Adipokinetic Hormone Receptor Mediates Trehalose Homeostasis to Promote Vitellogenin Uptake by Oocytes in Nilaparvata lugens
Adipokinetic Hormone Receptor Mediates Trehalose Homeostasis to Promote Vitellogenin Uptake by Oocytes in Nilaparvata lugens
复制标题
脂肪运动激素受体介导海藻糖稳态以促进褐飞虱卵母细胞对卵黄蛋白原的摄取
DOI：
10.3389/fphys.2018.01904
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发表时间：
2019-01-08
影响因子：
4
通讯作者：
Zeng, Rensen
中科院分区：
文献类型：
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作者：
Lu, Kai;Wang, Ying;Zeng, Rensen
众所周知，脂肪动力学激素（AKHs）可以调动昆虫体内的脂质和碳水化合物进行能量消耗活动。这些神经肽通过与脂肪体细胞质膜上的AKH受体（AKHRs）相互作用发挥作用，通过刺激三酰基甘油（TAG）脂解为二酰基甘油（DAG）和糖原转化为海藻糖来调节能量动员。本文研究了褐飞虱（Nilaparvata lugens）雌性繁殖过程中AKH/AKHR信号系统在海藻糖代谢和卵黄形成中的作用。通过RNA干扰（RNAi）敲低AKHR表达导致血淋巴循环海藻糖减少，脂肪体中两种海藻糖酶水平显著升高，提示AKHR对血淋巴海藻糖水平的调节可能是通过调节海藻糖降解来实现的。此外，注射双链RNA （dsRNA）用于AKHR的成年雌性表现为卵母细胞成熟延迟，产卵前期延长，卵数下降，繁殖力下降。考虑到AKHR沉默导致的这些表型与卵黄蛋白原受体（VgR） RNAi相似，我们进一步分析了AKHR与卵黄蛋白形成之间可能的联系。敲低AKHR对脂肪体的Vg合成没有影响，但显著降低卵巢的VgR水平。在rnai雌性小鼠中，我们观察到血淋巴中Vg积累增加，卵巢中Vg沉积减少。此外，通过向AKHR RNAi雌鼠注射海藻糖，可以部分地挽救发育中的卵母细胞中VgR表达的减少和Vg的掺入。本研究提示海藻糖参与了AKH/AKHR信号介导的生殖控制，并为AKH/AKHR调控海藻糖代谢在昆虫卵黄形成、卵母细胞成熟和繁殖力中的作用机制提供了新的认识。
Adipokinetic hormones (AKHs) are well known to mobilize lipids and carbohydrates for energy-consuming activities in insects. These neuropeptides exert their functions by interacting with AKH receptors (AKHRs) located on the plasma membrane of fat body cells, which regulates energy mobilization by stimulating lipolysis of triacylglycerols (TAG) to diacylglycerols (DAG) and conversion of glycogen into trehalose. Here, we investigated the roles of AKH/AKHR signaling system in trehalose metabolism and vitellogenesis during female reproduction in the brown planthopper, Nilaparvata lugens. Knockdown of AKHR expression by RNA interference (RNAi) resulted in a decrease of the circulating trehalose in hemolymph and significantly increased levels of two trehalases in fat bodies, indicating that the modulation of hemolymph trehalose levels by AKHR may be mediated by regulating trehalose degradation. In addition, adult females that had been injected with double-stranded RNA (dsRNA) for AKHR exhibited delayed oocyte maturation, prolonged pre-oviposition period, as well as decline in egg number and reduction in fecundity. Considering that these phenotypes resulting from AKHR silencing are similar to those of vitellogenin receptor (VgR) RNAi, we further analyzed a possible connection between AKHR and vitellogenesis. Knockdown of AKHR showed no effects on the Vg synthesis in fat bodies, whereas it significantly reduced the levels of VgR in ovaries. With RNAi-females, we observed an increase of Vg accumulation in hemolymph and a decrease of Vg deposition in ovaries. Moreover, the decrease in VgR expression and Vg incorporation by developing oocytes could be partially rescued by injection of trehalose into AKHR RNAi females. The present study has implicated trehalose in the AKH/AKHR signaling-mediated control of reproduction and provided new insight into mechanisms of AKH/AKHR regulation of trehalose metabolism in insect vitellogenesis, oocyte maturation and fecundity.