螯虾鞣化激素调控IMD/Relish信号通路参与免疫的机制研究

Tanning hormone (Bursicon) is a neuropeptide hormone in arthropods that promotes the tanning of the new cuticle after each molt. The bursicon homodimers induce the expression of antimicrobial peptides, as a prophylactic immune strategy to help arthropods after molting through the soft-cuticle stage, which is particularly vulnerable to invading pathogens. However, the regulation mechanism of bursicon homodimers on immune response and its role in the process of pathogen infection are not clear at present. In the previous study, we found that crayfish bursicon homodimers induced the expression of a variety of antimicrobial peptides, and activated the transcription factor Relish of one specific immune signaling pathway, the IMD pathway . On the basis of previous studies, this project intends to further clarify the induction of antimicrobial peptides in crayfish, explore the mechanism of bursicon regulation on IMD/Relish pathway and the key components involved, and reveal the role of bursicon in the response of crayfish to its pathogenic Vibrio parahaemolyticus and WSSV pathogen infection. The project is expected to establish a model for the involvement of tanning hormone bursicon in the immune response of crustaceans, to find new mechanisms for prophylactic immunity of crustaceans to respond to potential pathogen invasions, to enrich the theory of endocrine system regulation on immune response, and to provide reference for molecular breeding and fishery drug development of crayfish and other ecnomic crustaceans.

鞣化激素(bursicon)是节肢动物中一种神经肽激素，促进节肢动物蜕皮后新表皮的鞣化。其同二聚体可以诱导抗菌肽表达，作为预防性免疫策略帮助蜕皮后的节肢动物渡过表皮柔软危险期。但目前鞣化激素对免疫反应的调控机制和在病原感染过程中起到的作用尚不明确。在前期研究中我们发现克氏原螯虾(小龙虾)鞣化激素同二聚体诱导多种抗菌肽的表达，并激活免疫信号通路IMD途径的转录因子Relish。本项目拟在前期研究基础上，进一步明确螯虾中鞣化激素对抗菌肽的诱导，探索鞣化激素激活IMD/Relish途径的机制和参与其中的关键组分，并揭示鞣化激素在螯虾应对其病原副溶血弧菌和WSSV感染中的作用。项目预期建立鞣化激素参与甲壳动物免疫反应的模型，发现甲壳动物预防性免疫来应对潜在病原入侵的新机制，丰富内分泌系统调控免疫反应的理论，为小龙虾和其他近源甲壳动物的分子育种和渔药开发提供参考。

鞣化激素(bursicon)是节肢动物中一种神经肽激素，促进节肢动物蜕皮后新表皮的鞣化。鞣化激素同二聚体可以诱导抗菌肽表达，但其对免疫反应的调控机制和在病原感染过程中起到的作用尚不明确。在本研究中我们发现克氏原螯虾(小龙虾)鞣化激素同二聚体激活免疫信号通路IMD途径的转录因子Relish，并诱导下游多种抗菌肽的表达，包括甲壳肽、抗脂多糖因子和溶菌酶。进一步的研究证实了IMD途径的关键分子IMD并不参与鞣化激素对抗菌肽表达的调节，而另外一关键分子TAK1在该信号通路中起到了关键作用。我们的研究结果还显示鞣化激素能够帮助克氏原螯虾抵抗嗜水气单胞菌的感染，但对白斑综合征病毒的感染没有效果。本项目发现了甲壳动物预防性免疫来应对潜在病原入侵的新机制，丰富了内分泌系统调控免疫反应的理论，为小龙虾的分子育种和渔药开发提供了参考。