AUTHOR=Mou Cheng-Yan , Li Shun , Lu Long-Feng , Wang Yang , Yu Peng , Li Zhi , Tong Jin-Feng , Zhang Qi-Ya , Wang Zhong-Wei , Zhang Xiao-Juan , Wang Guang-Xin , Zhou Li , Gui Jian-Fang 

TITLE=Divergent Antiviral Mechanisms of Two Viperin Homeologs in a Recurrent Polyploid Fish

JOURNAL=Frontiers in Immunology

VOLUME=12

YEAR=2021

URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2021.702971

DOI=10.3389/fimmu.2021.702971

ISSN=1664-3224

ABSTRACT=<p>Polyploidy and subsequent diploidization provide genomic opportunities for evolutionary innovations and adaptation. The researches on duplicated gene evolutionary fates in recurrent polyploids have seriously lagged behind that in paleopolyploids with diploidized genomes. Moreover, the antiviral mechanisms of Viperin remain largely unclear in fish. Here, we elaborate the distinct antiviral mechanisms of two <italic>viperin</italic> homeologs (<italic>Cgviperin-A</italic> and <italic>Cgviperin-B</italic>) in auto-allo-hexaploid gibel carp (<italic>Carassius gibelio</italic>). First, <italic>Cgviperin-A</italic> and <italic>Cgviperin-B</italic> showed differential and biased expression patterns in gibel carp adult tissues. Subsequently, using co-immunoprecipitation (Co-IP) screening analysis, both <italic>Cg</italic>Viperin-A and <italic>Cg</italic>Viperin-B were found to interact with crucian carp (<italic>C. auratus</italic>) herpesvirus (<italic>Ca</italic>HV) open reading frame 46 right (ORF46R) protein, a negative herpesvirus regulator of host interferon (IFN) production, and to promote the proteasomal degradation of ORF46R <italic>via</italic> decreasing K63-linked ubiquitination. Additionally, <italic>Cg</italic>Viperin-B also mediated ORF46R degradation through autophagosome pathway, which was absent in <italic>Cg</italic>Viperin-A. Moreover, we found that the N-terminal α-helix domain was necessary for the localization of <italic>Cg</italic>Viperin-A and <italic>Cg</italic>Viperin-B at the endoplasmic reticulum (ER), and the C-terminal domain of <italic>Cg</italic>Viperin-A and <italic>Cg</italic>Viperin-B was indispensable for the interaction with degradation of ORF46R. Therefore, the current findings clarify the divergent antiviral mechanisms of the duplicated <italic>viperin</italic> homeologs in a recurrent polyploid fish, which will shed light on the evolution of teleost duplicated genes.</p>