Normal histone modifications on the inactive X chromosome in ICF and Rett syndrome cells: implications for methyl-CpG binding proteins |
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Authors: | Email author" target="_blank">Stanley?M?GartlerEmail author Kartik?R?Varadarajan Ping?Luo Theresa?K?Canfield Jeff?Traynor Uta?Francke R?Scott?Hansen |
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Institution: | (1) Department of Medicine, University of Washington, Seattle, WA, USA;(2) Department of Genome Sciences, University of Washington, Seattle, WA, USA;(3) Department of Genetics, Stanford University, Stanford, CA, USA |
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Abstract: | Background In mammals, there is evidence suggesting that methyl-CpG binding proteins may play a significant role in histone modification
through their association with modification complexes that can deacetylate and/or methylate nucleosomes in the proximity of
methylated DNA. We examined this idea for the X chromosome by studying histone modifications on the X chromosome in normal
cells and in cells from patients with ICF syndrome (Immune deficiency, Centromeric region instability, and Facial anomalies syndrome). In normal cells the inactive X has characteristic silencing type histone modification patterns
and the CpG islands of genes subject to X inactivation are hypermethylated. In ICF cells, however, genes subject to X inactivation
are hypomethylated on the inactive X due to mutations in the DNA methyltransferase (DNMT3B) genes. Therefore, if DNA methylation
is upstream of histone modification, the histones on the inactive X in ICF cells should not be modified to a silent form.
In addition, we determined whether a specific methyl-CpG binding protein, MeCP2, is necessary for the inactive X histone modification
pattern by studying Rett syndrome cells which are deficient in MeCP2 function. |
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