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淘汰赛BR-C诱导E93的过早表达,从而在幼虫形态下触发成人分化

Chang Liu^1,2, Mian-Zhi Wu^1,2, Zi-Jing Zheng^1,2

¹School of Agriculture and Biotechnology, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.

Pest management science

|December 6, 2024

概括

广泛复杂 (BR-C) 基因通常会在昆虫转型过程中防止过早的成年发育. 它在Spodoptera frugiperda幼虫中缺席,通过允许E93基因激活,从而触发早期成年特征.

科学领域:

昆虫的变形是昆虫的变形
发育生物学是发展生物学.
分子遗传学分子遗传学

背景情况:

整体甲基变形依赖于幼特异性宽复合体 (BR-C) 和成年特异性埃克迪松诱导蛋白93F (E93).
目前尚不完全了解BR-C和E93之间的精确相互作用,以及它们在化过程中的细胞死亡和分化中的作用.

研究的目的:

为了研究BR-C和E93在变形过程中的相互作用.
阐明BR-C对编程细胞死亡和细胞分化的影响.
了解在Spodoptera frugiperda中的E93上的BR-C的调节作用.

主要方法:

在Spodoptera frugiperda中使用多个单导向RNA (sgRNA) 的BR-C的马赛克淘汰.
定量实时聚合酶连锁反应 (qPCR) 用于基因表达分析.
组织学观察和TUNEL测定以检测细胞亡和组织分化.

主要成果:

BR-C 淘汰赛导致了变形的幼/子中间表型.
在晚期幼虫阶段的BR-C突变体中观察到E93的过早表达.
在幼虫组织中激活了亡,成年中肠结构出现在BR-C突变中.

结论:

缺乏BR-C导致过早的E93表达,在幼虫阶段触发成人分化.
在Spodoptera frugiperda的转化过程中,BR-C对E93产生抑制作用.
这项研究揭示了一种控制昆虫变形的新型调节机制.

关键词:

这就是CRISPR/Cas9的作用.它们是花鸟 (Spodoptera frugiperda) 的种类.灭症 (apoptosis) 是一种死亡的过程.变形转化是一种转化.sgRNARNA 是一个

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In-vitro Mutagenesis

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