Functional characterization of grass carp (Ctenopharyngodon idella) jmjd8 gene in the anti-GCRV immune response.

Abstract

Grass carp (Ctenopharyngodon idella) is an economically important fish species that holds a central position in freshwater aquaculture in China, and its primary disease, grass carp hemorrhagic disease (GCHD), is caused by Grass Carp Reovirus (GCRV) infection. GCHD poses serious threats to aquaculture, but traditional prevention and control methods are limited. Currently, the primary measures for preventing and controlling the disease include vaccination and cultivating disease-resistant varieties. Breeding resistant varieties is an effective strategy to improve grass carp's disease resistance. In a previous study, the role of candidate gene jmjd8 (JmjC domain-containing 8), which is related to grass carp hemorrhagic disease resistance, in the mechanism of grass carp disease resistance was identified through multi-omics association analysis. We conducted functional studies on the grass carp jmjd8 gene and cloned its open reading frame (ORF). Bioinformatics analysis revealed that the encoded protein possesses a conserved JmjC domain, which is highly homologous to those of zebrafish and carp. Tissue expression analysis showed that jmjd8 was highly expressed in the head kidney and gill of healthy grass carp, and its expression was significantly upregulated in the spleen and mesonephros after GCRV infection, suggesting that it was involved in the immune response. Subcellular localization analysis demonstrated that jmjd8 was predominantly localized in the nucleus. By establishing stable transient overexpression cell lines, we found that jmjd8 overexpression significantly inhibited GCRV replication in Ctenopharyngodon idella kidney cells (CIK), suggesting its potential to enhance antiviral immunity by regulating host epigenetic modifications. These findings indicate that jmjd8 may play a significant role in breeding disease-resistant grass carp and provide novel insights for enhancing GCRV resistance via a potential epigenetic mechanism.