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Human Molecular Genetics Advance Access originally published online on January 31, 2006
Human Molecular Genetics 2006 15(6):883-895; doi:10.1093/hmg/ddl006
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Parkin enhances mitochondrial biogenesis in proliferating cells

Yukiko Kuroda1, Takao Mitsui1,*, Makoto Kunishige1, Masayuki Shono2, Masashi Akaike1, Hiroyuki Azuma1 and Toshio Matsumoto1

1Department of Medicine and Bioregulatory Sciences, University of Tokushima Graduate School of Medicine, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan and 2General Laboratory for Medical Research, University of Tokushima Graduate School of Medicine, Kuramoto-3, Tokushima 770-8503, Japan

* To whom correspondence should be addressed. Tel: +81 886337120; Fax: +81 886337121; Email: tmitsui{at}clin.med.tokushima-u.ac.jp

Received October 28, 2005; Accepted January 25, 2006

We describe a novel function of parkin, a RING protein, which is elaborately involved in mitochondrial biogenesis. Parkin was located within the mitochondrial organelle of proliferating cells. Anti-proliferative treatments released parkin from mitochondria to cytosol. Results of pharmacological treatments indicate that parkin was released from mitochondria when permeability transition pore was opened. The extra-mitochondrial localization was also observed in differentiated cells. In proliferating cells, transcription and replication of mitochondrial DNA was enhanced by parkin overexpression and attenuated by parkin suppression with siRNA. Parkin was associated with mitochondrial transcription factor A (TFAM) and enhanced TFAM-mediated mitochondrial transcription. These results indicate that parkin is involved in the regulation of mitochondrial transcription/replication other than the ubiquitin-mediated protein degradation system in proliferating cells.


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