Downregulation of a transcription factor associated with resistance to Bt toxin Vip3Aa in the invasive fall armyworm

Downregulation of a transcription factor associated with resistance to Bt toxin Vip3Aa in the invasive fall armyworm
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DOI:
10.1073/pnas.2306932120
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发表时间:
2023-10-31
影响因子:
11.1
通讯作者:
Xiao,Yutao
Xiao,Yutao
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Jin,Minghui;Shan,Yinxue;Xiao,Yutao

文献摘要

相似文献

从苏云金芽孢杆菌(Bt)产生杀虫蛋白的转基因作物已经彻底改变了对一些主要害虫的控制。然而,超过25例田间进化的实际抗药性降低了产生晶体(Cry)Bt蛋白的转基因作物的效力,促使替代作物的采用,包括产生Bt营养杀虫蛋白Vip3Aa的作物。虽然对Vip3Aa的实际抗性还没有报道,但迫切需要更好地了解对Vip3Aa的抗性的遗传基础,以便主动监测、延迟和对抗害虫的抗性。这对秋季粘虫尤其重要,它已经进化出对Cry蛋白的实际抵抗力,是世界上最具破坏性的害虫之一。在这里,我们报告了转录因子基因SfMyband对Vip3Aa INS的抗性与下调之间的关系。果子酱。全基因组关联研究、精细作图和RNA-Seq的结果表明,该基因是实验室选择的菌株对Vip3Aa产生206倍抗药性的有力候选者。用RNA干扰(RNAi)或CRISPR/Cas9基因编辑降低了敏感品系中SfMyb的表达,降低了对Vip3Aa的敏感性,证实了该基因的表达降低可以导致对Vip3Aa的抗性。相对于SfMyb的野生型启动子,抗性品系中的启动子缺失且活性较低。来自酵母单杂交分析、基因组学、RNA-Seq、RNAi和蛋白质组学的数据表明,这些基因是介导SfMybon Vip3Aa抗性的有力候选基因。本文报道的结果可能有助于了解和管理害虫对Vip3Aa的抗性。
Transgenic crops producing insecticidal proteins fromBacillus thuringiensis(Bt) have revolutionized control of some major pests. However, more than 25 cases of field-evolved practical resistance have reduced the efficacy of transgenic crops producing crystalline (Cry) Bt proteins, spurring adoption of alternatives including crops producing the Bt vegetative insecticidal protein Vip3Aa. Although practical resistance to Vip3Aa has not been reported yet, better understanding of the genetic basis of resistance to Vip3Aa is urgently needed to proactively monitor, delay, and counter pest resistance. This is especially important for fall armyworm (Spodoptera frugiperda), which has evolved practical resistance to Cry proteins and is one of the world’s most damaging pests. Here, we report the identification of an association between downregulation of the transcription factor geneSfMyband resistance to Vip3Aa inS. frugiperda. Results from a genome-wide association study, fine-scale mapping, and RNA-Seq identified this gene as a compelling candidate for contributing to the 206-fold resistance to Vip3Aa in a laboratory-selected strain. Experimental reduction ofSfMybexpression in a susceptible strain using RNA interference (RNAi) or CRISPR/Cas9 gene editing decreased susceptibility to Vip3Aa, confirming that reduced expression of this gene can cause resistance to Vip3Aa. Relative to the wild-type promoter forSfMyb, the promoter in the resistant strain has deletions and lower activity. Data from yeast one-hybrid assays, genomics, RNA-Seq, RNAi, and proteomics identified genes that are strong candidates for mediating the effects ofSfMybon Vip3Aa resistance. The results reported here may facilitate progress in understanding and managing pest resistance to Vip3Aa.