Garvin R T, Rosset R, Gorini L
Proc Natl Acad Sci U S A. 1973 Oct;70(10):2762-6. doi: 10.1073/pnas.70.10.2762.
Translational leakiness (i.e., nonspecific suppression) of nonsense mutants of bacteriophage T4 is increased in cells of certain streptomycin-resistant strains previously grown in the presence of streptomycin. Concomitantly, ribosomes extracted from these streptomycin-grown cells possess a high level of misreading. Increased suppression ability as well as ribosomes that highly misread accumulate with kinetics expected for a constant differential rate of synthesis of a new product induced by drug action. The misreading ribosomes do not contain appreciable amounts of streptomycin and the misreading property is lost by exposure to high salt concentrations. It is suggested that streptomycin (or dihydrostreptomycin, or paromomycin) induces a reversible modification in 30S subunit assembly without physically participating in the modified structure. The extent of this modification appears dependent upon the strA allele.
噬菌体T4无义突变体的翻译渗漏（即非特异性抑制）在某些先前在链霉素存在下生长的链霉素抗性菌株的细胞中有所增加。与此同时，从这些在链霉素存在下生长的细胞中提取的核糖体具有高水平的错读。抑制能力的增强以及高度错读的核糖体以药物作用诱导的新产物恒定差异合成速率所预期的动力学积累。错读的核糖体不含可观量的链霉素，并且通过暴露于高盐浓度会丧失错读特性。有人提出链霉素（或双氢链霉素，或巴龙霉素）在不实际参与修饰结构的情况下诱导30S亚基组装的可逆修饰。这种修饰的程度似乎取决于strA等位基因。
