Failure to control Palmer amaranth with glyphosate and protoporphyrinogen IX oxidase (PPO)-inhibitor herbicides was reported across southwestern Nebraska in 2017. The objectives of this study were to 1) confirm and 2) validate glyphosate and PPO-inhibitor (fomesafen and lactofen) resistance in 51 Palmer amaranth accessions from southwestern Nebraska using genotypic and whole-plant phenotypic assay correlations and cluster analysis, and 3) determine which agronomic practices might be influencing glyphosate resistance in Palmer amaranth accessions in that location. Based on genotypic assay, 88% of 51 accessions contained at least one individual with amplification (>2 copies) of the 5-enolypyruvyl-shikimate-3-phosphate synthase (EPSPS) gene, which confers glyphosate resistance; and/or a mutation in the PPX2 gene, either ΔG210 or R128G, which endows PPO-inhibitor resistance in Palmer amaranth. Cluster analysis and high correlation (0.83) between genotypic and phenotypic assays demonstrated that EPSPS gene amplification is the main glyphosate resistance mechanism in Palmer amaranth accessions from southwestern Nebraska. In contrast, there was poor association between genotypic and phenotypic responses for PPO-inhibitor resistance, which was attributed to segregation for PPO-inhibitor resistance within these accessions and/or the methodology that was adopted herein. Genotypic assays can expedite the process of confirming known glyphosate and PPO-inhibitor resistance mechanisms in Palmer amaranth from southwestern Nebraska and other locations. Phenotypic assays are also a robust method for confirming glyphosate resistance but not necessarily PPO-inhibitor resistance in Palmer amaranth. Moreover, random forest analysis of glyphosate resistance in Palmer amaranth indicated that EPSPS gene amplification, county, and current and previous crops are the main factors influencing glyphosate resistance within that geographic area. Most glyphosate-susceptible Palmer amaranth accessions were found in a few counties in areas with high crop diversity. Results presented here confirm the spread of glyphosate resistance and PPO-inhibitor resistance in Palmer amaranth accessions from southwestern Nebraska and demonstrate that less diverse cropping systems are an important driver of herbicide resistance evolution in Palmer amaranth.

据报道，2017年内布拉斯加州西南部地区未能使用草甘膦和原卟啉原IX氧化酶（PPO）抑制剂除草剂控制Palm菜。这项研究的目标是：1）确认和2）验证草甘膦和PPO抑制剂（fomesafen和乳铁芬）的耐药性使用基因型和整株表型分析的相关性和聚类分析，从内布拉斯加州西南部的51个Palmer mar菜中，研究了3种农艺方法可能影响该位置的Palm菜中草甘膦的抗性。根据基因型分析，在51个种质中，有88％包含至少一个个体（具有5个烯丙基丙酮酸-shi草酸酯-3-磷酸合酶（EPSPS）基因）的扩增（> 2个拷贝）；该基因赋予草甘膦抗性。和/或PPX2基因ΔG210或R128G，在Palmer mar菜中赋予PPO抑制剂抗性。基因型和表型分析之间的聚类分析和高度相关性（0.83）表明EPSPS基因扩增是内布拉斯加州西南部Palmer mar菜品种的主要抗草甘膦机制。相反，对于PPO-抑制剂抗性的基因型和表型反应之间的关联性较差，这归因于这些材料和/或本文采用的方法中PPO-抑制剂抗性的分离。基因型检测可以加快确认来自内布拉斯加州西南部和其他地区的帕默a菜中已知的草甘膦和PPO抑制剂抗性机制的过程。表型化验也是一种可靠的方法，可用于确认帕默a菜中的草甘膦抗性，但不一定是PPO抑制剂抗性。此外，帕尔默a菜中草甘膦抗性的随机森林分析表明，EPSPS基因扩增，县以及当前和以前的作物是影响该地区草甘膦抗性的主要因素。大多数草甘膦易感的Palmer a菜品种在作物多样性高的几个县发现。此处提供的结果证实了内布拉斯加州西南部Palmer mar菜品种中的草甘膦抗性和PPO抑制剂抗性的扩散，并表明多样化的种植体系是Palmer mar菜中抗除草剂抗性演变的重要驱动力。