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[大肠杆菌核糖体蛋白S1基因中的突变ssF29,抑制跨膜蛋白转运缺陷是由IS10R元件插入所致]

[Mutation ssF29 in the gene for E. coli ribosomal protein S1, suppressing a defect in transmembrane protein transport results from insertion of the IS10R element].

作者信息

Artamonova V S, Boni I V

出版信息

Bioorg Khim. 1996 Dec;22(12):941-3.

PMID:9054345
Abstract

The nature of the ssyF29 mutation causing the synthesis of a truncated form of the ribosomal protein S1 and its location in the rpsA gene were determined. The ssyF mutation was found to result from insertion of the IS10(R) element which causes the termination of translation of the corresponding mRNA at the first insertion nucleotide and the production of the S1 protein which is truncated at the C-terminus and composed of 464 amino acid residues (instead of 557 residues in the wild-type protein). The mutant rpsA gene (ssyF) encodes no additional amino acid residues as compared with the wild-type rpsA gene.

摘要

确定了导致核糖体蛋白S1截短形式合成的ssyF29突变的性质及其在rpsA基因中的位置。发现ssyF突变是由IS10(R)元件插入引起的,该元件导致相应mRNA在第一个插入核苷酸处翻译终止,并产生在C末端截短且由464个氨基酸残基组成的S1蛋白(而野生型蛋白为557个残基)。与野生型rpsA基因相比,突变的rpsA基因(ssyF)不编码额外的氨基酸残基。

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