A Role for Epigenetics in Psoriasis: Methylated Cytosine–Guanine Sites Differentiate Lesional from Nonlesional Skin and from Normal Skin  Johann E. Gudjonsson,

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A Role for Epigenetics in Psoriasis: Methylated Cytosine–Guanine Sites Differentiate Lesional from Nonlesional Skin and from Normal Skin  Johann E. Gudjonsson, Gerald Krueger  Journal of Investigative Dermatology  Volume 132, Issue 3, Pages 506-508 (March 2012) DOI: 10.1038/jid.2011.364 Copyright © 2012 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 1 DNA methylation and histone modifications. DNA methylation and histone modifications are two of the best-defined epigenetic mechanisms of gene expression, others being RNA-mediated gene silencing and mitotic retention of transcriptional regulatory machinery (not shown). Chromosomal DNA is packaged around histone cores to form nucleosomes. A nucleosome has 147 base pairs of DNA associated with an octomeric core of histone proteins. Nucleosome spacing (panel a, top) in active chromatin is an open structure that is accessible to nuclear factors and is maintained in part by posttranslational modification of histone tails, including lysine acetylation and specific lysine methylation. Cytosine–guanine (CpG) dinucleotides are distributed unequally throughout chromosomal DNA and may be concentrated in regions called CpG islands that typically overlap with gene promoters. Methylation of cytosine in CpG dinucleotides is associated with inactive, condensed states of the chromosome (panel a, bottom). This inactive state is also maintained by specific histone lysine modifications. DNA methylation involves attachment of a methyl group to the C5 position of cytosine residues in CpG dinucleotide sequences and typically results in silencing of gene transcription (panel b, top). Histone modifications occur posttranslationally, and different combination changes (phosphorylation, ubiquitination, acetylation, and methylation) may regulate chromatin structure and transcriptional status (Handy et al., 2011; panel b, bottom). Adapted with permission from Handy et al. (2011) and Zaidi et al. (2011). Journal of Investigative Dermatology 2012 132, 506-508DOI: (10.1038/jid.2011.364) Copyright © 2012 The Society for Investigative Dermatology, Inc Terms and Conditions

Journal of Investigative Dermatology 2012 132, 506-508DOI: (10 Journal of Investigative Dermatology 2012 132, 506-508DOI: (10.1038/jid.2011.364) Copyright © 2012 The Society for Investigative Dermatology, Inc Terms and Conditions