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Nucleic Acids Research Advance Access published online on September 9, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn576
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© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

The human mitochondrial ribosome recycling factor is essential for cell viability

Joanna Rorbach1, Ricarda Richter1, Hans J. Wessels2, Mateusz Wydro1, Marcin Pekalski3, Murtada Farhoud2, Inge Kühl4, Mauricette Gaisne4, Nathalie Bonnefoy4, Jan A. Smeitink2, Robert N. Lightowlers1,* and Zofia M.A. Chrzanowska-Lightowlers1

1Mitochondrial Research Group, Institute of Cellular Medicine, Medical School, Newcastle University, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK, 2Nijmegen Centre for Mitochondrial Disorders, Radboud University Nijmegen Medical Centre, 6500 HB Nijmegen, The Netherlands, 3Institute of Cellular Medicine, Medical School, Newcastle University, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK and 4Centre de Génétique Moléculaire, CNRS Batiment 26, Avenue de la Terrasse, 91198 Gif sur Yvette Cedex, France

*To whom correspondence should be addressed. Tel: +44 191 222 8028; Fax: +44 191 222 8553; Email: r.n.lightowlers{at}ncl.ac.uk

Received June 9, 2008. Revised August 12, 2008. Accepted August 27, 2008.

The molecular mechanism of human mitochondrial translation has yet to be fully described. We are particularly interested in understanding the process of translational termination and ribosome recycling in the mitochondrion. Several candidates have been implicated, for which subcellular localization and characterization have not been reported. Here, we show that the putative mitochondrial recycling factor, mtRRF, is indeed a mitochondrial protein. Expression of human mtRRF in fission yeast devoid of endogenous mitochondrial recycling factor suppresses the respiratory phenotype. Further, human mtRRF is able to associate with Escherichia coli ribosomes in vitro and can associate with mitoribosomes in vivo. Depletion of mtRRF in human cell lines is lethal, initially causing profound mitochondrial dysmorphism, aggregation of mitoribosomes, elevated mitochondrial superoxide production and eventual loss of OXPHOS complexes. Finally, mtRRF was shown to co-immunoprecipitate a large number of mitoribosomal proteins attached to other mitochondrial proteins, including putative members of the mitochondrial nucleoid.


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