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题名: Genome-wide loss of 5-hmC is a novel epigenetic feature of Huntingtons disease
作者: Wang, Fengli1; Yang, Yeran2; Lin, Xiwen3; Wang, Jiu-Qiang1; Wu, Yong-Sheng2; Xie, Wenjuan1; Wang, Dandan1; Zhu, Shu1; Liao, You-Qi2; Sun, Qinmiao1; Yang, Yun-Gui2; null(罗怀容)4; Guo, Caixia2; Han, Chunsheng3; Tang, Tie-Shan1
刊名: HUMAN MOLECULAR GENETICS
关键词: EMBRYONIC STEM-CELLS ; ADULT HIPPOCAMPAL NEUROGENESIS ; TRANSGENIC MOUSE MODEL ; DNA METHYLATION ; GENE-EXPRESSION ; MUTANT HUNTINGTIN ; NERVOUS-SYSTEM ; POLYGLUTAMINE PATHOGENESIS ; MITOCHONDRIAL DYSFUNCTION ; MAMMALIAN DEVELOPMENT
英文摘要: 5-Hydroxymethylcytosine (5-hmC) may represent a new epigenetic modification of cytosine. While the dynamics of 5-hmC during neurodevelopment have recently been reported, little is known about its genomic distribution and function(s) in neurodegenerative diseases such as Huntingtons disease (HD). We here observed a marked reduction of the 5-hmC signal in YAC128 (yeast artificial chromosome transgene with 128 CAG repeats) HD mouse brain tissues when compared with age-matched wild-type (WT) mice, suggesting a deficiency of 5-hmC reconstruction in HD brains during postnatal development. Genome-wide distribution analysis of 5-hmC further confirmed the diminishment of the 5-hmC signal in striatum and cortex in YAC128 HD mice. General genomic features of 5-hmC are highly conserved, not being affected by either disease or brain regions. Intriguingly, we have identied disease-specific (YAC128 versus WT) differentially hydroxymethylated regions (DhMRs), and found that acquisition of DhmRs in gene body is a positive epigenetic regulator for gene expression. Ingenuity pathway analysis (IPA) of genotype-specific DhMR-annotated genes revealed that alternation of a number of canonical pathways involving neuronal development/differentiation (Wnt/-catenin/Sox pathway, axonal guidance signaling pathway) and neuronal function/survival (glutamate receptor/calcium/CREB, GABA receptor signaling, dopamine-DARPP32 feedback pathway, etc.) could be important for the onset of HD. Our results indicate that loss of the 5-hmC marker is a novel epigenetic feature in HD, and that this aberrant epigenetic regulation may impair the neurogenesis, neuronal function and survival in HD brain. Our study also opens a new avenue for HD treatment; re-establishing the native 5-hmC landscape may have the potential to slow/halt the progression of HD.
出版日期: 2013-09-15
卷号: 22, 期号:18, 页码:3641-3653
语种: 英语
收录类别: SCI
学科分类: Biochemistry & Molecular Biology; Genetics & Heredity
ISSN号: 0964-6906
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内容类型: 期刊论文
URI标识: http://ir.kib.ac.cn/handle/151853/16661
Appears in Collections:植物化学与西部植物资源持续利用国家重点实验室_期刊论文

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作者单位: 1.Chinese Acad Sci, Inst Zool, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100101, Peoples R China
2.Chinese Acad Sci, Beijing Inst Genom, Lab Dis Genom & Individual Med, Beijing 100101, Peoples R China
3.Chinese Acad Sci, Inst Zool, State Key Lab Reprod Biol, Beijing 100101, Peoples R China
4.Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochem, Kunming 650201, Yunnan, Peoples R China

Recommended Citation:
Wang, Fengli; Yang, Yeran; Lin, Xiwen; Wang, Jiu-Qiang; Wu, Yong-Sheng; Xie, Wenjuan; Wang, Dandan; Zhu, Shu; Liao, You-Qi; Sun, Qinmiao; Yang, Yun-Gui; Luo, Huai-Rong; Guo, Caixia; Han, Chunsheng; Tang, Tie-Shan.Genome-wide loss of 5-hmC is a novel epigenetic feature of Huntingtons disease,HUMAN MOLECULAR GENETICS,2013,22(18):3641-3653
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