Maness M J, Foster G C, Sparling P F
J Bacteriol. 1974 Dec;120(3):1293-9. doi: 10.1128/jb.120.3.1293-1299.1974.
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.
利用无细胞蛋白质合成系统研究了淋病奈瑟菌实验室突变株和临床分离株对链霉素(Str)和壮观霉素(Spc)的耐药机制。敏感菌株的70S核糖体对Str和Spc对几种合成多核苷酸信使指导的合成的影响敏感,而耐药菌株的70S核糖体对这些相同的影响具有抗性。在每种情况下,通过研究由敏感菌株和耐药菌株的亚基组合形成的杂交70S核糖体的抗生素敏感性,发现这种改变定位于30S核糖体亚基。未发现链霉素或壮观霉素失活酶的证据。