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Human Molecular Genetics Advance Access originally published online on July 31, 2007
Human Molecular Genetics 2007 16(19):2306-2314; doi:10.1093/hmg/ddm182
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The yeast Holliday junction resolvase, CCE1, can restore wild-type mitochondrial DNA to human cells carrying rearranged mitochondrial DNA

Hiroshi Sembongi, Miriam Di Re, Monika Bokori-Brown and Ian J. Holt*

MRC-Dunn Human Nutrition Unit, Hills Road, Cambridge CB2 0XY, UK

* To whom correspondence should be addressed. Tel: +44 1223252840; Fax: +44 1223252845; Email: holt{at}mrc-dunn.cam.ac.uk

Received May 9, 2007; Revised June 12, 2007; Accepted July 6, 2007

Rearrangements of mitochondrial DNA (mtDNA) are a well-recognized cause of human disease; deletions are more frequent, but duplications are more readily transmitted to offspring. In theory, partial duplications of mtDNA can be resolved to partially deleted and wild-type (WT) molecules, via homologous recombination. Therefore, the yeast CCE1 gene, encoding a Holliday junction resolvase, was introduced into cells carrying partially duplicated or partially triplicated mtDNA. Some cell lines carrying the CCE1 gene had substantial amounts of WT mtDNA suggesting that the enzyme can mediate intramolecular recombination in human mitochondria. However, high levels of expression of CCE1 frequently led to mtDNA loss, and so it is necessary to strictly regulate the expression of CCE1 in human cells to ensure the selection and maintenance of WT mtDNA.


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