Ribosomal resistance to streptomycin and spectinomycin in Neisseria gonorrhoeae.
A cell-free protein synthesizing system was used to study the mechanism of resistance to streptomycin (Str) and spectinomycin (Spc) in laboratory mutants and clinical isolates of Neisseria gonorrhoeae. The 70S ribosomes from sensitive strains were sensitive to the effects of Str and Spc on synthesis directed by several synthetic polynucleotide messengers, whereas 70S ribosomes from resistant strains were resistant to these same effects. In each case, the alteration was localized to the 30S ribosomal subunit by studying antibiotic sensitivities of hybrid 70S ribosomes formed by combining subunits from sensitive and resistant strains. No evidence was found for streptomycin- or spectinomycin-inactivating enzymes.
D000596:Amino Acids / Q000378:metabolism; D001426:Bacterial Proteins / Q000096:biosynthesis; D002250:Carbon Radioisotopes; D002458:Cell Fractionation; D002474:Cell-Free System; D004352:Drug Resistance, Microbial; D008274:Magnesium / Q000494:pharmacology; D008851:Micropore Filters; D009154:Mutation; D009344:Neisseria gonorrhoeae / Q000187:drug effects* / Q000648:ultrastructure; D011119:Polynucleotides / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D012270:Ribosomes / Q000187:drug effects* / Q000378:metabolism; D000198:Spectinomycin / Q000494:pharmacology*; D013307:Streptomycin / Q000494:pharmacology*
D000596:Amino Acids; D001426:Bacterial Proteins; D002250:Carbon Radioisotopes; D011119:Polynucleotides; D012333:RNA, Messenger; D000198:Spectinomycin; D008274:Magnesium; D013307:Streptomycin