The impact of metabolism on DNA methylation
1Department of Biology, 2Center for Aging and 3Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA
* To whom correspondence should be addressed at: Department of Biology, 175 Campbell Hall, 1300 University Boulevard, University of Alabama at Birmingham, Birmingham, AL 35294-1170, USA. Tel: +1 2059344573; Fax: +1 2059756097; Email: trygve{at}uab.edu
Received December 15, 2004; Revised February 7, 2005; Accepted February 23, 2005
Methylation of genomic cytosines is one of the best characterized epigenetic mechanisms, and investigation of its relationship with other biochemical pathways represents a critical stage in the elucidation of biological information processing. The field also has immense potential for the development of medical treatments for any number of conditions ranging from aging to neurological disorders. The DNA methylation status of genes is responsible for many heritable traits and varies more or less independently of the genetic code. This variation is often a result of cellular environmental factors including metabolism. A key metabolite in this regard is homocysteine. Knowledge of homocysteine metabolism continues to be amassed, yet the part played by aberrant DNA methylation in homocysteine-related pathologies is often, at best, conjectural. In this analysis, we will review recent insights and attempt to speculate meaningfully concerning the dynamics of the methionine cycle in relation to DNA methylation and disease.
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