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Human Molecular Genetics Advance Access originally published online on December 1, 2005
Human Molecular Genetics 2006 15(1):143-154; doi:10.1093/hmg/ddi435
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© The Author 2005. Published by Oxford University Press. All rights reserved.
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact: journals.permissions@oxfordjournals.org

Natural competence of mammalian mitochondria allows the molecular investigation of mitochondrial gene expression

Milana Koulintchenko1,2,3, Richard J. Temperley1, Penelope A. Mason1,{dagger}, André Dietrich2 and Robert N. Lightowlers1,*

1Mitochondrial Research Group, Institutes of Neuroscience and Cell and Molecular Bioscience, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, UK, 2Institut de Biologie Moléculaire des Plantes du CNRS, Université Louis Pasteur, 12 Rue du Général Zimmer, 67084 Strasbourg, France and 3Siberian Institute of Plant Physiology and Biochemistry of the RAS, Lermontov St 132, PO Box 1243, 664033 Irkutsk, Russia

* To whom correspondence should be addressed. Tel: +44 1912228028; Fax: +44 1912228553; Email: r.n.lightowlers{at}ncl.ac.uk

Received November 14, 2005; Accepted November 20, 2005

Respiration, a fundamental process in mammalian cells, requires two genomes, those of the nucleus and the mitochondrion (mtDNA). Mutations of mtDNA are being increasingly recognized in disease and may play an important role in the ageing process. Accepting the vital role of mtDNA gene products, our limited knowledge concerning the details of mitochondrial gene expression is surprising. This is, in part, due to our inability to transfect mitochondria and to manipulate their genome. There have been claims of successful DNA import into isolated organelles, but most reports lacked evidence of expression and no method has furthered our understanding of gene expression. Here, we report that mammalian mitochondria possess a natural competence for DNA import. Using five functional assays, we show imported DNA can act as templates for DNA synthesis or promoter-driven transcription, with the resultant polycistronic RNA being processed (5' and 3') and excised mt-tRNA matured. Exploiting this natural competence will allow us to explore mitochondrial gene expression in organello and provides the potential for mitochondrial transfection in vivo.

{dagger} Present address: Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.


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