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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
REVIEW
Mitochondrial translation factors reflect coordination between organelles and cytoplasmic translation via mTOR signaling: Implication in disease.
Free Radical Biology & Medicine 2016 November
Mitochondria are semi-autonomous organelle possessing their own translation machinery to biosynthesize mitochondrial DNA (mtDNA)-encoded polypeptides, which are the core subunits of oxidative phosphorylation (OXPHOS) complexes. Mitochondrial translation elongation factor 4 (mtEF4) is a key quality control factor in mitochondrial translation (mt-translation) that regulates mitochondrial tRNA translocation and modulates cellular responses by influencing cytoplasmic translation (ct-translation). In addition to mtEF4, mt-translational activators, mitochondrial microRNAs (mitomiRs), and MITRAC have been reported recently as crucial mt-translation regulators. Here, we focus on the novel ways how these factors regulate mt-translation, discuss the main cellular response of mammalian target of rapamycin (mTOR) signalling upon mt-translation defects, and summarize the related human diseases.
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