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Metodiev, Metodi D.,Lesko, Nicole,Park, Chan Bae,Cá,mara, Yolanda,Shi, Yonghong,Wibom, Rolf,Hultenby, Kjell,Gustafsson, Claes M.,Larsson, Nils-Gö,ran Elsevier 2009 Cell metabolism Vol.9 No.4
<P><B>Summary</B></P><P>The 3′ end of the rRNA of the small ribosomal subunit contains two extremely highly conserved dimethylated adenines. This modification and the responsible methyltransferases are present in all three domains of life, but its function has remained elusive. We have disrupted the mouse <I>Tfb1m</I> gene encoding a mitochondrial protein homologous to bacterial dimethyltransferases and demonstrate here that loss of TFB1M is embryonic lethal. Disruption of <I>Tfb1m</I> in heart leads to complete loss of adenine dimethylation of the rRNA of the small mitochondrial ribosomal subunit, impaired assembly of the mitochondrial ribosome, and abolished mitochondrial translation. In addition, we present biochemical evidence that TFB1M does not activate or repress transcription in the presence of TFB2M. Our results thus show that TFB1M is a nonredundant dimethyltransferase in mammalian mitochondria. In addition, we provide a possible explanation for the universal conservation of adenine dimethylation of rRNA by showing a critical role in ribosome maintenance.</P>
Cá,mara, Yolanda,Asin-Cayuela, Jorge,Park, Chan ,Bae,Metodiev, Metodi ,D.,Shi, Yonghong,Ruzzenente, Benedetta,Kukat, Christian,Habermann, Bianca,Wibom, Rolf,Hultenby, Kjell,Franz, Thomas Elsevier 2011 Cell metabolism Vol.13 No.5
<P><B>Summary</B></P><P>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.</P> <P><B>Highlights</B></P><P>► Loss of MTERF4 leads to abolished mitochondrial translation ► MTERF4 forms a complex with the rRNA methyltransferase NSUN4 ► MTERF4 targets NSUN4 to the mitochondrial large ribosomal subunit</P>