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5'-非翻译前导区的一个点突变,影响线粒体COX3 mRNA的翻译激活。

A point mutation in the 5'-untranslated leader that affects translational activation of the mitochondrial COX3 mRNA.

作者信息

Costanzo M C, Fox T D

机构信息

Section of Genetics and Development, Cornell University, Ithaca, NY 14853-2703, USA.

出版信息

Curr Genet. 1995 Jun;28(1):60-6. doi: 10.1007/BF00311882.

Abstract

The 613-base 5'-untranslated leader (5'-UTL) of the Saccharomyces cerevisiae mitochondrial COX3 mRNA contains the target of an mRNA-specific translational activator complex composed of at least three nuclearly encoded proteins. We have genetically mapped a collection of cox3 point mutations, using a set of defined COX3 deletions, and found one to be located in the region coding the 5'-UTL. The strain carrying this allele was specifically defective in translation of the COX3 mRNA. Nucleotide-sequence analysis showed that the allele was in fact a double mutation comprised of a single-base insertion in the 5'-UTL (T inserted between bases -428 and -427 with respect to the start of translation) and a G to A substitution at +3 that changed the ATG initiation codon to ATA. Both mutations were required to block translation completely. The effects of the ATG to ATA mutation alone (cox3-1) had previously been analyzed in this laboratory: it reduces, but does not eliminate, translation, causing a slow respiratory growth phenotype. The T insertion in the 5'-UTL had no detectable respiratory growth phenotype as a single mutation. However, the 5'-UTL insertion mutation enhanced the respiratory defective phenotype of missense mutations in pet54, one of the COX3-specific translational-activator genes. This phenotypic enhancement suggests that the -400 region of the 5'-UTL, where the mutation is located, is important for Pet54p-COX3 mRNA interaction.

摘要

酿酒酵母线粒体COX3 mRNA的613个碱基的5'-非翻译前导序列(5'-UTL)包含一种由至少三种核编码蛋白组成的mRNA特异性翻译激活复合物的作用靶点。我们利用一组确定的COX3缺失突变,对一系列cox3点突变进行了遗传定位,发现其中一个位于编码5'-UTL的区域。携带该等位基因的菌株在COX3 mRNA的翻译方面存在特异性缺陷。核苷酸序列分析表明,该等位基因实际上是一个双重突变,由5'-UTL中的一个单碱基插入(相对于翻译起始位点,T插入在-428和-427碱基之间)和+3处的G到A替换组成,该替换将ATG起始密码子变为ATA。这两个突变都是完全阻断翻译所必需的。此前本实验室已分析过单独的ATG到ATA突变(cox3-1)的影响:它会降低但不会消除翻译,导致呼吸生长缓慢的表型。5'-UTL中的T插入作为单一突变没有可检测到的呼吸生长表型。然而,5'-UTL插入突变增强了pet54(COX3特异性翻译激活基因之一)错义突变的呼吸缺陷表型。这种表型增强表明,突变所在的5'-UTL的-400区域对于Pet54p与COX3 mRNA的相互作用很重要。

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