期刊
CELL
卷 167, 期 2, 页码 471-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2016.09.003
关键词
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资金
- Deutsche Forschungsgemeinschaft [SFB860]
- ERC [ERCAdG 339580]
- BIOSS
- MWK FoP [88b]
- Max Planck Society
- GGNB [EXC 294]
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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