Mitochondrial Protein Synthesis Adapts to Influx of Nuclear-Encoded Protein

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...

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Bibliographic Details
Published in:Cell Vol. 167; no. 2; p. 471
Main Authors: Richter-Dennerlein, Ricarda, Oeljeklaus, Silke, Lorenzi, Isotta, Ronsör, Christin, Bareth, Bettina, Schendzielorz, Alexander Benjamin, Wang, Cong, Warscheid, Bettina, Rehling, Peter, Dennerlein, Sven
Format: Journal Article
Language:English
Published: United States 06.10.2016
Subjects:
Active Transport, Cell Nucleus
Cell Line, Tumor
Cyclooxygenase 1 - biosynthesis
Cyclooxygenase 1 - genetics
Cyclooxygenase 1 - metabolism
DNA, Mitochondrial - genetics
Electron Transport Complex IV - biosynthesis
Electron Transport Complex IV - genetics
Electron Transport Complex IV - metabolism
HEK293 Cells
Humans
Membrane Proteins - biosynthesis
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mitochondria - enzymology
Mitochondrial Proteins - biosynthesis
Mitochondrial Proteins - genetics
Mitochondrial Proteins - metabolism
Oxidative Phosphorylation
Ribosomes - metabolism
RNA, Messenger - biosynthesis
RNA, Messenger - genetics
RNA, Mitochondrial
mitochondrial translation
assembly
OXPHOS
C12ORF62
COX1
cytochrome c oxidase
translation regulation
mitochondrial ribosome
MITRAC
translational plasticity
ISSN:1097-4172, 1097-4172
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Summary: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.
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ISSN:1097-4172
1097-4172
DOI:10.1016/j.cell.2016.09.003