Nucleic acid delivery to mammalian mitochondria - myth or reality?
M. Koulintchenko, A. Dietrich, R.N. Lightowlers
Mitochondrial Research Group, School of Neurology, Neurobiology and Psychiatry, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne NE2 4HH, UK
All nucleated cells in the body contain mitochondria and all
mitochondria contain copies of their own genome, mtDNA. This small
molecule is present in hundreds or thousands of copies per cell and
encodes thirteen subunits of the apparatus that couples ATP synthesis
to cellular respiration. Thus, mutations of this genome can have
profound consequences. This area of research has gathered new momentum
with the inference that mtDNA mutations can underlie neurodegenerative
disease and have been implicated in the ageing process. As
mitochondrial gene expression is believed to be a relatively simple
process, can the genome be manipulated to alleviate the debilitating
disorders associated with mtDNA mutations ? To date, the answer is no,
although there have been encouraging reports in isolated cell lines.
Progress in this area is frustratingly slow, due in major part to our
inability to transfect mammalian mitochondria. Over the past twenty
years, there have been numerous claims of successful transfection,
although evidence of any functionality associated with this 'imported'
DNA has been extremely limited.
In this lecture, I intend to discuss several of these claims and to
introduce the concept of natural competence in mitochondria.
Key words:
mtDNA, mitochondrial transfection, mitochondrial gene expression
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