Abstract

Summary The mechanism of action of kasugamycin, an aminoglycosidic antibiotic, has been comparatively studied with those of other aminoglycosides. The initiation complex formation on 30S ribosomes is inhibited by kasugamycin but not by streptomycin, kanamycin or gentamicin, although the binding of fMet-tRNA to 70S ribosomes is inhibited both by kasugamycin and by streptomycin. The 70S complex formation is inhibited by kasugamycin but not by streptomycin when GTP is replaced by GMPPCP. The results indicate that the 30S initiation complex formation is a primary site of kasugamycin action but the other aminoglycosides interfere with a certain process after forming the complex.

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