Vertebrate interferon (IFN) response defenses against viral infection through the induction of hundreds of IFN-stimulated genes (ISGs). Most ISGs are conserved across vertebrates; however, little is known about the species-specific ISGs. In this study, we reported that grass carp reovirus (GCRV)-induced gene 1 (Gig1), previously screened as a virus-induced gene from UV-inactivated GCRV-infected crucian carp (Carassius auratus) blastulae embryonic (CAB) cells, was a typical fish ISG, which was significantly induced by intracellular poly(I:C) through retinoic acid-inducible gene I (RIG-I)-like receptors-triggered IFN signaling pathway. Transient or stable overexpression of Gig1 prevented GCRV replication efficiently in cultured fish cells. Strikingly, Gig1 homologs were found exclusively in fish species forming a novel gene family. These results illustrate that there exists a Gig1 gene family unique to fish species and the founding gene mediates a novel fish IFN antiviral pathway. (C) 2013 Elsevier Inc. All rights reserved.
英文摘要:
Vertebrate interferon (IFN) response defenses against viral infection through the induction of hundreds of IFN-stimulated genes (ISGs). Most ISGs are conserved across vertebrates; however, little is known about the species-specific ISGs. In this study, we reported that grass carp reovirus (GCRV)-induced gene 1 (Gig1), previously screened as a virus-induced gene from UV-inactivated GCRV-infected crucian carp (Carassius auratus) blastulae embryonic (CAB) cells, was a typical fish ISG, which was significantly induced by intracellular poly(I:C) through retinoic acid-inducible gene I (RIG-I)-like receptors-triggered IFN signaling pathway. Transient or stable overexpression of Gig1 prevented GCRV replication efficiently in cultured fish cells. Strikingly, Gig1 homologs were found exclusively in fish species forming a novel gene family. These results illustrate that there exists a Gig1 gene family unique to fish species and the founding gene mediates a novel fish IFN antiviral pathway. (C) 2013 Elsevier Inc. All rights reserved.
