IDENTIFICATION AND CHARACTERIZATION OF A CRUCIAL ANTIOXIDANT GENE FROM JAPANESE EEL (ANGUILLA JAPONICA): REVEALING ITS POST INNATE-IMMUNE RESPONSES    

The Japanese eel (Anguilla japonica) is one of the most economically important aquaculture species in Korea. Due to the mass mortalities caused by pathogenic infections, the eel aquaculture industry has been suffering a severe economic loss. Understanding of immune components and their functions is an additional advantage for develop novel therapeutics for disease prevention. Catalase is a critical antioxidant enzyme present in all kind of living organisms, which plays an important role in the protection of host organism against oxidative stress. This study was carried out to identification and molecular characterization of catalase counterpart from Anguilla japonica (AjCat). Furthermore its potent post innate immune responses were investigated using several immune stimulants.

The AjCat protein contained 526 amino acids with a predicted molecular mass of 59.7kDa and theoretical iso-electric point of 6.79. Characteristic catalase domain profile (24-503 aa), catalase proximal active site signature (64-80 aa) and catalase proximal heme-ligand signature (354-362 aa) were identified. Pairwise sequence showed AjCat shares highest amino acid identity (89.6%) with Oplegnathus fasciatus. In a phylogenetic analysis using deduced amino acid sequences, the AjCat was clustered with other teleost counterparts. The AjCat was ubiquitously expressed in all the immune and non-immune tissues we tested. Innate immune responses of AjCat were examined after pathogenic challenge (3h - 72h). Data revealed that, the AjCat mRNA transcripts were upregulated in spleen upon immune stimulation (Fig.1.). Fluctuated up regulation pattern of AjCat was observed throughout the experiment after post E. tarda injection, while AjCat was significantly upregulated later phase of the experiment upon LPS and Poly I:C injection (Fig.1). Collectively our findings suggested that AjCat might be involved in post innate immune responses upon pathogenic infection.