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首页> 外文期刊>Molecular and Cellular Biology >Suppression of a defect in the 5' untranslated leader of mitochondrial COX3 mRNA by a mutation affecting an mRNA-specific translational activator protein.
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Suppression of a defect in the 5' untranslated leader of mitochondrial COX3 mRNA by a mutation affecting an mRNA-specific translational activator protein.

机译：通过影响mRNA特异性翻译激活蛋白的突变，抑制线粒体COX3 mRNA 5'非翻译前导序列的缺陷。

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摘要

Translation of the Saccharomyces cerevisiae mitochondrial COX3 mRNA, encoding subunit III of cytochrome c oxidase, specifically requires the action of the nuclear gene products PET54, PET122, and PET494 at a site encoded in the 612-base 5' untranslated leader. To identify more precisely the site of action of the translational activators, we constructed two large deletions of the COX3 mRNA 5' untranslated leader. Both deletions blocked translation without affecting mRNA stability. However, one of the large deletions was able to revert to partial function by a small secondary deletion within the remaining 5' leader sequences. Translation of the resulting mutant (cox3-15) mRNA was still dependent on the nuclear-encoded specific activators but was cold sensitive. We selected revertants of this mitochondrial mutant at low temperature to identify genes encoding proteins that might interact with the COX3 mRNA 5' leader. One such revertant carried a missense mutation in the PET122 gene that was a strong and dominant suppressor of the cold-sensitive defect in the mRNA, indicating that the PET122 protein interacts functionally (possibly directly) with the COX3 mRNA 5' leader. The cox3-15 mutation was not suppressed by overproduction of the wild-type PET122 protein but was very weakly suppressed by overproduction of PET494 and slightly better suppressed by co-overproduction of PET494 and PET122.
机译：酿酒酵母线粒体COX3 mRNA的编码细胞色素C氧化酶的亚基III的翻译特别需要核基因产物PET54，PET122和PET494在612位碱基的5'非翻译前导序列中编码的位点起作用。为了更准确地确定翻译激活剂的作用位点，我们构建了COX3 mRNA 5'非翻译前导序列的两个大缺失。两种缺失均阻止翻译而不影响mRNA的稳定性。然而，大的缺失之一能够通过在剩余的5'前导序列内的小的二次缺失而恢复为部分功能。产生的突变体（cox3-15）mRNA的翻译仍然依赖于核编码的特定激活剂，但对冷敏感。我们在低温下选择了该线粒体突变体的回复体，以鉴定编码可能与COX3 mRNA 5'前导序列相互作用的蛋白质的基因。一种这样的回复株在PET122基因中携带了一个错义突变，该突变是mRNA的冷敏感缺陷的强力和主要抑制因子，表明PET122蛋白在功能上（可能直接）与COX3 mRNA 5'前导分子相互作用。野生型PET122蛋白的过量生产并不能抑制cox3-15突变，而PET494的过量生产则可以非常弱地抑制cox3-15突变，而PET494和PET122的共同过量生产则可以更好地抑制cox3-15突变。

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