1. Mitochondrial Protein Synthesis Adapts to Influx of Nuclear-Encoded Protein
- Author
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Ricarda Richter-Dennerlein, Silke Oeljeklaus, Alexander Benjamin Schendzielorz, Bettina Bareth, Sven Dennerlein, Bettina Warscheid, Peter Rehling, Christin Ronsör, Cong Wang, and Isotta Lorenzi
- Subjects
assembly ,0301 basic medicine ,Nuclear-Encoded Protein ,Mitochondrial Protein Synthesis ,mitochondrial ribosome ,Mitochondrial translation ,RNA, Mitochondrial ,Active Transport, Cell Nucleus ,translation regulation ,Mitochondrion ,Biology ,mitochondrial translation ,Ribosome ,DNA, Mitochondrial ,General Biochemistry, Genetics and Molecular Biology ,Oxidative Phosphorylation ,Electron Transport Complex IV ,Mitochondrial Proteins ,03 medical and health sciences ,0302 clinical medicine ,cytochrome c oxidase ,Cell Line, Tumor ,Translational regulation ,Mitochondrial ribosome ,Cytochrome c oxidase ,Humans ,RNA, Messenger ,Biochemistry, Genetics and Molecular Biology(all) ,C12ORF62 ,Membrane Proteins ,Translation (biology) ,MITRAC ,OXPHOS ,Mitochondria ,030104 developmental biology ,HEK293 Cells ,Biochemistry ,biology.protein ,Cyclooxygenase 1 ,ATP–ADP translocase ,translational plasticity ,Ribosomes ,030217 neurology & neurosurgery ,COX1 - Abstract
Mitochondrial ribosomes translate membrane integral core subunits of the oxidative phosphorylation system encoded by mtDNA. These translation products associate with nuclear-encoded, imported proteins to form enzyme complexes that produce ATP. Here, we show that human mitochondrial ribosomes display translational plasticity to cope with the supply of imported nuclear-encoded subunits. Ribosomes expressing mitochondrial-encoded COX1 mRNA selectively engage with cytochrome c oxidase assembly factors in the inner membrane. Assembly defects of the cytochrome c oxidase arrest mitochondrial translation in a ribosome nascent chain complex with a partially membrane-inserted COX1 translation product. This complex represents a primed state of the translation product that can be retrieved for assembly. These findings establish a mammalian translational plasticity pathway in mitochondria that enables adaptation of mitochondrial protein synthesis to the influx of nuclear-encoded subunits. peerReviewed
- Published
- 2016