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Mitochondrial translation factors reflect coordination between organelles and cytoplasmic translation via mTOR signaling: Implication in disease
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 c...
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Published in: | Free radical biology & medicine 2016-11, Vol.100, p.231-237 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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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•mtEF4 is an elongation factor regulating tRNA translocation in mitoribosome.•Activators, mitomiRs and MITRAC are direct regulators of mt-translation machinery.•Mitochondrial and cytoplasmic translations are coordinated via mTOR signaling.•Mitochondrial translation (regulatory) factors defects induce various human diseases. |
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ISSN: | 0891-5849 1873-4596 |
DOI: | 10.1016/j.freeradbiomed.2016.04.010 |