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构巢曲霉的suaC109和suaA101抑制因子在体外改变核糖体表型。

Suppressors suaC109 and suaA101 of Aspergillus nidulans alter the ribosomal phenotype in vitro.

作者信息

Zamir A, Martinelli S S

机构信息

Department of Biology, Birkbeck College, University of London.

出版信息

Biosci Rep. 1987 Dec;7(12):941-8. doi: 10.1007/BF01122127.

Abstract

A new homologous, cell-free system for protein synthesis has been devised for use with ribosomes and elongation factors from Aspergillus nidulans. Ribosome preparations from strains with either the suaA101 or suaC109 mutations have a higher misreading ratio (non-cognate:cognate amino acid incorporation) in the presence of hygromycin than controls. They can be classed as fidelity mutants. These results also prove that the mutations must be in genes coding for ribosomal proteins or enzymes which modify ribosomal proteins post-translationally. Alternatively, the genes could code for translation factors.

摘要

已设计出一种新的同源无细胞蛋白质合成系统,用于与构巢曲霉的核糖体和延伸因子配合使用。在潮霉素存在的情况下,具有suaA101或suaC109突变的菌株的核糖体制剂比对照具有更高的错读率(非同源:同源氨基酸掺入)。它们可被归类为保真度突变体。这些结果还证明,这些突变必定存在于编码核糖体蛋白的基因中,或者存在于翻译后修饰核糖体蛋白的酶的基因中。或者,这些基因可能编码翻译因子。

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