Asatryan L S, Spirin A S
Mol Gen Genet. 1975 Jul 10;138(4):315-21. doi: 10.1007/BF00264801.
The capablity of ribosomes of four types of streptomycin-resistant mutants (A1, A2, A40 and A60) for non-enzymatic (EF-G--GTP-independent) translocation was tested. It was found that an A40 type mutation (amino acid replacement in position 87 of the protein S12 polypeptide chain) leads to activation of the capablity of the ribosome to perform spontaneous non-enzymatic translocation, while type A1, A2 and A60 mutations (amino acid replacements in position 42 of protein S12) does not give such an effect. Thus, it is shown that non-enzymatic translocation can be activated not only by the earlier described damage of the protein S12 by para-chloromercuribenzoate or by the complete removal of protein S12, but also by a definate mutational alteration of the protein. Preliminary data are also reported on the possibility of activating non-enzymatic translocation by combinations of mutational alterations of the ribosomal proteins other than protein S12 but interdepending with it (such as S4 and S5).
对四种抗链霉素突变体(A1、A2、A40和A60)核糖体进行非酶促(不依赖EF - G - GTP)转位能力的测试。发现A40型突变(蛋白质S12多肽链第87位氨基酸替换)导致核糖体进行自发非酶促转位的能力激活,而A1、A2和A60型突变(蛋白质S12第42位氨基酸替换)未产生这种效应。因此,表明非酶促转位不仅可被先前描述的对氯汞苯甲酸对蛋白质S12的损伤或蛋白质S12的完全去除激活,还可被蛋白质的特定突变改变激活。还报告了关于除蛋白质S12外但与之相互依赖的核糖体蛋白质(如S4和S5)的突变改变组合激活非酶促转位可能性的初步数据。