反向工程在Plutella xylostella中对Bt Cry1Ac毒素的高水平耐药性揭示了荷尔蒙调节反通路
Dan Sun1, Mingyun Wang1, Le Guo2
1Key Laboratory of Microbiological Metrology, Measurement & Bio-product Quality Security, State Administration for Market Regulation, College of Life Science, China Jiliang University, Hangzhou 310018, China.
Pesticide biochemistry and physiology
|April 22, 2025
概括
昆虫对Bacillus thuringiensis (Bt) 毒素的耐药性涉及一种新的荷尔蒙反循环. 这条由SE2逆转移素插入引发的途径,可调节MAP4K4,从而在Plutella xylostella中产生Bt耐药性.
科学领域:
- 分子生物学分子生物学
- 昆虫学 昆虫学是一门学科.
- 遗传学 是一个遗传学.
背景情况:
- 昆虫对Bacillus thuringiensis (Bt) 毒素的耐药性威胁着生物杀虫剂的有效性.
- 之前的工作将FOXO转录因子与SE2逆转录素结合,MAP4K4过度表达和Plutella xylostella中的Bt耐药性联系在一起.
- 在耐药菌株中观察到较高的激素水平,但其作用仍然不清楚.
研究的目的:
- 阐明在Plutella xylostella中Bt Cry1Ac耐药性背后的分子机制和激素调节.
- 调查SE2逆转移子插入在敏感菌株中的作用.
- 为了确认潜在的荷尔蒙反通路.
主要方法:
- 使用反向遗传学建立了一个同卵性敲进菌株 (SE2-KI).
- 将SE2逆转移子插入敏感的Plutella xylostella菌株的MAP4K4促进体中.
- 分析了MAP4K4表达,中肠受体水平,激素标位和抵抗表型.
主要成果:
- 在MAP4K4促进体中插入SE2成功诱导了MAP4K4.4的过度表达.
- 诱导的MAP4K4过度表达导致中肠受体下调和Bt Cry1Ac抵抗表型.
- 插入SE2显著提高了两种关键昆虫激素的水平,证实了积极的反循环.
结论:
- 发现了一种新的荷尔蒙调节反通路,可以控制Plutella xylostella中的Cry1Ac抵抗.
- 证明SE2逆转移素的插入可以通过MAP4K4和荷尔蒙信号传递驱动Bt抵抗.
- 提供了对Bt耐药性机制的见解,这对于开发耐药性管理策略至关重要.
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