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大肠杆菌K-12中的新型UGA抑制子

Novel UGA-suppressors in Escherichia coli K-12.

作者信息

Chang Z, Inokuchi H, Ozeki H

机构信息

Department of Biophysics, Faculty of Science, Kyoto University.

出版信息

Jpn J Genet. 1990 Apr;65(2):71-81. doi: 10.1266/jjg.65.71.

Abstract

UGA-specific nonsense suppressors from Escherichia coli K-12 were isolated and characterized. One of them (Su+UGA-11) was identified as a mutant of the prfB gene for the peptide releasing factor RF2. It appears that in this strain, while peptide release at sites of UGA mutations is retarded, the UGA stop codon is read through even in the absence of a tRNA suppressor, exhibiting a novel type of passive nonsense suppression. Three suppressors (Su+UGA-12, -16 and -34) were capable of restoring the streptomycin sensitive phenotype in resistant bacteria (strAr). Because of their drug-related phenotype, these are possibly mutations in the components of the ribosomal machinery, particularly those concerned with peptide release at UGA nonsense codons. A tRNA suppressor was also obtained which was derived from the tRNA(Trp) gene. In this strain, a long region between rrnC (84.5 min) and rrnB (89.5 min) was duplicated and one of the duplicated genes of tRNA(Trp) was mutated to the suppressor. The mechanism of UGA-suppression is discussed in terms of translation termination at the nonsense codon in both active and passive fashions.

摘要

从大肠杆菌K-12中分离并鉴定了UGA特异性无义抑制子。其中一个(Su + UGA-11)被鉴定为肽释放因子RF2的prfB基因突变体。在该菌株中,UGA突变位点处的肽释放似乎受到阻碍,然而即使在没有tRNA抑制子的情况下,UGA终止密码子也能被通读,表现出一种新型的被动无义抑制。三种抑制子(Su + UGA-12、-16和-34)能够恢复抗性细菌(strAr)中的链霉素敏感表型。由于它们与药物相关的表型,这些可能是核糖体机制组分中的突变,特别是那些与UGA无义密码子处的肽释放有关的组分。还获得了一种源自tRNA(Trp)基因的tRNA抑制子。在该菌株中,rrnC(84.5分钟)和rrnB(89.5分钟)之间的一个长区域发生了重复,并且tRNA(Trp)的一个重复基因突变为抑制子。从主动和被动方式在无义密码子处的翻译终止方面讨论了UGA抑制的机制。

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