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核仁蛋白Tma23和Nop6中的突变可抑制Nep1蛋白的功能异常。

Mutations in the nucleolar proteins Tma23 and Nop6 suppress the malfunction of the Nep1 protein.

作者信息

Buchhaupt Markus, Kötter Peter, Entian Karl-Dieter

机构信息

Center of Excellence, Macromolecular Complexes, Institute of Molecular Biosciences, Johann Wolfgang Goethe-University, Frankfurt, Germany.

出版信息

FEMS Yeast Res. 2007 Sep;7(6):771-81. doi: 10.1111/j.1567-1364.2007.00230.x. Epub 2007 Apr 10.

Abstract

The nucleolar Saccharomyces cerevisiae protein Nep1 was previously shown to bind to a specific site of the 18S rRNA and to be involved in assembly of Rps19p into pre-40S ribosome subunits. Here we report on the identification of tma23 and nop6 mutations as recessive suppressors of a nep1(ts) mutant allele and the nep1 deletion as well. Green fluorescent protein fusions localized Tma23p and Nop6p within the nucleolus, indicating their function in ribosome biogenesis. The high lysine content of both proteins and an RNA binding motif in the Nop6p amino acid sequence suggest RNA-binding functions for both factors. Surprisingly, in contrast to Nep1p, Tma23p and Nop6p seem to be specific for fungi as no homologues could be found in higher eukaryotes. In contrast to most other ribosome biogenesis factors, Tma23p and Nop6p are nonessential in S. cerevisiae. Interestingly, the tma23 mutants showed a considerably increased resistance against the aminoglycoside G418, probably due to a structural change in the 40S ribosomal subunit, which could be the result of incorrectly folded 18S rRNA gene, missing rRNA modifications or the lack of a ribosomal protein.

摘要

酿酒酵母的核仁蛋白Nep1先前已被证明可与18S rRNA的特定位点结合,并参与Rps19p组装到40S核糖体亚基前体中。在此,我们报告了tma23和nop6突变作为nep1(ts)突变等位基因以及nep1缺失的隐性抑制子的鉴定结果。绿色荧光蛋白融合物将Tma23p和Nop6p定位在核仁内,表明它们在核糖体生物发生中的功能。这两种蛋白质的高赖氨酸含量以及Nop6p氨基酸序列中的RNA结合基序表明这两种因子都具有RNA结合功能。令人惊讶的是,与Nep1p不同,Tma23p和Nop6p似乎是真菌特有的,因为在高等真核生物中未发现同源物。与大多数其他核糖体生物发生因子不同,Tma23p和Nop6p在酿酒酵母中并非必需。有趣的是,tma23突变体对氨基糖苷类G418的抗性显著增加,这可能是由于40S核糖体亚基的结构变化,这可能是18S rRNA基因折叠错误、缺少rRNA修饰或缺乏核糖体蛋白的结果。

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