Functional synergy and genomic linkage of glyphosate resistance traits in Canada fleabane.

IF 3.8 1区农林科学 Q1 AGRONOMY

Pest Management Science Pub Date : 2025-09-04 DOI:10.1002/ps.70194

Eric R Page,Sara L Martin,Sydney Meloche,Alyssa Thibodeau,Martin Laforest

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引用次数: 0

Abstract

BACKGROUND Glyphosate resistance in Conyza canadensis (Canada fleabane) has been primarily attributed to non-target-site resistance (NTSR) mechanisms such as vacuolar sequestration, though these have not been formally elucidated. While a target-site mutation at EPSPS2 (P106S) was recently identified, it failed to account for many resistant cases. These findings underscore the need to re-evaluate the genetic basis of glyphosate resistance in this species. RESULTS Using an F2 population derived from glyphosate-resistant and susceptible biotypes, we disentangled the individual and combined effects of target-site resistance (TSR) and NTSR. Dose-response phenotyping and genotyping revealed that NTSR conferred broad protection across a wide range of glyphosate doses, while TSR provided a more limited, dose-dependent benefit. When both mechanisms were present, median lethal dose (LD50) values greatly exceeded additive expectations, indicating a synergistic interaction. Quantitative trait locus (QTL) mapping identified a major-effect locus associated with NTSR on chromosome 4, with candidate genes linked to membrane transport and subcellular compartmentalization processes. Segregation distortion and recombination frequency estimates suggest moderate genetic linkage between TSR and NTSR loci, facilitating co-inheritance of resistance alleles. CONCLUSION This study provides the first explicit quantitative analysis of gene × gene interactions underlying herbicide resistance in C. canadensis. By disentangling TSR and NTSR, we show that single copies of the TSR and NTSR alleles confer approximately nine-fold and seven-fold glyphosate resistance, respectively. When combined, these mechanisms exhibit synergism, resulting in resistance levels that exceed additive LD50 expectations by more than two-fold. Both TSR and NTSR loci have been mapped to chromosome 4, and moderate genomic linkage (~27% recombination) between them will likely contribute to the persistence and spread of high-level resistance, even under low selection pressure. © 2025 His Majesty the King in Right of Canada. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry. Reproduced with the permission of the Minister of Agriculture and Agri-Food Canada.

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加拿大藜抗草甘膦性状的功能协同和基因组连锁。

背景：加拿大Conyza canadensis（加拿大fleabane）的草甘膦抗性主要归因于非靶点抗性（NTSR）机制，如液泡封存，尽管这些尚未正式阐明。虽然最近发现了EPSPS2 （P106S）的靶位点突变，但它无法解释许多耐药病例。这些发现强调需要重新评估该物种对草甘膦抗性的遗传基础。结果利用来自草甘膦抗性和敏感生物型的F2群体，揭示了目标位点抗性（TSR）和NTSR的个体效应和联合效应。剂量反应表型和基因分型显示，NTSR在广泛的草甘膦剂量范围内具有广泛的保护作用，而TSR提供了更有限的剂量依赖性益处。当两种机制都存在时，中位致死剂量（LD50）值大大超过相加性预期，表明存在协同相互作用。数量性状位点（QTL）定位在4号染色体上发现了一个与NTSR相关的主要影响位点，候选基因与膜运输和亚细胞区隔化过程有关。分离畸变和重组频率估计表明，TSR和NTSR位点之间存在适度的遗传连锁，有利于抗性等位基因的共遗传。结论本研究首次对加拿大草抗除草剂基因间相互作用进行了明确的定量分析。通过解开TSR和NTSR的缠结，我们发现TSR和NTSR等位基因的单拷贝分别赋予大约9倍和7倍的草甘膦抗性。当这些机制结合在一起时，表现出协同作用，导致抗性水平超过添加剂LD50预期的两倍以上。TSR和NTSR位点均定位于4号染色体，它们之间的适度基因组连锁（~27%的重组）可能有助于高水平抗性的持续和传播，即使在低选择压力下也是如此。©2025加拿大在位国王陛下。由John Wiley & Sons Ltd代表化学工业协会出版的《害虫管理科学》。经加拿大农业和农业食品部许可转载。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Pest Management Science 农林科学-昆虫学

CiteScore

7.90

自引率

9.80%

发文量

553

审稿时长

4.8 months

期刊介绍： Pest Management Science is the international journal of research and development in crop protection and pest control. Since its launch in 1970, the journal has become the premier forum for papers on the discovery, application, and impact on the environment of products and strategies designed for pest management. Published for SCI by John Wiley & Sons Ltd.