Functional interactions between yeast mitochondrial ribosomes and mRNA 5′ untranslated leaders
Functional interactions between yeast mitochondrial ribosomes and mRNA 5′ untranslated leaders
复制标题
DOI：
10.1128/mcb.18.4.1826
复制
发表时间：
1998-04-01
影响因子：
5.3
通讯作者：
Costanzo, MC
中科院分区：
文献类型：
--
作者：
Green-Willms, NS;Fox, TD;Costanzo, MC
酿酒酵母线粒体mRNAs的翻译依赖于识别其目标mRNAs的5‘未翻译前导(5’-UTL)的mRNA特异性翻译激活子。我们已经发现了两个新的核基因的突变，这两个新的核基因由于COX2和COX3 mRNAs的5‘-UTL的某些改变而抑制了翻译缺陷，表明了翻译激活的一般功能，LEAN基因MRP21编码一个与细菌核糖体蛋白S21相关的蛋白和几种动物的未知蛋白，另一个基因MRP51编码一个新的蛋白，其唯一已知的同源基因是由Kluyveri中的一个未知基因编码的。MRP21或MRP51的缺失完全阻断了线粒体基因的表达。亚线粒体分离表明，mrp21p和mrp51p都与线粒体核糖体小亚基共生，抑制突变是错义替换，而影响mrp21p的突变改变了与大肠杆菌S21同源的区域，已知该区域与mRNAs相互作用。抑制子突变和线粒体起始密码子泄漏突变的相互作用强烈表明，抑制子通常不会提高翻译效率，因为一些强烈抑制5‘-UTL突变的等位基因无法抑制起始密码子突变。我们认为线粒体核糖体本身识别mRNA5‘-UTL的一个共同特征，这与mRNA特异性翻译激活一起，是细胞器翻译启动所必需的。
Translation of mitochondrial mRNAs in Saccharomyces cerevisiae depends on mRNA-specific translational activators that recognize the 5' untranslated leaders (5'-UTLs) of their target mRNAs. We have identified mutations in two new nuclear genes that suppress translation defects due to certain alterations in the 5'-UTLs of both the COX2 and COX3 mRNAs, indicating a general function in translational activation, lane gene, MRP21, encodes a protein with a domain related to the bacterial ribosomal protein S21 and to unidentified proteins of several animals, The other gene, MRP51, encodes a novel protein whose only known homolog is encoded by an unidentified gene in S. kluyveri. Deletion of either MRP21 or MRP51 completely blocked mitochondrial gene expression. Submitochondrial fractionation showed that both Mrp21p and Mrp51p cosediment with the mitochondrial ribosomal small subunit, That suppressor mutations are missense substitutions, and those affecting Mrp21p alter the region homologous to E. coli S21, which is known to interact with mRNAs. Interactions of the suppressor mutations with leaky mitochondrial initiation codon mutations strongly suggest that the suppressors do not generally increase translational efficiency, since some alleles that strongly suppress 5'-UTL mutations fail to suppress initiation codon mutations. We propose that mitochondrial ribosomes themselves recognize a common feature of mRNA 5'-UTLs which, in conjunction with mRNA-specific translational activation, is required for organellar translation initiation.