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ISSN: 2161-0436

Human Genetics & Embryology
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Editorial

Epigenetic Programming via DNA Deamination

David Kazadi1 and Uttiya Basu2*

1Department of Microbiology & Immunology, College of Physicians & Surgeons, Columbia University, New York, NY 10032

2Integrated Program in Cellular, Molecular, and Biomedical Studies, College of Physicians & Surgeons, Columbia University, New York, NY 10032

*Corresponding Author:
Dr. Uttiya Basu
Integrated Program in Cellular Molecular and Biomedical Studies
College of Physicians & Surgeons
Columbia University
New York, NY 10032
E-mail: [email protected]

Received Date: June 28, 2011; Accepted Date: August 05, 2011; Published Date: September 30, 2011

Citation: Kazadi D, Basu U (2011) Epigenetic Programming via DNA Deamination. Human Genet Embryol 1:e102. doi: 10.4172/2161-0436.1000e102

Copyright: © 2011 Kazadi D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Methylation of DNA has evolved across many organisms as an epigenetic marker typically associated with transcriptional repression. As cells develop, their epigenetic profile changes to reflect their differentiated state, with the promoters of genes to be silenced getting methylated, and the promoters of genes whose expression is required losing their methylation. Although a significant amount of insight has been gained in the mechanisms of DNA methylation, those of active DNA demethylation are yet to be determined. It has long been postulated that replication-dependent "passive" DNA demethylation is one route of transcriptional regulation. In addition, recent studies suggest that the DNA deamination activity of Apo-lipoprotein B (APOBEC) family member Activation Induced cytidine Deaminase (AID) determines genomic DNA methylation patterns. Here, we discuss the evidence and the arguments regarding AID function in DNA demethylation. Understanding how methylation and demethylation are established and regulated is crucial for at least two reasons. First, some diseases, exhibit a change in their epigenetic profile due to DNA methylation dysregulation. Second, considerable efforts have been expended in the reprogramming of somatic cells to give rise to other cell types. The substantial therapeutic advantages that would result from such technology are invaluable, but they have been hampered in part by our inability to fully understand how DNA demethylation occurs.

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