类固醇激素20-羟基蜕皮激素与多巴胺受体结合，抑制鳞翅目昆虫摄食并促进化up。,PLOS Genetics

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类固醇激素20-羟基蜕皮激素与多巴胺受体结合，抑制鳞翅目昆虫摄食并促进化up。
PLOS Genetics ( IF 4.0 ) Pub Date : 2019-08-14 , DOI: 10.1371/journal.pgen.1008331
Xin-Le Kang ₁ , Jun-Ying Zhang ₁ , Di Wang ₁ , Yu-Meng Zhao ₁ , Xiao-Lin Han ₁ , Jin-Xing Wang ₁ , Xiao-Fan Zhao ₁

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完全代谢的昆虫在幼虫期的最后阶段停止觅食，然后发生变态。但是，机制尚不清楚。在本研究中，使用严重的鳞翅目农业害虫棉铃虫（Helicoverpa armigera）作为模型，我们揭示了20-羟基蜕皮酮（20E）与G蛋白偶联受体多巴胺受体（DopEcR）结合，以停止幼虫摄食并促进化promote。在20E调节下的蜕皮蜕皮过程中，DopEcR在各种组织中表达，其水平升高。幼虫摄食阶段的20E滴度较低，而徘徊阶段的20E滴度较高。相比之下，幼虫摄食阶段的多巴胺（DA）滴度较高，而徘徊阶段的多巴胺（DA）滴度较低。使用抑制剂flupentixol注射20E或阻断多巴胺受体可减少幼虫的食物消耗和体重。击倒DopEcR可以抑制幼虫的摄食，生长和化脓。20E通过DopEcR促进细胞凋亡；DA通过DopEcR诱导细胞增殖。20E通过抑制DA诱导的细胞增殖和AKT磷酸化来对抗DA功能。20E通过DopEcR诱导基因表达，并使细胞内钙离子和cAMP迅速增加。20E诱导DopEcR与G蛋白αs和αq相互作用。20E，通过DopEcR，诱导蛋白磷酸化和EcRB1-USP1转录复合物与蜕皮激素响应元件的结合。DopEcR可以在细胞膜内部或从细胞膜分离后结合20E。DopEcR的突变降低了20E结合水平和相关的细胞反应。20E与DA竞争与DopEcR结合。本研究的结果表明20E通过与DopEcR结合，

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The steroid hormone 20-hydroxyecdysone binds to dopamine receptor to repress lepidopteran insect feeding and promote pupation.

Holometabolous insects stop feeding at the final larval instar stage and then undergo metamorphosis; however, the mechanism is unclear. In the present study, using the serious lepidopteran agricultural pest Helicoverpa armigera as a model, we revealed that 20-hydroxyecdysone (20E) binds to the dopamine receptor (DopEcR), a G protein-coupled receptor, to stop larval feeding and promote pupation. DopEcR was expressed in various tissues and its level increased during metamorphic molting under 20E regulation. The 20E titer was low during larval feeding stages and high during wandering stages. By contrast, the dopamine (DA) titer was high during larval feeding stages and low during the wandering stages. Injection of 20E or blocking dopamine receptors using the inhibitor flupentixol decreased larval food consumption and body weight. Knockdown of DopEcR repressed larval feeding, growth, and pupation. 20E, via DopEcR, promoted apoptosis; and DA, via DopEcR, induced cell proliferation. 20E opposed DA function by repressing DA-induced cell proliferation and AKT phosphorylation. 20E, via DopEcR, induced gene expression and a rapid increase in intracellular calcium ions and cAMP. 20E induced the interaction of DopEcR with G proteins αs and αq. 20E, via DopEcR, induced protein phosphorylation and binding of the EcRB1-USP1 transcription complex to the ecdysone response element. DopEcR could bind 20E inside the cell membrane or after being isolated from the cell membrane. Mutation of DopEcR decreased 20E binding levels and related cellular responses. 20E competed with DA to bind to DopEcR. The results of the present study suggested that 20E, via binding to DopEcR, arrests larval feeding and promotes pupation.

更新日期：2019-08-31

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