A novel JNK from Litopenaeus vannamei involved in white spot syndrome virus infection

The c-Jun N-terminal kinase (JNK), a member of MAP kinases, is a serine/threonine-specific protein kinase which responds to extracellular stimuli and regulate various cellular activities. It is well documented in innate immune responses and reported to be involved in various viral infections of mammals. In present study, we cloned JNK homolog in a crustacean, Litopenaeus vannamei (designated as LvJNK) and studied its role in white spot syndrome virus (WSSV) infection. Sequence analysis displayed that LvJNK shared high similarity with other members of the JNK subfamily, including the conserved TPY motif and serine/threonine protein kinase (S_TKc) domain. Western blot analysis showed that the activation of LvJNK took place in WSSV infection. LvJnk silencing mediated by specific dsRNA in shrimps could significantly inhibit the proliferation of the virus. Moreover, inhibition of shrimp JNK signaling pathway by specific inhibitor resulted in the reduction of WSSV replication and the delay of WSSV gene transcription. These results indicate for the first time that shrimp JNK is activated in response to WSSV infection and WSSV could benefit from JNK activation. It may facilitate our understanding of the molecular mechanism of virus infection and provided a potential target for preventing the WSSV infection.

► JNK from Litopenaeus vannamei (LvJNK) was cloned and recognized as a novel homolog of JNK subfamily.
► The activation of LvJNK took place in WSSV infection.
► WSSV may acquire the ability to activate JNK to aid its replication.