M.V. Lomonosov Moscow State University, Faculty of Biology, 119234 Moscow, Russia.
M.V. Lomonosov Moscow State University, Institute of Functional Genomics, 119234 Moscow, Russia.
Cells. 2019 Jun 26;8(7):645. doi: 10.3390/cells8070645.
After billions of years of evolution, mitochondrion retains its own genome, which gets expressed in mitochondrial matrix. Mitochondrial translation machinery rather differs from modern bacterial and eukaryotic cytosolic systems. Any disturbance in mitochondrial translation drastically impairs mitochondrial function. In budding yeast , deletion of the gene coding for mitochondrial translation initiation factor 3 - , leads to an imbalance in mitochondrial protein synthesis and significantly delays growth after shifting from fermentable to non-fermentable carbon sources. Molecular mechanism underlying this adaptation to respiratory growth was unknown. Here, we demonstrate that slow adaptation from glycolysis to respiration in the absence of Aim23p is accompanied by a gradual increase of cytochrome c oxidase activity and by increased levels of Tma19p protein, which protects mitochondria from oxidative stress.
经过数十亿年的进化，线粒体保留了自己的基因组，该基因组在线粒体基质中表达。线粒体翻译机制与现代细菌和真核细胞质系统有很大的不同。线粒体翻译的任何干扰都会严重损害线粒体的功能。在 budding yeast 中，删除编码线粒体翻译起始因子 3 的基因会导致线粒体蛋白合成失衡，并在从可发酵碳源转换到不可发酵碳源后显著延迟生长。这种对呼吸生长的适应的分子机制尚不清楚。在这里，我们证明了在没有 Aim23p 的情况下，从糖酵解到呼吸的缓慢适应伴随着细胞色素 c 氧化酶活性的逐渐增加和 Tma19p 蛋白水平的升高，该蛋白可保护线粒体免受氧化应激。
