Myosuppressin signaling deficiency affects ovarian development via repression of 20-hydroxyecdysone biosynthesis in Grapholita molesta

IF 4.2 1区 农林科学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pesticide Biochemistry and Physiology Pub Date : 2024-09-02 DOI:10.1016/j.pestbp.2024.106116
{"title":"Myosuppressin signaling deficiency affects ovarian development via repression of 20-hydroxyecdysone biosynthesis in Grapholita molesta","authors":"","doi":"10.1016/j.pestbp.2024.106116","DOIUrl":null,"url":null,"abstract":"<div><p>The steroid 20-hydroxyecdysone (20E) is crucial in regulating ovarian development. However, the neuropeptidergic mechanisms underlying ovarian development via 20E are underexplored. In this study, we investigated myosuppressin (MS) signaling in the dominant fruit pest <em>Grapholita molesta</em> and revealed that MS signaling is necessary for 20E biosynthesis during ovarian maturation. Pharmacological and molecular docking analyses confirmed that the GmMS mature peptide could activate its receptor GmMSR. Additionally, transcript expression analyses of <em>GmMS</em> and <em>GmMSR</em> showed different distribution patterns in adults. Notably, <em>GmMSR</em> was also detected in the ovaries of sexually mature females. RNAi-mediated dysfunction of <em>GmMS</em> or <em>GmMSR</em> specifically decreased fertility in females. Furthermore, <em>GmMS</em> or <em>GmMSR</em> knockdown decreased vitellogenin synthesis and uptake, thereby delaying ovarian development. RNA-seq, gene expression validation, and hormone quantification further revealed that GmMS signaling depletion blocked 20E biosynthesis in the ovary. Finally, exogenous MS rescued most dsGmMS<em>-</em> or dsGmMSR-induced ovarian defects and 20E titers. These results suggest that MS/MSR-to-20E signaling regulates ovarian development through vitellogenesis, providing a new perspective on the development of neuroendocrine targets that suppress pest field populations.</p></div>","PeriodicalId":19828,"journal":{"name":"Pesticide Biochemistry and Physiology","volume":null,"pages":null},"PeriodicalIF":4.2000,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pesticide Biochemistry and Physiology","FirstCategoryId":"97","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0048357524003493","RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

The steroid 20-hydroxyecdysone (20E) is crucial in regulating ovarian development. However, the neuropeptidergic mechanisms underlying ovarian development via 20E are underexplored. In this study, we investigated myosuppressin (MS) signaling in the dominant fruit pest Grapholita molesta and revealed that MS signaling is necessary for 20E biosynthesis during ovarian maturation. Pharmacological and molecular docking analyses confirmed that the GmMS mature peptide could activate its receptor GmMSR. Additionally, transcript expression analyses of GmMS and GmMSR showed different distribution patterns in adults. Notably, GmMSR was also detected in the ovaries of sexually mature females. RNAi-mediated dysfunction of GmMS or GmMSR specifically decreased fertility in females. Furthermore, GmMS or GmMSR knockdown decreased vitellogenin synthesis and uptake, thereby delaying ovarian development. RNA-seq, gene expression validation, and hormone quantification further revealed that GmMS signaling depletion blocked 20E biosynthesis in the ovary. Finally, exogenous MS rescued most dsGmMS- or dsGmMSR-induced ovarian defects and 20E titers. These results suggest that MS/MSR-to-20E signaling regulates ovarian development through vitellogenesis, providing a new perspective on the development of neuroendocrine targets that suppress pest field populations.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
肌抑素信号缺乏通过抑制 20-hydroxyecdysone 生物合成影响 Grapholita molesta 的卵巢发育
类固醇 20-羟基蜕皮激素(20E)对调节卵巢发育至关重要。然而,通过 20E 实现卵巢发育的神经肽能机制尚未得到充分探索。在这项研究中,我们研究了优势果实害虫 Grapholita molesta 的肌抑素(MS)信号传导,发现 MS 信号传导是卵巢成熟过程中 20E 生物合成所必需的。药理和分子对接分析证实,GmMS成熟肽可激活其受体GmMSR。此外,GmMS和GmMSR的转录本表达分析显示了它们在成体中的不同分布模式。值得注意的是,在性成熟雌性动物的卵巢中也检测到了GmMSR。RNAi- 介导的 GmMS 或 GmMSR 功能障碍特异性地降低了雌性的生育能力。此外,GmMS或GmMSR敲除会减少卵黄素的合成和吸收,从而延迟卵巢发育。RNA-seq、基因表达验证和激素定量分析进一步表明,GmMS信号消耗阻碍了卵巢中20E的生物合成。最后,外源MS能挽救大多数dsGmMS或dsGmMSR诱导的卵巢缺陷和20E滴度。这些结果表明,MS/MSR-20E 信号通过卵黄发生调节卵巢发育,为抑制害虫田间种群的神经内分泌靶标的发展提供了一个新的视角。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
7.00
自引率
8.50%
发文量
238
审稿时长
4.2 months
期刊介绍: Pesticide Biochemistry and Physiology publishes original scientific articles pertaining to the mode of action of plant protection agents such as insecticides, fungicides, herbicides, and similar compounds, including nonlethal pest control agents, biosynthesis of pheromones, hormones, and plant resistance agents. Manuscripts may include a biochemical, physiological, or molecular study for an understanding of comparative toxicology or selective toxicity of both target and nontarget organisms. Particular interest will be given to studies on the molecular biology of pest control, toxicology, and pesticide resistance. Research Areas Emphasized Include the Biochemistry and Physiology of: • Comparative toxicity • Mode of action • Pathophysiology • Plant growth regulators • Resistance • Other effects of pesticides on both parasites and hosts.
期刊最新文献
Factors influencing pesticide-biocontrol agent compatibility: A metadata-based review Two critical detoxification enzyme genes, NlCYP301B1 and NlGSTm2 confer pymetrozine resistance in the brown planthopper (BPH), Nilaparvata lugens Stål Editorial Board Resistance risk and mechanism of Ustilaginoidea virens to pydiflumetofen Functional analysis of dopa decarboxylase in the larval pupation and immunity of the diamondback moth, Plutella xylostella
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1