A genetic link between an mRNA-specific translational activator and the translation system in yeast mitochondria.

A genetic link between an mRNA-specific translational activator and the translation system in yeast mitochondria.
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酵母线粒体中 mRNA 特异性翻译激活剂和翻译系统之间的遗传联系。

DOI:
10.1093/genetics/125.3.495
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发表时间:
1990
期刊:
影响因子:
3.3
通讯作者:
Fox,TD
Fox,TD
中科院分区:
生物学2区
文献类型:
--
作者:
Haffter,P;McMullin,TW;Fox,TD

文献摘要

被引文献

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编码细胞色素c氧化酶亚基III (coxIII)的Saccharomyces cerevisiae线粒体mRNA的翻译需要至少三个核基因PET122、PET494和PET54的产物。从基因产物的羧基端去除24-67个氨基酸残基的Pet122突变被发现受到非连锁核突变的抑制。这些非连锁抑制子不能抑制pet122错义突变和pet122完全缺失。其中一种抑制突变在野生型菌株中引起热敏感的非呼吸生长表型,并减少在高温下生长的细胞中所有线粒体基因产物的翻译。该抑制基因定位于XV染色体上一个新发现的基因PET123。携带PET123的DNA片段序列包含一个主要的开放阅读框,编码318个氨基酸的基本蛋白。通过中断这个开放阅读框,使PET123染色体副本失活,导致细胞变成rho(-)(在它们的mtDNA中维持大量缺失)。这种表型的特征是基因的零等位基因,其产物是一般线粒体蛋白质合成所必需的。因此,我们的数据强烈表明,PET123蛋白是线粒体翻译装置的一个组成部分,直接与coxiii - mrna特异性翻译激活子PET122相互作用。
Translation of the Saccharomyces cerevisiae mitochondrial mRNA encoding cytochrome c oxidase subunit III (coxIII) specifically requires the products of at least three nuclear genes, PET122, PET494 and PET54. pet122 mutations that remove 24-67 amino acid residues from the carboxyterminus of the gene product were found to be suppressed by unlinked nuclear mutations. These unlinked suppressors fail to suppress both a pet122 missense mutation and a complete pet122 deletion. One of the suppressor mutations causes a heat-sensitive nonrespiratory growth phenotype in an otherwise wild-type strain and reduces translation of all mitochondrial gene products in cells grown at high temperature. This suppressor maps to a newly identified gene on chromosome XV termed PET123. The sequence of a DNA fragment carrying PET123 contains one major open reading frame encoding a basic protein of 318 amino acids. Inactivation of the chromosomal copy of PET123 by interruption of this open reading frame causes cells to become rho(-) (sustain large deletions in their mtDNA). This phenotype is characteristic for null alleles of genes whose products are essential for general mitochondrial protein synthesis. Thus our data strongly suggest that the PET123 protein is a component of the mitochondrial translation apparatus that interacts directly with the coxIII-mRNA-specific translational activator PET122.