Aim-less translation: loss of Saccharomyces cerevisiae mitochondrial translation initiation factor mIF3/Aim23 leads to unbalanced protein synthesis.
Aim-less translation: loss of Saccharomyces cerevisiae mitochondrial translation initiation factor mIF3/Aim23 leads to unbalanced protein synthesis.
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DOI：
10.1038/srep18749
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发表时间：
2016-01-05
影响因子：
4.6
通讯作者：
Hauryliuk V
中科院分区：
文献类型：
--
作者：
Kuzmenko A;Derbikova K;Salvatori R;Tankov S;Atkinson GC;Tenson T;Ott M;Kamenski P;Hauryliuk V
线粒体基因组几乎专门编码氧化磷酸化（OXPHOS）系统的少数跨膜成分。这些基因的协调表达确保了系统组分的正确化学计量。线粒体中的翻译起始由两种通用起始因子mIF2和mIF3辅助，其在细菌中的直向同源物对于蛋白质合成和活力是不可或缺的。mIF3被认为是缺乏酿酒酵母，直到我们最近确定线粒体蛋白Aim23作为失踪的直系同源物。令人惊讶的是，在S.酿酒酵母不会不加选择地消除线粒体翻译，而是导致蛋白质生产的不平衡：F1F0 ATP合酶（复合物V）的Atp9亚基的合成速率增加，而细胞色素c氧化酶（复合物IV）的Cox1，Cox2和Cox3亚基的表达受到抑制。我们的研究结果提供了一个例子，线粒体翻译偏离其细菌起源。
The mitochondrial genome almost exclusively encodes a handful of transmembrane constituents of the oxidative phosphorylation (OXPHOS) system. Coordinated expression of these genes ensures the correct stoichiometry of the system’s components. Translation initiation in mitochondria is assisted by two general initiation factors mIF2 and mIF3, orthologues of which in bacteria are indispensible for protein synthesis and viability. mIF3 was thought to be absent in Saccharomyces cerevisiae until we recently identified mitochondrial protein Aim23 as the missing orthologue. Here we show that, surprisingly, loss of mIF3/Aim23 in S. cerevisiae does not indiscriminately abrogate mitochondrial translation but rather causes an imbalance in protein production: the rate of synthesis of the Atp9 subunit of F1F0 ATP synthase (complex V) is increased, while expression of Cox1, Cox2 and Cox3 subunits of cytochrome c oxidase (complex IV) is repressed. Our results provide one more example of deviation of mitochondrial translation from its bacterial origins.