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Journal Article

MTERF4 regulates translation by targeting the methyltransferase NSUN4 to the mammalian mitochondrial ribosome

MPS-Authors
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Metodiev,  M.D.
Department Partridge - Biological Mechanisms of Ageing, Max Planck Institute for Biology of Ageing, Max Planck Society;

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Ruzzenente,  B.
Department Larsson - Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Max Planck Society;

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Kukat,  C.
FACS & Imaging, Core Facilities, Max Planck Institute for Biology of Ageing, Max Planck Society;

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Habermann,  B.H.
Dieterich – Computational RNA Biology and Ageing, Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society;

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Franz,  T.
Max Planck Institute for Biology of Ageing, Max Planck Society;

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Larsson,  N.G.
Department Larsson - Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Max Planck Society;

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http://www.ncbi.nlm.nih.gov/pubmed/21531335
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Citation

Camara, Y., Asin-Cayuela, J., Park, C. B., Metodiev, M., Shi, Y., Ruzzenente, B., et al. (2011). MTERF4 regulates translation by targeting the methyltransferase NSUN4 to the mammalian mitochondrial ribosome. Cell Metab, 13(5), 527-39. doi:10.1016/j.cmet.2011.04.002.


Cite as: https://hdl.handle.net/21.11116/0000-000B-A957-5
Abstract
Precise control of mitochondrial DNA gene expression is critical for regulation of oxidative phosphorylation capacity in mammals. The MTERF protein family plays a key role in this process, and its members have been implicated in regulation of transcription initiation and site-specific transcription termination. We now demonstrate that a member of this family, MTERF4, directly controls mitochondrial ribosomal biogenesis and translation. MTERF4 forms a stoichiometric complex with the ribosomal RNA methyltransferase NSUN4 and is necessary for recruitment of this factor to the large ribosomal subunit. Loss of MTERF4 leads to defective ribosomal assembly and a drastic reduction in translation. Our results thus show that MTERF4 is an important regulator of translation in mammalian mitochondria.