Shen Chen-Hui, Xu Qing-Yu, Fu Kai-Yun, Guo Wen-Chao, Jin Lin, Li Guo-Qing
Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests, College of Plant Protection, Nanjing Agricultural University, Nanjing, China.
Institute of Plant Protection, Xinjiang Academy of Agricultural Sciences, Urumqi, China.
Front Physiol. 2020 Dec 1;11:593962. doi: 10.3389/fphys.2020.593962. eCollection 2020.
Insect ecdysis triggering hormone (ETH) receptors (ETHRs) are rhodopsin-like G protein-coupled receptors. Upon binding its ligand ETH, ETHR initiates a precisely programed ecdysis behavior series and physiological events. In , the gene produces two functionally distinct splicing isoforms, and . ETH/ETHRA activates eclosion hormone (EH), kinin, crustacean cardioactive peptide (CCAP), and bursicon (burs and pburs) neurons, among others, in a rigid order, to elicit the behavioral sequences and physiological actions for ecdysis at all developmental stages, whereas ETH/ETHRB is required at both pupal and adult ecdysis. However, the role of ETHRB in regulation of molting has not been clarified in any non-drosophila insects. In the present paper, we found that 20-hydroxyecdysone (20E) signaling triggers the expression of both and in a Coleopteran insect pest, the Colorado potato beetle . RNA interference (RNAi) was performed using double-stranded RNAs (dsRNAs) targeting the common (ds) or isoform-specific (ds, ds) regions of . RNAi of ds, ds, or ds by the final-instar larvae arrested larva development. The arrest was not rescued by feeding 20E. All the depleted larvae stopped development at prepupae stage; the body cavity was expanded by a large amount of liquid. Comparably, more than 80% of the RNAi larvae developmentally halted at the prepupae stage. The remaining hypomorphs became pupae, with blackened wings and highly-expressed , and four melanin biosynthesis genes. Therefore, ETHRA and ETHRB play isoform-specific roles in regulation of ecdysis during larva-pupa transition in .
昆虫蜕皮触发激素（ETH）受体（ETHRs）是视紫红质样G蛋白偶联受体。一旦与其配体ETH结合，ETHR就会启动精确编程的蜕皮行为序列和生理事件。在[具体物种名称未给出]中，[基因名称未给出]基因产生两种功能不同的剪接异构体，即[异构体名称1]和[异构体名称2]。ETH/ETHR A以严格的顺序激活羽化激素（EH）、激肽、甲壳类心脏活性肽（CCAP）和bursicon（burs和pburs）神经元等，以引发所有发育阶段蜕皮的行为序列和生理作用，而在蛹期和成虫蜕皮时则需要ETH/ETHR B。然而，在任何非果蝇昆虫中，ETHR B在蜕皮调节中的作用尚未阐明。在本文中，我们发现20-羟基蜕皮酮（20E）信号触发了鞘翅目害虫科罗拉多马铃薯甲虫[物种名称未给出]中[基因名称未给出]和[基因名称未给出]的表达。使用靶向[基因名称未给出]的共同（ds）或异构体特异性（ds[异构体名称1]、ds[异构体名称2]）区域的双链RNA（dsRNAs）进行RNA干扰（RNAi）。末龄幼虫对ds[异构体名称1]、ds[异构体名称2]或ds进行RNAi会导致幼虫发育停滞。通过喂食20E无法挽救这种停滞。所有[基因名称未给出]缺失的幼虫在蛹前期停止发育；体腔因大量液体而扩张。相比之下，超过80%的[基因名称未给出]RNAi幼虫在蛹前期发育停滞。其余的[基因名称未给出]低表达型变成了蛹，翅膀变黑，[基因名称未给出]、[基因名称未给出]和四个黑色素生物合成基因高度表达。因此，在[物种名称未给出]幼虫-蛹转变过程中，ETHR A和ETHR B在蜕皮调节中发挥异构体特异性作用。
