-G-dependent translocation of Ac-Phe-tRNA. These results suggest that interaction of neomycin B and related antibiotics with the 30S subunit induces misreading and inhibits translocation, and interaction with the 50S subunit stabilizes EF-G on the ribosome and also inhibits translocation.

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