Functional interactions among two yeast mitochondrial ribosomal proteins and an mRNA-specific translational activator.
Functional interactions among two yeast mitochondrial ribosomal proteins and an mRNA-specific translational activator.
复制标题
两种酵母线粒体核糖体蛋白和 mRNA 特异性翻译激活剂之间的功能相互作用。
DOI：
10.1093/genetics/127.2.319
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发表时间：
1991
期刊：
影响因子：
3.3
通讯作者：
Fox,TD
中科院分区：
文献类型：
--
作者：
Haffter,P;McMullin,TW;Fox,TD
编码细胞色素c氧化酶亚基III的酵母线粒体基因在翻译水平上被至少三个核基因（PET122、PET494和PET54）特异性激活。我们之前已经证明，PET122的羧基端缺失被一个称为PET123的非连锁核基因的突变特异性抑制，该基因编码一个小亚基核糖体蛋白。在这里，我们描述了由第二个基因突变产生的额外的pet122抑制子，我们证明了这个基因是先前鉴定的核基因MRP1。像PET123一样，MRP1编码线粒体核糖体小亚基的一个组成部分。我们的mrp1突变是PET122蛋白羧基末端截断的等位基因特异性抑制因子，并且不绕过PET122对剩余功能的要求。我们的mrp1突变在其他野生型背景中都没有内在表型。然而，一些mrp1突变与某些pet123等位基因结合会导致非条件呼吸缺陷表型。这种合成缺陷表型表明核糖体蛋白PET123和MRP1在功能上相互作用。它们都可以突变抑制mRNA特异性翻译激活子PET122的某些等位基因，这一事实强烈表明PET122蛋白通过与线粒体核糖体小亚基的相互作用促进coxIII mRNA的翻译。
Expression of the Saccharomyces cerevisiae mitochondrial gene coding cytochrome c oxidase subunit III is specifically activated at the level of translation by at least three nuclear genes, PET122, PET494 and PET54. We have shown previously that carboxy-terminal deletions of PET122 are allele-specifically suppressed by mutations in an unlinked nuclear gene, termed PET123, that encodes a small subunit ribosomal protein. Here we describe additional pet122 suppressors generated by mutations in a second gene which we show to be the previously identified nuclear gene MRP1. Like PET123, MRP1 encodes a component of the small subunit of mitochondrial ribosomes. Our mrp1 mutations are allele-specific suppressors of carboxyl-terminal truncations of the PET122 protein and do not bypass the requirement for residual function of PET122. None of our mrp1 mutations has an intrinsic phenotype in an otherwise wild-type background. However, some of the mrp1 mutations cause a non-conditional respiratory-defective phenotype in combination with certain pet123 alleles. This synthetic defective phenotype suggests that the ribosomal proteins PET123 and MRP1 interact functionally with each other. The fact that they can both mutate to suppress certain alleles of the mRNA-specific translational activator PET122 strongly suggests that the PET122 protein promotes translation of the coxIII mRNA via an interaction with the small subunit of mitochondrial ribosomes.