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特定转座元件家族内的 DNA 低甲基化与组织特异性增强子景观相关。

DNA hypomethylation within specific transposable element families associates with tissue-specific enhancer landscape.

机构信息

Department of Genetics, Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, MO, USA.

出版信息

Nat Genet. 2013 Jul;45(7):836-41. doi: 10.1038/ng.2649. Epub 2013 May 26.

DOI:10.1038/ng.2649
PMID:23708189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3695047/
Abstract

Transposable element (TE)-derived sequences comprise half of the human genome and DNA methylome and are presumed to be densely methylated and inactive. Examination of genome-wide DNA methylation status within 928 TE subfamilies in human embryonic and adult tissues identified unexpected tissue-specific and subfamily-specific hypomethylation signatures. Genes proximal to tissue-specific hypomethylated TE sequences were enriched for functions important for the relevant tissue type, and their expression correlated strongly with hypomethylation within the TEs. When hypomethylated, these TE sequences gained tissue-specific enhancer marks, including monomethylation of histone H3 at lysine 4 (H3K4me1) and occupancy by p300, and a majority exhibited enhancer activity in reporter gene assays. Many such TEs also harbored binding sites for transcription factors that are important for tissue-specific functions and showed evidence of evolutionary selection. These data suggest that sequences derived from TEs may be responsible for wiring tissue type-specific regulatory networks and may have acquired tissue-specific epigenetic regulation.

摘要

转座元件 (TE) 衍生序列构成人类基因组和 DNA 甲基组的一半，据推测它们被高度甲基化且处于非活性状态。在人类胚胎和成人组织中对 928 个 TE 亚家族的全基因组 DNA 甲基化状态进行检查，发现了意想不到的组织特异性和亚家族特异性低甲基化特征。与组织特异性低甲基化 TE 序列临近的基因富集了与相关组织类型重要的功能，并且它们的表达与 TE 内的低甲基化密切相关。当这些 TE 序列发生低甲基化时，它们获得了组织特异性增强子标记，包括组蛋白 H3 在赖氨酸 4 上的单甲基化 (H3K4me1) 和 p300 的占据，并且大多数在报告基因检测中表现出增强子活性。许多这样的 TE 还具有转录因子的结合位点，这些转录因子对于组织特异性功能很重要，并且表现出进化选择的证据。这些数据表明，源自 TE 的序列可能负责构建组织类型特异性调控网络，并且可能已经获得了组织特异性的表观遗传调控。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74ac/3695047/b3ce0446df4c/nihms-475505-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74ac/3695047/08561f340bfa/nihms-475505-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74ac/3695047/817eb3b836cc/nihms-475505-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74ac/3695047/b244a89a3ef5/nihms-475505-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74ac/3695047/b3ce0446df4c/nihms-475505-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74ac/3695047/08561f340bfa/nihms-475505-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74ac/3695047/817eb3b836cc/nihms-475505-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74ac/3695047/b244a89a3ef5/nihms-475505-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74ac/3695047/b3ce0446df4c/nihms-475505-f0004.jpg

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