The evolution of resistance to multiple herbicides in Palmer amaranth is a major challenge for its management. In this study, a Palmer amaranth population from Hutchinson, Kansas (HMR), was characterized for resistance to inhibitors of photosystem II (PSII) (e.g., atrazine), acetolactate synthase (ALS) (e.g., chlorsulfuron), and EPSP synthase (EPSPS) (e.g., glyphosate), and this resistance was investigated. About 100 HMR plants were treated with field-recommended doses (1×) of atrazine, chlorsulfuron, and glyphosate, separately along with Hutchinson multiple-herbicide (atrazine, chlorsulfuron, and glyphosate)–susceptible (HMS) Palmer amaranth as control. The mechanism of resistance to these herbicides was investigated by sequencing or amplifying the psbA, ALS, and EPSPS genes, the molecular targets of atrazine, chlorsulfuron, and glyphosate, respectively. Fifty-two percent of plants survived a 1× (2,240 g ai ha−1) atrazine application with no known psbA gene mutation, indicating the predominance of a non–target site resistance mechanism to this herbicide. Forty-two percent of plants survived a 1× (18 g ai ha−1) dose of chlorsulfuron with proline197serine, proline197threonine, proline197alanine, and proline197asparagine, or tryptophan574leucine mutations in the ALS gene. About 40% of the plants survived a 1× (840 g ae ha−1) dose of glyphosate with no known mutations in the EPSPS gene. Quantitative PCR results revealed increased EPSPS copy number (50 to 140) as the mechanism of glyphosate resistance in the survivors. The most important finding of this study was the evolution of resistance to at least two sites of action (SOAs) (~50% of plants) and to all three herbicides due to target site as well as non–target site mechanisms. The high incidence of individual plants with resistance to multiple SOAs poses a challenge for effective management of this weed.

中文翻译：

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堪萨斯州单个棕榈苋（Amaranthus palmeri）种群中基于目标和非目标的多种除草剂抗性的演变

帕尔默苋菜对多种除草剂的抗性演变是其管理的主要挑战。在这项研究中，来自堪萨斯州哈钦森 (HMR) 的帕尔默苋菜种群被表征为对光系统 II (PSII)（例如阿特拉津）、乙酰乳酸合酶 (ALS)（例如氯磺隆）和 EPSP 合酶 (EPSPS) 抑制剂具有抗性。 )（例如草甘膦），并研究了这种抗性。大约 100 株 HMR 植物分别用田间推荐剂量 (1x) 的阿特拉津、氯磺隆和草甘膦以及 Hutchinson 多种除草剂（阿特拉津、氯磺隆和草甘膦）敏感 (HMS) 棕榈苋菜作为对照进行处理。通过测序或扩增对这些除草剂的抗性机制进行了研究psbA,肌萎缩侧索硬化症， 和每股收益基因，分别是阿特拉津、氯磺隆和草甘膦的分子靶点。52% 的植物在 1× (2,240 g ai ha-1) 阿特拉津应用与未知psbA基因突变，表明对该除草剂的非靶位点抗性机制占优势。42% 的植物在 1 倍（18 g ai ha-1) 氯磺隆与脯氨酸的剂量197丝氨酸，脯氨酸197苏氨酸、脯氨酸197丙氨酸和脯氨酸197天冬酰胺或色氨酸574亮氨酸突变肌萎缩侧索硬化症基因。大约 40% 的植物在 1× (840 g ae ha-1) 剂量的草甘膦没有已知的突变每股收益基因。定量 PCR 结果显示增加每股收益拷贝数（50 到 140）作为幸存者草甘膦抗性的机制。这项研究最重要的发现是由于目标位点和非目标位点机制，对至少两个作用位点 (SOA)（约 50% 的植物）和所有三种除草剂的抗性演变。对多种 SOA 具有抗性的个体植物的高发病率对这种杂草的有效管理提出了挑战。