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马尼拉蜂寄生调控宿主胰岛素信号通路基因转录对幼虫发育的控制。

Transcriptional regulation of host insulin signaling pathway genes controlling larval development by Microplitis manilae parasitization.

机构信息

Hainan Institute, Zhejiang University, Sanya, China.

Sanya Nanfan Research Institute & School of Tropical Crops, Hainan University, Sanya, China.

出版信息

Arch Insect Biochem Physiol. 2023 May;113(1):e22003. doi: 10.1002/arch.22003. Epub 2023 Jan 24.

DOI:10.1002/arch.22003
PMID:36694471
Abstract

Idiobiont parasitoids using other insects as hosts sabotage the host growth and development to ensure their offspring survival. Numerous studies have discovered that insect development is subtly regulated by the conserved insulin signaling pathway. However, little is known about how wasp parasitization disrupts host development controlled by the insulin signaling pathway. Here we address this study to determine the effect of wasp parasitism on host Spodoptera frugiperda development using the idiobiont parasitoid Microplitis manilae as a model. Upon M. manilae parasitization, the body weight, body length, and food consumption of host insect were dramatically reduced compared to the unparasitized S. frugiperda. We next identified the core genes involved in host insulin signaling pathway and further analyzed the domain organizations of these genes. Phylogenetic reconstruction based on the insulin receptors clustered S. frugiperda together with other noctuidae insects. In the latter study, we profiled the expression patterns of host insulin signaling pathway genes in response to M. manilae parasitization at 2, 24, and 48 h, significant decreases in mRNA levels were recorded in S. frugiperda larvae upon 24 and 48 h parasitization. These current findings substantially add to our understanding of the physiological interaction between parasitoid and host insects, thus contributing to revealing the molecular mechanism of parasitic wasps regulating host development.

摘要

拟寄生物种利用其他昆虫作为宿主,破坏宿主的生长和发育,以确保其后代的生存。许多研究已经发现,昆虫的发育受到保守的胰岛素信号通路的微妙调节。然而,对于寄生蜂如何破坏受胰岛素信号通路控制的宿主发育,人们知之甚少。在这里,我们以拟寄生物种微孢子虫(Microplitis manilae)为模型,研究了寄生对宿主烟夜蛾(Spodoptera frugiperda)发育的影响。与未被寄生的烟夜蛾相比,寄生后,宿主昆虫的体重、体长和食物消耗明显减少。接下来,我们鉴定了参与宿主胰岛素信号通路的核心基因,并进一步分析了这些基因的结构域组织。基于胰岛素受体的系统发育重建将烟夜蛾与其他夜蛾科昆虫聚类在一起。在后一项研究中,我们分析了宿主胰岛素信号通路基因在微孢子虫寄生后 2、24 和 48 小时的表达模式,记录到在 24 和 48 小时寄生后,烟夜蛾幼虫的 mRNA 水平显著下降。这些发现极大地增加了我们对寄生蜂和宿主昆虫之间生理相互作用的理解,从而有助于揭示寄生蜂调节宿主发育的分子机制。

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