van Buul C P, Visser W, van Knippenberg P H
FEBS Lett. 1984 Nov 5;177(1):119-24. doi: 10.1016/0014-5793(84)80994-1.
The aminoglycoside kasugamycin, which has previously been shown to inhibit initiation of protein biosynthesis in vitro, also affects translational accuracy in vitro. This is deduced from the observation that the drug decreases the incorporation of histidine relative to alanine into the coat protein of phage MS2, the gene of which is devoid of histidine codons. The read-through of the MS2 coat cistron, due to frameshifts in vitro, is also suppressed by the antibiotic. In contrast, streptomycin enhances histidine incorporation and read-through in this system. The effects of kasugamycin take place at concentrations that do not inhibit coat protein biosynthesis. Kasugamycin-resistant mutants (ksgA) lacking dimethylation of two adjacent adenosines in 16 S ribosomal RNA, show an increased leakiness of nonsense and frameshift mutants (in the absence of antibiotic). They are therefore phenotypically similar to previously described ribosomal ambiguity mutants (ram).
氨基糖苷类春日霉素先前已被证明在体外可抑制蛋白质生物合成的起始，它在体外也会影响翻译准确性。这是从以下观察结果推断出来的：该药物会降低相对于丙氨酸的组氨酸掺入噬菌体MS2外壳蛋白中的量，其基因不含组氨酸密码子。由于体外移码导致的MS2外壳顺反子的通读也受到该抗生素的抑制。相比之下，链霉素会增强该系统中组氨酸的掺入和通读。春日霉素的作用发生在不抑制外壳蛋白生物合成的浓度下。缺乏16S核糖体RNA中两个相邻腺苷二甲基化的春日霉素抗性突变体（ksgA），在无抗生素的情况下，无义突变体和移码突变体的渗漏增加。因此，它们在表型上与先前描述的核糖体模糊突变体（ram）相似。
