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Mitochondrial DNA: A Blind Spot in Neuroepigenetics

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journal contribution
posted on 05.12.2013, 00:00 by Hari Manev, Svetlana Dzitoyeva, Hu Chen
Neuroepigenetics, which includes nuclear DNA modifications such as 5-methylcytosine and 5-hydoxymethylcytosine and modifications of nuclear proteins such as histones, is emerging as the leading field in molecular neuroscience. Historically, a functional role for epigenetic mechanisms, including in neuroepigenetics, has been sought in the area of the regulation of nuclear transcription. However, one important compartment of mammalian cell DNA, different from nuclear but equally important for physiological and pathological processes (including in the brain), mitochondrial DNA has for the most part not had a systematic epigenetic characterization. The importance of mitochondria and mitochondrial DNA (particularly its mutations) in central nervous system physiology and pathology has long been recognized. Only recently have mechanisms of mitochondrial DNA methylation and hydroxymethylation, including the discovery of mitochondrial DNA-methyltransferases and the presence and the functionality of 5-methylcytosine and 5-hydroxymethylcytosine in mitochondrial DNA (e.g., in modifying the transcription of mitochondrial genome), been unequivocally recognized as a part of mammalian mitochondrial physiology. Here we summarize for the first time evidence supporting the existence of these mechanisms and we propose the term “mitochondrial epigenetics” to be used when referring to them. Currently, neuroepigenetics does not include mitochondrial epigenetics - a gap that we expect to close in the near future.

Funding

National Institutes of Health (NIH) grant R01AG015347 from the National Institute on Aging (NIA)

History

Publisher Statement

This is a copy of an article published in the BioMolecular Concepts © 2012 Walter de Gruyter. The original version is available at http://www.degruyter.com/ doi: 10.1515/bmc-2011-0058

Publisher

Walter de Gruyter

Language

en_US

issn

1868-503X

Issue date

01/04/2012

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