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Ko, Myunggon
Molecular Immunology & Cancer Epigenetics
Research Interests
  • TET proteins, DNA hydroxymethylation, oncogenesis, cancer stem cells, cancer therapy

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Large conserved domains of low DNA methylation maintained by 5-hydroxymethycytosine and Dnmt3a

Cited 58 times inthomson ciCited 51 times inthomson ci
Title
Large conserved domains of low DNA methylation maintained by 5-hydroxymethycytosine and Dnmt3a
Author
Jeong, MiraSun, DeqiangLuo, MinHuang, YunChallen, Grant ARodriguez, BenjaminZhang, XiaotianChavez, LukasWang, HuiHannah, RebeccaKim, Sang-BaeYang, LiubinKo, Myung GonChen, RuiGottgens, BertholdLee, Ju-SeogGunaratne, PreethiGodley, LADarlington, GJRao, AnjanaLi, WeiGoodell, Margaret A
Keywords
5 hydroxymethylcytosine; 5 methylcytosine; DNA methyltransferase 3A; histone
Issue Date
2014-01
Publisher
NATURE PUBLISHING GROUP
Citation
NATURE GENETICS, v.46, no.1, pp.17 - 23
Abstract
Gains and losses in DNA methylation are prominent features of mammalian cell types. To gain insight into the mechanisms that promote shifts in DNA methylation and contribute to changes in cell fate, including malignant transformation, we performed genome-wide mapping of 5-methylcytosine and 5-hydroxymethylcytosine in purified mouse hematopoietic stem cells. We discovered extended regions of low methylation (canyons) that span conserved domains frequently containing transcription factors and are distinct from CpG islands and shores. About half of the genes in these methylation canyons are coated with repressive histone marks, whereas the remainder are covered by activating histone marks and are highly expressed in hematopoietic stem cells (HSCs). Canyon borders are demarked by 5-hydroxymethylcytosine and become eroded in the absence of DNA methyltransferase 3a (Dnmt3a). Genes dysregulated in human leukemias are enriched for canyon-associated genes. The new epigenetic landscape we describe may provide a mechanism for the regulation of hematopoiesis and may contribute to leukemia development. © 2014 Nature America, Inc.
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DOI
10.1038/ng.2836
ISSN
1061-4036
Appears in Collections:
PHY_Journal Papers
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