Duck RIG-I CARD Domain Induces the Chicken IFN-β by Activating NF-κB. (30th March 2015)

• Record Type: Journal Article
• Authors: Chen, Yang; Huang, Zhengyang; Wang, Bin; Yu, Qinming; Liu, Ran; Xu, Qi; Chang, Guobin; Ding, Jiatong; Chen, Guohong
• Other Names: Li Kui Academic Editor.
• Is Part Of: BioMed research international. Volume 2015(2015)
• Publication Date: 2015-03-30
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2015/348792
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : Retinoic acid-inducible gene I- (RIG-I-) like receptors (RLRs) have recently been identified as cytoplasmic sensors for viral RNA. RIG-I, a member of RLRs family, plays an important role in innate immunity. Although previous investigations have proved that RIG-I is absent in chickens, it remains largely unknown whether the chicken can respond to RIG-I ligand. In this study, the eukaryotic expression vectors encoding duRIG-I full length (duck RIG-I, containing all domains), duRIG-I N-terminal (containing the two caspase activation and recruitment domain, CARDs), and duRIG-I C-terminal (containing helicase and regulatory domains) labeled with 6*His tags were constructed successfully and detected by western blotting. Luciferase reporter assay and enzyme-linked immunosorbent assay (ELISA) detected the duRIG-I significantly activated NF- κ B and induced the expression of IFN- β when polyinosinic-polycytidylic acid (poly[I:C], synthetic double-stranded RNA) challenges chicken embryonic fibroblasts cells (DF1 cells), while the duRIG-I was inactive in the absence of poly[I:C]. Further analysis revealed that the CARDs (duRIG-I-N) induced IFN- β production regardless of the presence of poly[I:C], while the CARD-lacking duRIG-I (duRIG-I-C) was not capable of activating downstream signals. These results indicate that duRIG-I CARD domain plays an important role in the induction of IFN- β and provide a basis for further studying the function of RIG-I in avian innate immunity.