Zebrafish prmt7 negatively regulates antiviral responses by suppressing the retinoic acid-inducible gene-I-like receptor signaling.

Arginine methylation is a post-translational modification in histone and nonhistone proteins that can affect numerous cellular activities. Protein arginine methyltransferase 7 (Prmt7), a type III arginine methyltransferase, catalyzes the formation of stable monomethylarginines of histones. The role of PRMT7 in virus-induced innate immunity signaling, however, remains largely unknown. We demonstrate that zebrafish prmt7 could be inhibited by spring viremia of carp virus (SVCV) and grass carp reovirus (GCRV) infection. The overexpression of prmt7 suppresses cellular antiviral responses that are partially dependent on the arginine methyltransferase activity of prmt7. Consistently, prmt7-null zebrafish were more resistant to SVCV or GCRV infection, exhibiting enhanced expression of key antiviral genes and fewer necrotic cells in the liver and kidney upon viral infection. Furthermore, we established a zebrafish model to investigate grass carp hemorrhagic disease. Our findings suggest that by suppressing the RIG-I-like receptors signaling, zebrafish prmt7 negatively regulates antiviral responses, indicating the vital role of prmt7 and its arginine methyltransferase activity in innate immunity.

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