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C400572200v1
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Papers In Press, published online ahead of print December 24, 2004
J. Biol. Chem, 10.1074/jbc.C400572200
Submitted on December 10, 2004
Revised on December 23, 2004
Accepted on December 24, 2004

Correction of translational defects in patient-derived mutant mitochondria by complex-mediated import of a cytoplasmic tRNA

Bidesh Mahata, Suvendra Nath Bhattacharyya, Saikat Mukherjee, and Samit Adhya

Department of Genetic Engineering, Indian Institute of Chemical Biology, Calcutta 700032

Corresponding Author: sadhya{at}iicb.res.in

A variety of clinical disorders result from mutations in mitochondrial tRNA genes, leading to transaltional defects. We show here that a protein complex from the kinetoplastid protozoon Leishmania induces specific, ATP-dependent import of human cytoplasmic tRNALys1 into human mitochondria in vitro. The imported tRNA undergoes efficient aminoacylation within the organelle and supports organellar protein synthesis. Moreover, translation in mitochondria from patients with Myclonic Epilepsy with Ragged Red Fibers (MERRF) and Kearns-Sayre Syndrome (KSS), containing mutant tRNALys genes, is stimulated to near-wild type levels, and the formation of aberrant polypeptides suppressed, by complex-mediated import. These results suggest a novel way to introduce RNAs for the modulation of mitochondrial gene expression.


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