Reactive oxygen species and the segregation of mtdna sequence variants


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Access through your institution Buy or subscribe TO THE EDITOR: Mutations in mitochondrial DNA (mtDNA) are an important cause of a group of human diseases collectively referred to as


mitochondrial encephalomyopathies. Most pathogenic mtDNA mutations coexist with wild-type genomes, and an oxidative phosphorylation defect is not manifest until the proportion of mutant


genomes exceeds a particular cellular threshold. The pattern of segregation of mtDNA mutations is thus a key determinant of the onset and severity of disease. The mechanisms regulating


tissue-specific mtDNA segregation, however, remain largely unknown. This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution


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AFFILIATIONS * Montreal Neurological Institute and Department of Human Genetics, McGill University, 3801 University Street, Montreal, H3A 2B4, Quebec, Canada Brendan J Battersby & Eric A


Shoubridge Authors * Brendan J Battersby View author publications You can also search for this author inPubMed Google Scholar * Eric A Shoubridge View author publications You can also


search for this author inPubMed Google Scholar ETHICS DECLARATIONS COMPETING INTERESTS The authors declare no competing financial interests. RIGHTS AND PERMISSIONS Reprints and permissions


ABOUT THIS ARTICLE CITE THIS ARTICLE Battersby, B., Shoubridge, E. Reactive oxygen species and the segregation of mtDNA sequence variants. _Nat Genet_ 39, 571–572 (2007).


https://doi.org/10.1038/ng0507-571 Download citation * Issue Date: May 2007 * DOI: https://doi.org/10.1038/ng0507-571 SHARE THIS ARTICLE Anyone you share the following link with will be able


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