Streptomycin action: greater inhibition of Escherichia coli ribosome function with exogenous than with endogenous messenger ribonucleic acid.
Inhibition of protein synthesis by streptomycin was tested in extracts from a strain of Escherichia coli sensitive to streptomycin. Three kinds of messenger ribonucleic acid (RNA) were employed: endogenous cellular RNA, extracted cellular RNA, and phage R17 RNA. Protein synthesis directed by extracted cellular RNA was inhibited three- to fourfold more than protein synthesis directed by endogenous RNA. With R17 RNA as messenger, nearly total inhibition of protein synthesis at initiation was again observed. The greater inhibition of function of extracted RNA, which must initiate new polypeptide chains in vitro, is in accord with the observation that in whole cells streptomycin blocks ribosomes at an early stage in protein synthesis. When streptomycin was added at successively later times during protein synthesis, the subsequent inhibition was progressively less. This was observed with either extracted cellular RNA or phage R17 RNA. A model is presented that can explain the less drastic inhibition by streptomycin of messenger RNA that is already functioning on ribosomes.
D000409:Alanine / Q000378:metabolism; D001426:Bacterial Proteins / Q000096:biosynthesis; D002247:Carbon Isotopes; D002474:Cell-Free System; D003090:Coliphages; D004926:Escherichia coli / Q000187:drug effects* / Q000378:metabolism; D012329:RNA, Bacterial / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D012367:RNA, Viral / Q000378:metabolism; D012270:Ribosomes / Q000187:drug effects*; D013307:Streptomycin / Q000494:pharmacology*
D001426:Bacterial Proteins; D002247:Carbon Isotopes; D012329:RNA, Bacterial; D012333:RNA, Messenger; D012367:RNA, Viral; D000409:Alanine; D013307:Streptomycin