一种新的核糖体蛋白的突变影响的功能变异RF1 S4。
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达利,Ryden-Aulin M
一种新的核糖体蛋白的突变影响的功能变异RF1 S4。
Biochimie。2000年8月,82 (8):683 - 91。
- PubMed ID
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11018284 (在PubMed]
- 文摘
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释放的因素(RF) 1和2触发的肽的水解peptidyl-tRNA期间翻译终止。RF1与核糖体结合反应停止密码子UAG和UAA而RF2承认UAA和佐治亚大学。RF1和RF2显示绑定到几个核糖体蛋白质。prfA1,研究这种交互体内突变形式的RF1一直使用。prfA1突变的菌株是温度敏感(Ts)的增长在42摄氏度,显示了一个增加UAG和UAA的误读。在这个工作我们显示一个点突变核糖体蛋白S4,一方面,使RF1突变株Ts (+);另一方面,这种突变会增加UAG的误读,但不是UAA prfA1所致。rpsD101 S4突变等位基因,是一个错义突变(Tyr51 Asp),这使得细胞冷敏感。rpsD101的行为比较研究S4等位基因rpsD12, rpsD14, rpsD16。这三个突变都赋予Ts(44摄氏度)表型和核糖体歧义表型,rpsD101不。 The three alleles were sequenced and shown to be truncations of the S4 protein. None of the three mutations could compensate for the Ts phenotype caused by the prfA1 mutation. Hence, rpsD101 differs in all studied characteristics from the three above mentioned S4 mutants. Because rpsD101 can compensate for the Ts phenotype caused by prfA1 but enhances the misreading of UAG and not UAA, we suggest that S4 influences the interaction of RF1 with the decoding center of the ribosome and that the Ts phenotype is not a consequence of increased readthrough.