Abstract

The greenfin horse-faced filefish (Thamnaconus septentrionalis) is susceptible to recurrent Amyloodinium ocellatum (AO) infestation over the grow-out production cycle. This parasite breeds mainly on the gills, causing hypoxia in the fish body, and leading to many deaths. The host-parasite response drives a complex immune reaction, which is poorly understood. To generate a model for host-parasite interaction and the pathogenesis of AO in greenfin horse-faced filefish, an RNA-seq approach, differential gene expression, GO, and KEGG analyses were employed. Overall, 624 new genes and 2076 differentially expressed genes (DEGs) were detected, including 942 upregulated and 1134 downregulated genes in the gills. Compared with the control group, the expression of leptin a, GTPase IMAP family member 4, and NLR family CARD domain-containing protein 3 was significantly higher in the AO-infected group. Conversely, cell wall integrity and stress response component 1-like, and hepcidin-like were significantly downregulated in the gills of AO-infected fish. GO and KEGG enrichment analysis indicated that DEGs were significantly enriched in signaling pathways associated with viral protein interaction with cytokine and cytokine receptor and cytokine–cytokine receptor interaction. Collectively, this transcriptomic study provides novel molecular insights into the pathology caused by AO infestation and alternative theories for future research implementing strategies to control and manage AO.

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