Methiozolin is a new herbicide with an unknown mechanism of action (MOA) for control of annual bluegrass (Poa annua L.) in several warm- and cool-season turfgrasses. In the literature, methiozolin was proposed to be a pigment inhibitor via inhibition of tyrosine aminotransferases (TATs) or a cellulose biosynthesis inhibitor (CBI). Here, exploratory research was conducted to characterize the herbicide symptomology and MOA of methiozolin. Arabidopsis (Arabidopsis thaliana L.) and P. annua exhibited a similar level of susceptibility to methiozolin, and arrest of meristematic growth was the most characteristic symptomology. For example, methiozolin inhibited A. thaliana root growth (GR50 8 nM) and shoot emergence (GR80 ˜50 nM), and apical meristem growth was completely arrested at rates greater than 500 nM. We concluded that methiozolin was neither a TAT nor a CBI inhibitor. Methiozolin had a minor effect on chlorophyll and alpha-tocopherol content in treated seedlings (<500 nM), and supplements in the proposed TAT pathway could not lessen phytotoxicity. Examination of microscopic images of roots revealed that methiozolin-treated (100 nM) and untreated seedlings had similar root cell lengths. Thus, methiozolin inhibits cell proliferation and not elongation from meristematic tissue. Subsequently, we suspected methiozolin was an inhibitor of the mevalonic acid (MVA) pathway, because its herbicidal symptomologies were nearly indistinguishable from those caused by lovastatin. However, methiozolin did not inhibit phytosterol production, and MVA pathway metabolites did not rescue treated seedlings. Further experiments showed that methiozolin produced a physiological profile very similar to cinmethylin across a number of assays, a known inhibitor of fatty-acid synthesis through inhibition of thioesterases (FATs). Experiments with lesser duckweed (Lemna aequinoctialis Welw.; syn. Lemna paucicostata Hegelm.) showed that methiozolin also reduced fatty-acid content in Lemna with a profile similar, but not identical, to cinmethylin. However, there was no difference in fatty-acid content between treated (1 µM) and untreated A. thaliana seedlings. Methiozolin also bound to both A, thaliana and L. aequinoctialis FATs in vitro. Modeling suggested that methiozolin and cinmethylin have comparable and overlapping FAT binding sites. While there was a discrepancy in the effect of methiozolin on fatty-acid content between L. aequinoctialis and A. thaliana, the overall evidence indicates that methiozolin is a FAT inhibitor and acts in a similar manner as cinmethylin.

中文翻译：

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除草剂症状及甲硫唑啉的作用机制

甲硫唑啉是一种作用机制未知（MOA）的新型除草剂，用于防治一年生早熟禾（早熟禾L.) 在几个暖季和冷季的草坪草中。在文献中，甲硫唑啉被提议通过抑制酪氨酸氨基转移酶 (TAT) 或纤维素生物合成抑制剂 (CBI) 来作为色素抑制剂。在这里，进行了探索性研究，以表征甲硫唑啉的除草剂症状和 MOA。拟南芥(拟南芥土地青蒿表现出对甲硫唑啉的相似程度的敏感性，并且分生组织生长停滞是最具特征性的症状。例如，甲硫唑啉抑制拟南芥根系生长（GR508 nM）和出芽（GR80~50 nM)，并且顶端分生组织的生长在大于 500 nM 的速率下完全停止。我们得出结论，甲硫唑啉既不是 TAT 也不是 CBI 抑制剂。Methiozolin 对处理过的幼苗（<500 nM）中的叶绿素和 α-生育酚含量有轻微影响，并且建议的 TAT 途径中的补充剂不能减轻植物毒性。检查根的显微图像显示，甲硫唑啉处理 (100 nM) 和未处理的幼苗具有相似的根细胞长度。因此，甲硫唑啉抑制细胞增殖而不是分生组织的伸长。随后，我们怀疑甲硫唑啉是甲羟戊酸 (MVA) 途径的抑制剂，因为它的除草症状与洛伐他汀引起的症状几乎没有区别。然而，甲硫唑啉并没有抑制植物甾醇的产生，和 MVA 途径代谢物没有拯救处理过的幼苗。进一步的实验表明，在许多试验中，甲硫唑啉产生的生理学特征与辛甲基林非常相似，辛甲基林是一种通过抑制硫酯酶 (FAT) 抑制脂肪酸合成的已知抑制剂。小浮萍的实验（四季分明; 同义词淡藻Hegelm.) 表明，甲硫唑啉还降低了浮萍具有与cinmethylin相似但不相同的特征。然而，处理（1 µM）和未处理之间的脂肪酸含量没有差异拟南芥幼苗。甲硫唑啉也与两者结合一、拟南芥和L. aequinoctialis体外脂肪。建模表明，甲硫唑啉和 cinmethylin 具有可比较和重叠的 FAT 结合位点。虽然甲硫唑啉对脂肪酸含量的影响存在差异L. aequinoctialis和拟南芥，总体证据表明，甲硫唑啉是一种 FAT 抑制剂，其作用方式与 cinmethylin 相似。