Ddx1 is essential for zebrafish development to adulthood but has no detectable effect on the response to tilapia lake...

DExD/H-box RNA helicases are multifunctional regulators of RNA metabolism and some are associated with host defence against viruses. However, the in vivo roles of individual family members remain insufficiently characterised. Ddx1 is one such example, implicated in antiviral signalling as well as in the replication of several viruses. In this study, we investigated the function of Ddx1 during vertebrate development and viral infection in zebrafish (Danio rerio) model using both loss-of-function and gain-of-function approaches. CRISPR/Cas9-mediated knockout of ddx1 resulted in viable embryos and larvae without overt developmental abnormalities; however, knockouts failed to survive to adulthood, indicating that Ddx1 is required for later stages of development. To assess its role in antiviral defence, ddx1 knockout and wild-type larvae were experimentally infected with tilapia lake virus (TiLV), a virus known to induce a strong type I interferon response in zebrafish. Survival rates, viral loads, and expression of selected type I interferon pathway genes (rig-I, ifnφ1, mxa) were comparable between genotypes, demonstrating that Ddx1 is not essential for the larval antiviral response to TiLV. Consistently, overexpression of ddx1 did not enhance resistance to infection. Together, these findings indicate that while Ddx1 is critical for zebrafish survival to adulthood, it does not play a measurable role in early antiviral immunity against TiLV in zebrafish larvae.