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Mre11A is considered as a cytosolic DNA receptor in mammals. However, it is rarely known about Mre11A in other vertebrates. Recently, a mammalian ortholog of Mre11A has been identified in grass carp (Ctenopharyngodon idellus) in our lab. Phylogenetic-tree analysis provided evidence for a close genetic relationship between C.idellus Mre11A and Carassius auratus Mre11A. The tissue expression profile of CiMre11A was detected, with a relatively higher level of expression in kidney, intestines, liver and spleen than that in other tissues after grass carp reovirus (GCRV) infection. Similarly, CiMre11A was also up-regulated in CIK cells after treatment with GCRV. Q-PCR and dual-luciferase assays indicated that the transcription levels of IFN1 and ISG15 were inhibited by Ci Mre11A knockdown, but were gradually augmented after CIK cells were transfected with increasing amounts of Ci Mre11A. Subcellular localization assays showed that a part of Ci Mre11A was translocated from the nucleus to the cytoplasm. Co-immunoprecipitation and co-localization assays demonstrated that Ci Mre11A interacts with Ci STING in response to GCRV infection. In CIK cells, the expressions of both IFN1 and ISG15 were acutely up-regulated by Ci Mre11A overexpression, as well as by co-overexpression of Ci Mre11A and Ci STING. Ci Mre11A and Ci STING induced the phosphorylation and cytoplasmic-to-nuclear translocation of IRF7 in CIK cells. The multiplication of GCRV in CIK cells was inhibited by the overexpression of Ci Mre11A and Ci STING. • A Mre11A orthologous gene from grass carp (Ctenopharyngodon idella) is cloned and characterized. • GCRV induces the nuclear-to-cytoplasm translocation of Mre11A. • Mre11A interacts with STING and then initiates IFN 1 and ISG15 expression. • Mre11A and STING promote the phosphorylation and nuclear translocation of IRF7. • Mre11A and STING protect CIK cells against GCRV infection. [ABSTRACT FROM AUTHOR]