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(Walker)中对 Vip3Aa 杀虫蛋白的抗性迅速演变与中肠受体结合的改变无关。

The Rapid Evolution of Resistance to Vip3Aa Insecticidal Protein in (Walker) Is Not Related to Altered Binding to Midgut Receptors.

机构信息

Instituto de Biotecnología y Biomedicina (BIOTECMED), Department of Genetics, Universitat de València, 46100 Burjassot, Spain.

State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, No. 2, West Yuanmingyuan Road, Beijing 100193, China.

出版信息

Toxins (Basel). 2021 May 20;13(5):364. doi: 10.3390/toxins13050364.

DOI:10.3390/toxins13050364
PMID:34065247
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8190635/
Abstract

Laboratory selection for resistance of field populations is a well-known and useful tool to understand the potential of insect populations to evolve resistance to insecticides. It provides us with estimates of the frequency of resistance alleles and allows us to study the mechanisms by which insects developed resistance to shed light on the mode of action and optimize resistance management strategies. Here, a field population of was subjected to laboratory selection with either Vip3Aa, Cry1Ab, or Cry1F insecticidal proteins from . The population rapidly evolved resistance to Vip3Aa reaching, after eight generations, a level of >3061-fold resistance, compared with the unselected insects. In contrast, the same population did not respond to selection with Cry1Ab or Cry1F. The Vip3Aa resistant population did not show cross resistance to either Cry1Ab or Cry1F. Radiolabeled Vip3Aa was tested for binding to brush border membrane vesicles from larvae from the susceptible and resistant insects. The results did not show any qualitative or quantitative difference between both insect samples. Our data, along with previous results obtained with other Vip3Aa-resistant populations from other insect species, suggest that altered binding to midgut membrane receptors is not the main mechanism of resistance to Vip3Aa.

摘要

田间种群的抗药性实验室选择是一种众所周知且有用的工具,可以帮助我们了解昆虫种群对杀虫剂产生抗药性的潜力。它为我们提供了抗性等位基因频率的估计,并使我们能够研究昆虫产生抗药性的机制,从而揭示作用方式,并优化抗药性管理策略。在这里,我们用来自 的 Vip3Aa、Cry1Ab 或 Cry1F 杀虫蛋白对田间种群 进行了实验室选择。该种群对 Vip3Aa 的抗药性迅速进化,在经过 8 代后,与未选择的昆虫相比,其抗药性达到了 >3061 倍。相比之下,同一种群对 Cry1Ab 或 Cry1F 的选择没有反应。Vip3Aa 抗性种群对 Cry1Ab 或 Cry1F 没有表现出交叉抗性。放射性标记的 Vip3Aa 被用于测试对来自敏感和抗性昆虫幼虫的刷状缘膜囊泡的结合。结果显示,两种昆虫样本之间没有任何定性或定量的差异。我们的数据,以及之前从其他昆虫物种获得的其他 Vip3Aa 抗性种群的结果表明,对中肠膜受体的结合改变不是对 Vip3Aa 产生抗药性的主要机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c0f/8190635/734a6c1d5da5/toxins-13-00364-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c0f/8190635/734a6c1d5da5/toxins-13-00364-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c0f/8190635/734a6c1d5da5/toxins-13-00364-g001.jpg

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