Nakka Sridevi, Godar Amar S, Wani Prashant S, Thompson Curtis R, Peterson Dallas E, Roelofs Jeroen, Jugulam Mithila
Department of Agronomy, Kansas State University, ManhattanKS, USA.
Department of Plant Sciences, University of California, DavisCA, USA.
Front Plant Sci. 2017 Apr 11;8:555. doi: 10.3389/fpls.2017.00555. eCollection 2017.
Herbicides that inhibit hydroxyphenylpyruvate dioxygenase (HPPD) such as mesotrione are widely used to control a broad spectrum of weeds in agriculture. is an economically troublesome weed throughout the United States. The first case of evolution of resistance to HPPD-inhibiting herbicides in was documented in Kansas (KS) and later in Nebraska (NE). The objective of this study was to investigate the mechansim of HPPD-inhibitor (mesotrione) resistance in Dose response analysis revealed that this population (KSR) was 10-18 times more resistant than their sensitive counterparts (MSS or KSS). Absorbtion and translocation analysis of [C] mesotrione suggested that these mechanisms were not involved in the resistance in . Importantly, mesotrione (>90%) was detoxified markedly faster in the resistant populations (KSR and NER), within 24 hours after treatment (HAT) compared to sensitive plants (MSS, KSS, or NER). However, at 48 HAT all populations metabolized the mesotrione, suggesting additional factors may contribute to this resistance. Further evaluation of mesotrione-resistant did not reveal any specific resistance-conferring mutations nor amplification of gene, the molecular target of mesotrione. However, the resistant populations showed 4- to 12-fold increase in gene expression. This increase in transcript levels was accompanied by increased HPPD protein expression. The significant aspects of this research include: the mesotrione resistance in is conferred primarily by rapid detoxification (non-target-site based) of mesotrione; additionally, increased gene expression (target-site based) also contributes to the resistance mechanism in the evolution of herbicide resistance in this naturally occurring weed species.
抑制对羟基苯丙酮酸双加氧酶（HPPD）的除草剂，如甲基磺草酮，在农业中被广泛用于控制多种杂草。[杂草名称未给出]在美国是一种造成经济麻烦的杂草。在堪萨斯州（KS）首次记录了对抑制HPPD的除草剂产生抗性进化的案例，随后在内布拉斯加州（NE）也有记录。本研究的目的是调查[杂草名称未给出]对HPPD抑制剂（甲基磺草酮）的抗性机制。剂量反应分析表明，该种群（KSR）的抗性比其敏感对应种群（MSS或KSS）高10 - 18倍。[C]甲基磺草酮的吸收和转运分析表明，这些机制与[杂草名称未给出]的抗性无关。重要的是，与敏感植物（MSS、KSS或NER）相比，抗性种群（KSR和NER）中的甲基磺草酮（>90%）在处理后24小时内解毒速度明显更快。然而，在处理后48小时，所有种群都代谢了甲基磺草酮，这表明可能有其他因素导致这种抗性。对甲基磺草酮抗性[杂草名称未给出]的进一步评估未发现任何特定的抗性赋予突变，也未发现甲基磺草酮的分子靶标[基因名称未给出]基因的扩增。然而，抗性种群的[基因名称未给出]基因表达增加了4至12倍。[基因名称未给出]转录水平的这种增加伴随着HPPD蛋白表达的增加。本研究的重要方面包括：[杂草名称未给出]对甲基磺草酮的抗性主要是由甲基磺草酮的快速解毒（非靶标位点基础）赋予的；此外，[基因名称未给出]基因表达的增加（靶标位点基础）也有助于这种天然存在的杂草物种除草剂抗性进化中的抗性机制。
