スポドプテラ・フリペルダのエマレクチンベンゾアート耐性菌株のGSTe2プロモーターの変異は,エマレクチンベンゾアートに対する高い発現レベルと強化された代謝解毒能力に貢献する
Zhongxiang Sun1, Yuhan Chen1, Zhihui Lu1
1State Key Laboratory of Conservation and Utilization of Biological Resources of Yunnan, College of Plant Protection, Yunnan Agricultural University, Kunming 650201, China.
Journal of agricultural and food chemistry
|September 3, 2025
まとめ
エマレクチンベンゾ酸 (EB) 耐性は,GSTe2遺伝子と関連しています. プロモーター変異はGSTe2発現を増加させ,EB代謝を促進し,殺虫剤の有効性を低下させます.
科学分野:
- 昆虫学
- 分子生物学
- 生物化学
背景:
- エマレクチンベンゾ酸 (EB) は,秋の軍虫 (Spodoptera frugiperda) の制御に不可欠である.
- 昆虫剤の耐性,特にEBに対する耐性は,害虫管理に増大する脅威です.
- 耐性メカニズムの理解は 持続可能な制御戦略の開発に不可欠です
研究 の 目的:
- スポドプテラ フルギペルダに耐性を与える遺伝子や変異を特定する.
- グルタチオンS-トランスファーゼ (GSTs) を含む特定の遺伝子のEB耐性における役割を明らかにする.
- この害虫のEB耐性の 分子メカニズムを提案する
主な方法:
- EB耐性および感受性S. frugiperda株のゲノム再配列化とトランスクリプトーム解析
- 耐性候補遺伝子 (GST,シトクロームP450,ABCトランスポーター) の選択と機能的検証
- 遺伝子サイレンシング (dsRNA注射),インビトロ酵素測定 (UPLC-MS/MS),およびプロモーター活性分析.
主要な成果:
- 177の候補耐性遺伝子が特定され,GSTe2は有意なアップレギュレーションと高いEB親和性を示した.
- GSTe2を静止すると,EBストレス下での幼虫死亡率が増加し,耐性におけるその役割が確認された.
- GSTe2はEBを in vitroで代謝することが確認された.
- 耐性菌株のGSTe2プロモーターの3つの単核型ポリモルフィズムが,その転写活動を強化した.
結論:
- GSTe2のプロモーター変異は,その転写とEBの代謝解毒を促進し,重要な抵抗メカニズムを表しています.
- この研究は,スポドプテラ・フルギペルダのEB耐性に関する重要な洞察を提供します.
- 対象となる害虫対策戦略や耐性管理プログラムの開発に役立つ.
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