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Inhibitor of growth protein 3 epigenetically silences endogenous retroviral elements and prevents innate immune activation

文献类型： 外文期刊

作者： Song, Yanhua 1 ; Hou, Gaopeng 5 ; Diep, Jonathan 1 ; Ooi, Yaw Shin 1 ; Akopyants, Natalia S. 5 ; Beverley, Stephen M. 5 ; Carette, Jan E. 1 ; Greenberg, Harry B. 1 ; Ding, Siyuan 5 ;

作者机构： 1.Stanford Univ, Dept Microbiol & Immunol, Stanford, CA 94305 USA

2.Stanford Univ, Dept Med, Div Gastroenterol & Hepatol, Stanford, CA 94305 USA

3.VA Palo Alto Hlth Care Syst, Palo Alto Vet Inst Res, Palo Alto, CA USA

4.Jiangsu Acad Agr Sci, Inst Vet Med, Nanjing, Peoples R China

5.Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA

6.Duke Natl Univ Singapore Med Sch, Program Emerging Infect Dis, Singapore, Singapore

期刊名称：NUCLEIC ACIDS RESEARCH （ 影响因子：19.16； 五年影响因子：17.21 ）

ISSN： 0305-1048

年卷期： 2021 年 49 卷 22 期

页码：

收录情况： SCI

摘要： Endogenous retroviruses (ERVs) are subject to transcriptional repression in adult tissues, in part to prevent autoimmune responses. However, little is known about the epigenetic silencing of ERV expression. Here, we describe a new role for inhibitor of growth family member 3 (ING3), to add to an emerging group of ERV transcriptional regulators. Our results show that ING3 binds to several ERV promoters (for instance MER21C) and establishes an EZH2-mediated H3K27 trimethylation modification. Loss of ING3 leads to decreases of H3K27 trimethylation enrichment at ERVs, induction of MDA5-MAVS-interferon signaling, and functional inhibition of several virus infections. These data demonstrate an important new function of ING3 in ERV silencing and contributing to innate immune regulation in somatic cells.

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