Pc-JNK plays a crucial role in the comprehensive regulation of crayfish antibacterial innate immune responses.

The mitogen-activated protein kinase (MAPK) signaling pathway serves as a critical mediator of the cellular inflammatory response in mammals. Current evidence has also revealed that the MAPK cascade plays an important role in regulating the innate immune responses of some invertebrates. In this paper, we thoroughly investigated the innate immune regulatory functions of the c-Jun N-terminal kinase (JNK) gene in Procambarus clarkii, which is an important member of the MAPK signaling pathway. The results of the time course expression profiles indicated that the expression level of Pc-JNK gene was obviously up-regulated after Vibrio harveyi challenge. The rapid increase in expression levels revealed that Pc-JNK could be mobilized to defend against V. harveyi infection. In the RNAi assay, we found that the suppression in H2O2 content at relatively early stages after dsPc-JNK injection attenuated the bacteria-killing ability of crayfish. Moreover, the antimicrobial peptide (AMP) genes' expression in crayfish hepatopancreas was down-regulated at 12 h post V. harveyi infection, when the Pc-JNK gene was knocked down. And the knockdown of Pc-JNK also altered the prophenoloxidase (PPO) system and attenuated hemolymph melanization, ultimately leading to a significant reduction in crayfish survival following V. harveyi infection. Overall, we speculated that Pc-JNK gene plays a crucial role in the comprehensive regulation of crayfish antibacterial innate immune responses.