Sammons Robert Douglas, Gaines Todd A
Pest Manag Sci. 2014 Sep;70(9):1367-77. doi: 10.1002/ps.3743.
Studies of mechanisms of resistance to glyphosate have increased current understanding of herbicide resistance mechanisms. Thus far, single-codon non-synonymous mutations of EPSPS (5-enolypyruvylshikimate-3-phosphate synthase) have been rare and, relative to other herbicide mode of action target-site mutations, unconventionally weak in magnitude for resistance to glyphosate. However, it is possible that weeds will emerge with non-synonymous mutations of two codons of EPSPS to produce an enzyme endowing greater resistance to glyphosate. Today, target-gene duplication is a common glyphosate resistance mechanism and could become a fundamental process for developing any resistance trait. Based on competition and substrate selectivity studies in several species, rapid vacuole sequestration of glyphosate occurs via a transporter mechanism. Conversely, as the chloroplast requires transporters for uptake of important metabolites, transporters associated with the two plastid membranes may separately, or together, successfully block glyphosate delivery. A model based on finite glyphosate dose and limiting time required for chloroplast loading sets the stage for understanding how uniquely different mechanisms can contribute to overall glyphosate resistance.
对草甘膦抗性机制的研究增进了目前对除草剂抗性机制的理解。到目前为止,5-烯醇式丙酮酸莽草酸-3-磷酸合酶(EPSPS)的单密码子非同义突变很少见,而且相对于其他除草剂作用模式的靶位点突变而言,对草甘膦抗性的强度异常微弱。然而,杂草有可能出现EPSPS两个密码子的非同义突变,从而产生一种对草甘膦具有更强抗性的酶。如今,靶基因复制是一种常见的草甘膦抗性机制,并且可能成为产生任何抗性性状的基本过程。基于对多个物种的竞争和底物选择性研究,草甘膦可通过转运体机制快速被液泡隔离。相反,由于叶绿体需要转运体来摄取重要代谢物,与两个质体膜相关的转运体可能单独或共同成功阻止草甘膦的输送。基于有限草甘膦剂量和叶绿体装载所需的有限时间建立的模型,为理解截然不同的机制如何导致整体草甘膦抗性奠定了基础。