Virus Sensor RIG-I Represses RNA Interference by Interacting with TRBP through LGP2 in Mammalian Cells

被引:20
作者
Takahashi, Tomoko [1 ]
Nakano, Yuko [1 ]
Onomoto, Koji [2 ]
Yoneyama, Mitsutoshi [2 ]
Ui-Tei, Kumiko [1 ,3 ]
机构
[1] Univ Tokyo, Grad Sch Sci, Dept Biol Sci, Tokyo 1130033, Japan
[2] Chiba Univ, Med Mycol Res Ctr, Div Mol Immunol, Chiba 2608673, Japan
[3] Univ Tokyo, Grad Sch Frontier Sci, Dept Computat Biol & Med Sci, Chiba 2778561, Japan
基金
日本科学技术振兴机构;
关键词
RNA interference; RLRs; RIG-I; LGP2; TRBP; virus sensor; dsRNA; DOUBLE-STRANDED-RNA; BINDING-PROTEIN; ANTIVIRAL IMMUNITY; NUCLEAR EXPORT; RECOGNITION; HELICASE; DICER; SIRNA; INHIBITION; ACTIVATION;
D O I
10.3390/genes9100511
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Exogenous double-stranded RNAs (dsRNAs) similar to viral RNAs induce antiviral RNA silencing or RNA interference (RNAi) in plants or invertebrates, whereas interferon (IFN) response is induced through activation of virus sensor proteins including Toll like receptor 3 (TLR3) or retinoic acid-inducible gene I (RIG-I) like receptors (RLRs) in mammalian cells. Both RNA silencing and IFN response are triggered by dsRNAs. However, the relationship between these two pathways has remained unclear. Laboratory of genetics and physiology 2 (LGP2) is one of the RLRs, but its function has remained unclear. Recently, we reported that LGP2 regulates endogenous microRNA-mediated RNA silencing by interacting with an RNA silencing enhancer, TAR-RNA binding protein (TRBP). Here, we investigated the contribution of other RLRs, RIG-I and melanoma-differentiation-associated gene 5 (MDA5), in the regulation of RNA silencing. We found that RIG-I, but not MDA5, also represses short hairpin RNA (shRNA)-induced RNAi by type-I IFN. Our finding suggests that RIG-I, but not MDA5, interacts with TRBP indirectly through LGP2 to function as an RNAi modulator in mammalian cells.
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页数:13
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