期刊
NEURON
卷 81, 期 5, 页码 1024-1039出版社
CELL PRESS
DOI: 10.1016/j.neuron.2014.01.037
关键词
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资金
- ISCIII-Subdireccion General de Evaluacion
- Fondo Europeo de Desarrollo Regional (FEDER)
- Fundacion Cientifica de la Asociacion Espanola Contra el Cancer
- Departamento de Educacion Politica Linguistica y Cultura del Gobierno Vasco [PI2013-46]
- Ministerio de Economia y Competitividad-Plan Nacional de I+D+I [RYC2010-06901]
- Royal Society of Great Britain
- NIH [AT-1576]
- SAF [2011-29851]
- Sanidad Gobierno Vasco
- Wellcome Trust
- ETORTEK
- Educacion Gobierno Vasco
- Innovation Technology Department of the Bizkaia County
- Government of Navarra
- Instituto de Salud Carlos III
- [PI09/00094]
- [PI12/00005]
- [PI11/01588]
- MRC [G0600967] Funding Source: UKRI
- Medical Research Council [G0600967] Funding Source: researchfish
- ICREA Funding Source: Custom
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.
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