硫激肽及其受体抑制褐飞虱取食的分子机制

褐飞虱是为害水稻的重要害虫，已对多种杀虫剂产生抗性，生产上急需开发出新型作用机理的杀虫剂用于其田间防治。G蛋白偶联受体（GPCRs）调控着昆虫的各种生理与行为过程，研究昆虫GPCRs的药理及生理功能可为新型杀虫剂作用靶标研发提供依据。硫激肽（Sulfakinin, SK）在调控昆虫取食中扮演重要角色，其通过结合硫激肽受体（Sulfakinin Receptor, SKR）发挥作用，SKR即为典型的GPCRs家族成员。实验室前期研究发现，褐飞虱在饱腹状态时，硫激肽基因表达量明显上升，且注射硫激肽能够显著抑制褐飞虱取食，但硫激肽及其受体抑制褐飞虱取食的分子机制未知。本研究拟采用行为学、遗传学、免疫学、细胞生物学以及药理学等手段，从行为、生化、细胞到分子层面阐明硫激肽及其受体抑制褐飞虱取食的分子机制。本研究可丰富昆虫生理学研究内容，亦可为作用于昆虫硫激肽及其受体系统的新型杀虫剂研发提供依据。

The brown planthopper, Nilaparvata lugens, is one of the most economically important pests of rice. It has developed high-level of resistance to many kinds of insecticides. Therefore, it is urgent to develop insecticides with novel modes of action to control this pest. Insect G-protein coupled receptors (GPCRs) have important roles in modulating physiology and behaviour. Pharmacologists have focused their attention on the GPCRs, which are believed to represent promising targets for new insecticides. Sulfakinin (SK) is an insect neuropeptide that constitutes an important component of the neural factors that regulate feeding and digestion. The key modulating functions of SK are mediated by binding and signaling via sulfakinin receptor (SKR). SKR belongs to rhodopsin-like GPCR. It was shown by our previous experiments that the gene expression of nsk was strongly up-regulated in response to feeding and injection of sNSKⅡ demonstrate reduction of food intake in the brown planthopper. However, the molecular mechanisms of NSK/NSKR inhibition of food intake in the brown planthopper is unknown. In this proposal, we will illustrate this mechanism at behavioral, biochemical, cellular and molecular levels on the basis of ethological, genetic, immunological, cell biological and pharmacological methods. We believe this research will enrich the contents of the insect physiology and provide valuable information for developing new pesticides which target on SK/SKR system.