S-adenosylmethionine levels regulate the schwann cell DNA methylome.

Neuron

CIC bioGUNE, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Bizkaia Technology Park, Derio, 48160 Bizkaia, Spain; IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Spain. Electronic address:

Published: March 2014

AI Article Synopsis

  • Axonal myelination is crucial for fast nerve signal transmission, and issues with myelin can cause motor and sensory problems.
  • The study reveals that DNA methylation, an important process in gene regulation, plays a significant role in myelination and is influenced by S-adenosylmethionine (SAMe).
  • Findings suggest that SAMe may contribute to abnormal DNA methylation patterns in diabetic neuropathy, highlighting its potential impact on both normal biological processes and disease development.

Article Abstract

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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3960855PMC
http://dx.doi.org/10.1016/j.neuron.2014.01.037DOI Listing

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