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Title: A somatic role for the histone methyltransferase Setdb1 in endogenous retrovirus silencing
Authors: Kato, Masaki
Takemoto, Keiko  kyouindb  KAKEN_id
Shinkai, Yoichi
Author's alias: 加藤, 雅紀
竹本, 経緯子
眞貝, 洋一
Keywords: Gene silencing
Transcriptional regulatory elements
Issue Date: 27-Apr-2018
Publisher: Springer Nature
Journal title: Nature Communications
Volume: 9
Thesis number: 1683
Abstract: Subsets of endogenous retroviruses (ERVs) are derepressed in mouse embryonic stem cells (mESCs) deficient for Setdb1, which catalyzes histone H3 lysine 9 trimethylation (H3K9me3). Most of those ERVs, including IAPs, remain silent if Setdb1 is deleted in differentiated embryonic cells; however they are derepressed when deficient for Dnmt1, suggesting that Setdb1 is dispensable for ERV silencing in somatic cells. However, H3K9me3 enrichment on ERVs is maintained in differentiated cells and is mostly diminished in mouse embryonic fibroblasts (MEFs) lacking Setdb1. Here we find that distinctive sets of ERVs are reactivated in different types of Setdb1-deficient somatic cells, including the VL30-class of ERVs in MEFs, whose derepression is dependent on cell-type-specific transcription factors (TFs). These data suggest a more general role for Setdb1 in ERV silencing, which provides an additional layer of epigenetic silencing through the H3K9me3 modification.
Description: 内在性レトロウイルスを抑え込む普遍的な仕組み --抑制性ヒストン修飾の体細胞での機能を解明--. 京都大学プレスリリース. 2018-05-17.
Rights: © The Author(s) 2018. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit
DOI(Published Version): 10.1038/s41467-018-04132-9
PubMed ID: 29703894
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