Bioagricultural Sciences and Pest Management, Colorado State University, Fort Collins, CO, 80526, USA.
Weed Resistance Research Centre, Bayer AG, Industriepark Hoechst, Frankfurt, Germany.
Planta. 2019 Jun;249(6):1837-1849. doi: 10.1007/s00425-019-03124-3. Epub 2019 Mar 8.
Glufosinate is primarily toxic to plants due to a massive light-dependent generation of reactive oxygen species rather than ammonia accumulation or carbon assimilation inhibition. Glutamine synthetase (GS) plays a key role in plant nitrogen metabolism and photorespiration. Glufosinate (CHNOP) targets GS and causes catastrophic consequences leading to rapid plant cell death, and the causes for phytoxicity have been attributed to ammonia accumulation and carbon assimilation restriction. This study aimed to examine the biochemical and physiological consequences of GS inhibition to identify the actual cause for rapid phytotoxicity. Monocotyledonous and dicotyledonous species with different forms of carbon assimilation (C3 versus C4) were selected as model plants. Glufosinate sensitivity was proportional to the uptake of herbicide between species. Herbicide uptake also correlated with the level of GS inhibition and ammonia accumulation in planta even with all species having the same levels of enzyme sensitivity in vitro. Depletion of both glutamine and glutamate occurred in glufosinate-treated leaves; however, amino acid starvation would be expected to cause a slow plant response. Ammonia accumulation in response to GS inhibition, often reported as the driver of glufosinate phytotoxicity, occurred in all species, but did not correlate with either reductions in carbon assimilation or cell death. This is supported by the fact that plants can accumulate high levels of ammonia but show low inhibition of carbon assimilation and absence of phytotoxicity. Glufosinate-treated plants showed a massive light-dependent generation of reactive oxygen species, followed by malondialdehyde accumulation. Consequently, we propose that glufosinate is toxic to plants not because of ammonia accumulation nor carbon assimilation inhibition, but the production of reactive oxygen species driving the catastrophic lipid peroxidation of the cell membranes and rapid cell death.
草铵膦主要通过大量依赖光照的活性氧物种的产生而不是氨的积累或碳同化抑制对植物产生毒性。谷氨酰胺合成酶（GS）在植物氮代谢和光呼吸中起着关键作用。草铵膦（CHNOP）靶向 GS 并导致灾难性的后果，导致植物细胞迅速死亡，而植物毒性的原因归因于氨的积累和碳同化的限制。本研究旨在研究 GS 抑制的生化和生理后果，以确定快速植物毒性的实际原因。选择具有不同碳同化形式（C3 与 C4）的单子叶和双子叶物种作为模式植物。草铵膦敏感性与物种间除草剂的吸收成正比。除草剂的吸收也与体内 GS 抑制和氨积累的水平相关，即使所有物种在体外都具有相同水平的酶敏感性。在草铵膦处理的叶片中，谷氨酰胺和谷氨酸都耗尽；然而，氨基酸饥饿预计会导致植物缓慢反应。氨的积累作为草铵膦植物毒性的驱动力，在所有物种中都有发生，但与碳同化的减少或细胞死亡无关。事实上，植物可以积累高水平的氨，但表现出低的碳同化抑制和缺乏植物毒性，这一点得到了支持。草铵膦处理的植物表现出大量依赖光照的活性氧物种的产生，随后是丙二醛的积累。因此，我们提出，草铵膦对植物有毒，不是因为氨的积累或碳同化抑制，而是活性氧物种的产生导致细胞膜灾难性的脂质过氧化和快速细胞死亡。
