S-adenosylmethionine levels regulate the schwann cell DNA methylome.

Varela-Rey M, Iruarrizaga-Lejarreta M, Lozano JJ, Aransay AM, Fernandez AF, Lavin JL, Mósen-Ansorena D, Berdasco M, Turmaine M, Luka Z, Wagner C, Lu SC, Esteller M, Mirsky R, Jessen KR, Fraga MF, Martínez-Chantar ML, Mato JM, Woodhoo A
Neuron. 2014 81 (5): 1024-1039

PMID: 24607226 · PMCID: PMC3960855 · DOI:10.1016/j.neuron.2014.01.037

Axonal myelination is essential for rapid saltatory impulse conduction in the nervous system, and malformation or destruction of myelin sheaths leads to motor and sensory disabilities. DNA methylation is an essential epigenetic modification during mammalian development, yet its role in myelination remains obscure. Here, using high-resolution methylome maps, we show that DNA methylation could play a key gene regulatory role in peripheral nerve myelination and that S-adenosylmethionine (SAMe), the principal methyl donor in cytosine methylation, regulates the methylome dynamics during this process. Our studies also point to a possible role of SAMe in establishing the aberrant DNA methylation patterns in a mouse model of diabetic neuropathy, implicating SAMe in the pathogenesis of this disease. These critical observations establish a link between SAMe and DNA methylation status in a defined biological system, providing a mechanism that could direct methylation changes during cellular differentiation and in diverse pathological situations.

Copyright © 2014 Elsevier Inc. All rights reserved.

MeSH Terms (17)

Animals Cell Differentiation Cell Division DNA Methylation Female Genomics Genomics Male Mice Mice, Inbred C57BL Mice, Obese Myelin Sheath Peripheral Nerves Primary Cell Culture Rats S-Adenosylmethionine Schwann Cells

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