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Functional evaluation of the insulin/insulin‐like growth factor signaling pathway in determination of wing polyphenism in pea aphid

机译:胰岛素/胰岛素样生长因子信号通路在豌豆蚜翅多腈症测定中的功能评价

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摘要

Abstract Wing polyphenism is a common phenomenon that plays key roles in environmental adaptation of insects. Insulin/insulin‐like growth factor signaling (IIS) pathway is a highly conserved pathway in regulation of metabolism, development, and growth in metazoans. It has been reported that IIS is required for switching of wing morph in brown planthopper via regulating the development of the wing pad. However, it remains elusive whether and how IIS pathway regulates transgenerational wing dimorphism in aphid. In this study, we found that pairing and solitary treatments can induce pea aphids to produce high and low percentage winged offspring, respectively. The expression level of ILP5 (insulin‐like peptide 5) in maternal head was significantly higher upon solitary treatment in comparison with pairing, while silencing of ILP5 caused no obvious change in the winged offspring ratio. RNA interference‐mediated knockdown of FoxO (Forkhead transcription factor subgroup O) in stage 20 embryos significantly increased the winged offspring ratio. The results of pharmacological and quantitative polymerase chain reaction experiments showed that the embryonic insulin receptors may not be involved in wing polyphenism. Additionally, ILP4 and ILP11 exhibited higher expression levels in 1st wingless offspring than in winged offspring. We demonstrate that FoxO negatively regulates the wing morph development in embryos. ILPs may regulate aphid wing polyphenism in a developmental stage‐specific manner. However, the regulation may be not mediated by the canonical IIS pathway. The findings advance our understanding of IIS pathway in insect transgenerational wing polyphenism.
机译:摘要 翅多腈是一种常见现象,在昆虫的环境适应中起着关键作用。胰岛素/胰岛素样生长因子信号转导 (IIS) 通路是后生动物调节代谢、发育和生长的高度保守通路。据报道,通过调节翼垫的发育来改变褐飞虱的翅膀形态需要IIS。然而,IIS通路是否以及如何调控蚜虫的跨代翅二态性仍然难以捉摸。在这项研究中,我们发现配对和单独处理可以分别诱导豌豆蚜虫产生高百分比和低百分比的有翅后代。与配对相比,单独处理后母体头部ILP5(胰岛素样肽5)的表达水平显著升高,而ILP5的沉默导致有翅后代比例没有明显变化。RNA干扰介导的FoxO(叉头转录因子亚组O)在20期胚胎中的敲除显著增加了有翅后代的比例。药理学和定量聚合酶链反应实验结果表明,胚胎胰岛素受体可能不参与翅多酚增多症。此外,ILP4 和 ILP11 在第 1 个无翅后代中的表达水平高于有翅后代。我们证明FoxO负向调节胚胎中的翅膀形态发育。ILPs可能以发育阶段特异性的方式调节蚜虫翅多腱症。然而,该调节可能不是由经典 IIS 通路介导的。这些发现促进了我们对昆虫跨代翅多酚症IIS通路的理解。

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