Takano Hudson K, Beffa Roland, Preston Christopher, Westra Philip, Dayan Franck E
Agricultural Biology Department, Colorado State University, Fort Collins, CO, 80523, USA.
Weed Resistance Competence Centre, Bayer AG, Industriepark Hoechst, Frankfurt, Germany.
Photosynth Res. 2020 Jun;144(3):361-372. doi: 10.1007/s11120-020-00749-4. Epub 2020 May 5.
Glufosinate targets glutamine synthetase (GS), but its fast herbicidal action is triggered by reactive oxygen species (ROS). The relationship between GS inhibition and ROS accumulation was investigated in Amaranthus palmeri. Glufosinate's fast action is light-dependent with no visual symptoms or ROS formation in the dark. Inhibition of GS leads to accumulation of ammonia and metabolites of the photorespiration pathway, such as glycolate and glyoxylate, as well as depletion of other intermediates such as glycine, serine, hydroxypyruvate, and glycerate. Exogenous supply of glycolate to glufosinate-treated plants enhanced herbicidal activity and dramatically increased hydrogen peroxide accumulation (possibly from peroxisomal glycolate oxidase activity). Glufosinate affected the balance between ROS generation and scavenging. The activity of superoxide dismutase, catalase, ascorbate peroxidase, and glutathione reductase increased after glufosinate treatment in an attempt to quench the nascent ROS burst. Low doses of atrazine and dinoseb were used to investigate the sources of ROS by manipulating photosynthetic electron transport and oxygen (O) evolution. ROS formation depended on electron flow and O evolution in photosystem II (PSII). Inhibition of GS disrupted photorespiration, carbon assimilation, and linear electron flow in the light reactions. Consequently, the antioxidant machinery and the water-water cycle are overwhelmed in the presence of light and glufosinate. The O generated by the splitting of water in PSII becomes the acceptor of electrons, generating ROS. The cascade of events leads to lipid peroxidation and forms the basis for the fast action of glufosinate.
草铵膦作用于谷氨酰胺合成酶（GS），但其快速除草作用是由活性氧（ROS）引发的。本研究在糙果苋中探究了GS抑制与ROS积累之间的关系。草铵膦的快速作用依赖于光照，在黑暗中无可见症状或ROS形成。GS的抑制导致氨以及光呼吸途径的代谢产物（如乙醇酸和乙醛酸）积累，同时其他中间产物（如甘氨酸、丝氨酸、羟基丙酮酸和甘油酸）减少。向经草铵膦处理的植物外源供应乙醇酸可增强除草活性，并显著增加过氧化氢积累（可能源于过氧化物酶体乙醇酸氧化酶活性）。草铵膦影响了ROS产生与清除之间的平衡。草铵膦处理后，超氧化物歧化酶、过氧化氢酶、抗坏血酸过氧化物酶和谷胱甘肽还原酶的活性增加，试图淬灭新生的ROS爆发。使用低剂量的莠去津和地乐酚通过操纵光合电子传递和氧气（O）释放来研究ROS的来源。ROS的形成依赖于光系统II（PSII）中的电子流和O释放。GS的抑制破坏了光呼吸、碳同化以及光反应中的线性电子流。因此，在光照和草铵膦存在的情况下，抗氧化机制和水-水循环不堪重负。PSII中水分子裂解产生的O成为电子受体，从而产生活性氧。这一系列事件导致脂质过氧化，构成了草铵膦快速作用的基础。
