SUMMARY Puromycin, gougerotin, neomycin B, tetracycline, chloram- phenicol, and cycloheximide inhibit protein synthesis in various cell-free systems. Assays designed to determine the mechanism of action of these inhibitors indicat.e (a) that tetracycline inhibits the binding of aminoacyl soluble ribonucleic acid to messenger ribonucleic acid-containing ribosomes; (b) that the aminoacyl nucleoside, puromycin, releases peptide material from peptidyl soluble ribonucleic acid, messenger ribonucleic acid, ribosome complexes while the related aminoacyl nucleoside, gougerotin, blocks this release; (c) that neomycin B alters the binding of aminoacyl soluble ribonucleic acid onto messenger ribonucleic acid, ribosome complexes; (d) that chloramphenicol can compete with a messenger ribonucleic acid for sites on bacterial ribosomes; and (e) that cycloheximide does not influence the binding of aminoacyl soluble ribonucleic acid to ribosomes or the puromycin- dependent release of peptides from pept’idyl soluble ribonucleic acid, messenger ribonucleic acid, ribosome complexes. Aclcnowledgments-We wish to thank Dr. Richard Schweet for his encouragement of this work and Mrs. Ronnie Barker for invaluable technical assistance. REFERENCES
No takes yet. Share an insight, caveat, or question.
Clark et al. (1965) studied this question.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: