STAG2 deficiency induces interferon responses via cGAS-STING pathway and restricts virus infection
文献类型： 外文期刊
作者： Ding, Siyuan 1 ; Diep, Jonathan 1 ; Feng, Ningguo 1 ; Ren, Lili 1 ; Li, Bin 1 ; Ooi, Yaw Shin 1 ; Wang, Xin 6 ; Brulois, 1 ;
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 94304 USA
4.Nanjing Tech Univ, Sch Pharmaceut Sci, Nanjing 211816, Jiangsu, Peoples R China
5.Jiangsu Acad Agr Sci, Inst Vet Med, Nanjing 210014, Jiangsu, Peoples R China
6.Cleveland Clin, Dept Immunol, Cleveland, OH 44195 USA
7.Stanford Univ, Dept Pathol, Stanford, CA 94305 USA
8.Stanford Univ, Dept Med, Div Hematol, Stanford, CA 94305 USA
9.Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA
10.Ocean Univ China, Minist Educ, Key Lab Marine Drugs, Qingdao 266071, Peoples R China
期刊名称：NATURE COMMUNICATIONS （ 影响因子：14.919； 五年影响因子：15.805 ）
ISSN： 2041-1723
年卷期： 2018 年 9 卷
页码：
收录情况： SCI
摘要： Cohesin is a multi-subunit nuclear protein complex that coordinates sister chromatid separation during cell division. Highly frequent somatic mutations in genes encoding core cohesin subunits have been reported in multiple cancer types. Here, using a genome-wide CRISPR-Cas9 screening approach to identify host dependency factors and novel innate immune regulators of rotavirus (RV) infection, we demonstrate that the loss of STAG2, an important component of the cohesin complex, confers resistance to RV replication in cell culture and human intestinal enteroids. Mechanistically, STAG2 deficiency results in spontaneous genomic DNA damage and robust interferon (IFN) expression via the cGAS-STING cytosolic DNA-sensing pathway. The resultant activation of JAK-STAT signaling and IFN-stimulated gene (ISG) expression broadly protects against virus infections, including RVs. Our work highlights a previously undocumented role of the cohesin complex in regulating IFN homeostasis and identifies new therapeutic avenues for manipulating the innate immunity.
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