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调控德国小蠊雌成虫胰岛素样肽表达。

Regulation of insulin-like peptide expression in adult Blattella germanica females.

机构信息

Institute of Evolutionary Biology (CSIC.Universitat Pompeu Fabra), Passeig Marítim de la Barceloneta 37-49, 08003, Barcelona, Spain.

Institute of Evolutionary Biology (CSIC.Universitat Pompeu Fabra), Passeig Marítim de la Barceloneta 37-49, 08003, Barcelona, Spain.

出版信息

Insect Biochem Mol Biol. 2022 Feb;141:103706. doi: 10.1016/j.ibmb.2021.103706. Epub 2021 Dec 30.

DOI:10.1016/j.ibmb.2021.103706
PMID:34974083
Abstract

The insulin-IGF-signalling (IIS) pathway regulates key processes in metazoans. The pathway is activated through the binding of the ligands, which in insects are usually referred to as insulin-like peptides (ILPs), to a class of receptor tyrosine kinases, the insect insulin receptor. To study the pathway regulation, it is therefore essential to understand how ILPs are produced and released. In this study we analysed the factors that regulate the expression of the seven ILPs (BgILPs) expressed in adult females of the German cockroach, Blattella germanica. The results showed that the starvation-induced expression reduction of brain BgILP3, 5 and 6 and fat body BgILP7 is not due to reduced juvenile hormone (JH) or decreased TOR pathway activity. In addition, depletion of FoxO in starved females did not correct the low levels of these BgILPs, but even reduced further BgILP5 expression, indicating the need to maintain certain basal levels of BgILP5 even during starvation. Furthermore, JH promoted increased BgILP5 and decreased BgILP3 expression in the brain, an effect that required Methoprene-tolerant (Met), the JH receptor, but not Krüppel homolog 1 (Kr-h1), the main JH transducer. On the other hand, JH inhibited the expression of BgILP7 in the fat body, although in this case, the action required both Met and Kr-h1. In addition, JH reduction treatments produced a decrease in the expression of the insulin receptor in the fat body, which suggests an increase in IIS. The results show a peculiar regulation of ILP expression in adult B. germanica females, which is clearly different than that seen in other species. This is understandable given that gene duplications in recent clades have resulted in different sets of ILP genes, involving substantial changes in gene regulatory networks.

摘要

胰岛素-IGF 信号通路(IIS)调节后生动物的关键过程。该通路通过配体与一类受体酪氨酸激酶(昆虫胰岛素受体)的结合而被激活,在昆虫中,这些配体通常被称为胰岛素样肽(ILPs)。因此,为了研究该通路的调节,了解 ILPs 是如何产生和释放的是至关重要的。在这项研究中,我们分析了调节德国蟑螂(Blattella germanica)成年雌虫中表达的 7 种 ILPs(BgILPs)的因素。结果表明,饥饿诱导的脑 BgILP3、5 和 6 以及脂肪体 BgILP7 的表达减少并不是由于 JH 减少或 TOR 通路活性降低所致。此外,在饥饿的雌虫中耗尽 FoxO 并没有纠正这些 BgILPs 的低水平,反而进一步降低了 BgILP5 的表达,这表明即使在饥饿时也需要维持 BgILP5 的某些基础水平。此外,JH 促进了脑中 BgILP5 的增加和 BgILP3 的减少,这种效应需要 Methoprene-tolerant(Met),即 JH 受体,但不需要 Krüppel homolog 1(Kr-h1),即主要的 JH 转导物。另一方面,JH 抑制了脂肪体中 BgILP7 的表达,尽管在这种情况下,该作用需要 Met 和 Kr-h1。此外,JH 减少处理导致脂肪体中胰岛素受体的表达减少,这表明 IIS 增加。结果表明,德国蟑螂成年雌虫中 ILP 表达的调节具有特殊性,这与其他物种明显不同。考虑到最近进化枝中的基因重复导致了不同的 ILP 基因集,涉及基因调控网络的重大变化,这种情况是可以理解的。

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