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Download fileMitochondrial DNA: A Blind Spot in Neuroepigenetics
journal contribution
posted on 2013-12-05, 00:00 authored by Hari Manev, Svetlana Dzitoyeva, Hu ChenNeuroepigenetics, 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-2011-0058Publisher
Walter de GruyterLanguage
- en_US