*Result*: Transcriptome analysis and exploration of immune key genes of hepatopancreas after Poly(I:C) stimulation in Amphioctopus fangsiao.
*Further Information*
*Amphioctopus fangsiao is a commercially valuable cephalopod species prized for its distinctive flavor and nutritional profile. However, its large-scale aquaculture is hampered by significant challenges, particularly outbreaks of infectious diseases. Viral pathogens, which can be co-transmitted among marine species, pose a severe threat to sustainable population development. To elucidate the antiviral defense mechanisms in A. fangsiao, we conducted transcriptomic profiling of hepatopancreatic tissue following stimulation with polyinosinic-polycytidylic acid (Poly(I:C)), a well-established viral mimic known to activate innate immune pathways. Comparative transcriptomic profiling of the hepatopancreas-a key immune organ-at 6 h and 24 h post-stimulation identified 1406 and 904 differentially expressed genes (DEGs), respectively. Functional enrichment analysis revealed that these DEGs were significantly involved in critical immune-related pathways, including apoptosis, ECM-receptor interaction, and the MAPK and Hippo signaling pathways. Furthermore, by integrating protein-protein interaction (PPI) network analysis with KEGG pathway data, we identified 18 hub genes-such as TNFSF10, JUN, EGFR, and CTSB-that were potential key regulators of the antiviral response. The expression patterns of the aforementioned hub genes were successfully validated by means of quantitative reverse transcription polymerase chain reaction (qRT-PCR). This study comprehensively revealed the transcriptome characteristics of antiviral immune response of A. fangsiao for the first time. Our findings not only advance the understanding of innate immunity in cephalopods but also offer valuable genetic resources and potential molecular targets for developing strategies against viral diseases in octopus aquaculture.
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*Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.*