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Journal Article

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

MPS-Authors

Camara,  Y.
Max Planck Society;

Asin-Cayuela,  J.
Max Planck Society;

Park,  C. B.
Max Planck Society;

Metodiev,  M. D.
Max Planck Society;

Shi,  Y.
Max Planck Society;

Ruzzenente,  B.
Max Planck Society;

Kukat,  C.
Max Planck Society;

Habermann,  B.
Max Planck Society;

Wibom,  R.
Max Planck Society;

Hultenby,  K.
Max Planck Society;

Franz,  T.
Max Planck Society;

Erdjument-Bromage,  H.
Max Planck Society;

Tempst,  P.
Max Planck Society;

Hallberg,  B. M.
Max Planck Society;

Gustafsson,  C. M.
Max Planck Society;

Larsson,  N. G.
Max Planck Society;

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Citation

Camara, Y., Asin-Cayuela, J., Park, C. B., Metodiev, M. D., 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: http://hdl.handle.net/11858/00-001M-0000-0028-58AE-7
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.