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.
- 1/biosynthesis/genetics/*metabolism,cytochrome
- active
- c
- cell
- cells,humans,membrane
- complex
- iv/biosynthesis/genetics/*metabolism,hek293
- line
- messenger/biosynthesis/genetics,rna
- mitochondrial,to_read,translation
- mitochondrial/genetics,electron
- nucleus,assembly,c12orf62,cell
- oxidase,dna
- phosphorylation,oxphos,ribosomes/metabolism,rna
- plasticity
- proteins/biosynthesis/genetics/*metabolism,mitochondria/*enzymology,mitochondrial
- proteins/biosynthesis/genetics/*metabolism,mitochondrial
- regulation,translational
- ribosome,mitochondrial
- translation,mitrac,oxidative
- transport
- tumor,cox1,cyclooxygenase
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