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J. Biol. Chem., Vol. 280, Issue 16, 15659-15665, April 22, 2005

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Mitochondrial Initiation Factor 2 of Trypanosoma brucei Binds Imported Formylated Elongator-type tRNA^Met*

Fabien Charrière, Timothy H. P. Tan, and André Schneider¶

From the Department of Biology/Zoology, University of Fribourg, Chemin du Musée 10, CH-1700 Fribourg, Switzerland

The mitochondrion of Trypanosoma brucei lacks tRNA genes. Its translation system therefore depends on the import of nucleus-encoded tRNAs. Thus, except for the cytosol-specific initiator tRNA^Met, all trypanosomal tRNAs function in both the cytosol and the mitochondrion. The only tRNA^Met present in T. brucei mitochondria is therefore the one which, in the cytosol, is involved in translation elongation. Mitochondrial translation initiation depends on an initiator tRNA^Met carrying a formylated methionine. This tRNA is then recognized by initiation factor 2, which brings it to the ribosome. To guarantee mitochondrial translation initiation, T. brucei has an unusual methionyl-tRNA formyltransferase that formylates elongator tRNA^Met. In the present study, we have identified initiation factor 2 of T. brucei and shown that its carboxyl-terminal domain specifically binds formylated trypanosomal elongator tRNA^Met. Furthermore, the protein also recognizes the structurally very different Escherichia coli initiator tRNA^Met, suggesting that the main determinant recognized is the formylated methionine. In vivo studies using stable RNA interference cell lines showed that knock-down of initiation factor 2, depending on which construct was used, causes slow growth or even growth arrest. Moreover, concomitantly with ablation of the protein, a loss of oxidative phosphorylation was observed. Finally, although ablation of the methionyl-tRNA formyltransferase on its own did not impair growth, a complete growth arrest was observed when it was combined with the initiation factor 2 RNA interference cell line showing the slow growth phenotype. Thus, these experiments illustrate the importance of mitochondrial translation initiation for growth of procyclic T. brucei.

Received for publication, October 12, 2004 , and in revised form, February 23, 2005.

^* This study was supported by Grant 31–067906.02 from the Swiss National Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Both authors contributed equally to this work.

Present address: Institute of Molecular and Cell Biology, Singapore 117609.

^¶ To whom correspondence should be addressed: University of Fribourg, Chemin du Musée 10, CH-1700 Fribourg, Switzerland. Tel.: 41-26-3008877; Fax: 41-26-3009741; E-mail: andre.schneider{at}unifr.ch.

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