Glufosinate targets glutamine synthetase (GS), a key enzyme for nitrogen metabolism and photorespiration. Unlike other amino acid biosynthesis inhibitors, glufosinate is a fast-acting herbicide with limited translocation. <i>Amaranthus palmeri</i> was used as a model species to investigate the physiological basis for the contact activity of glufosinate. Two series of experiments were performed. Initially, we developed a method to quantify glufosinate translocation through xylem and phloem. Then, physiological and biochemical responses were evaluated in plants treated and untreated with glufosinate. Leaf translocation was 43% acropetal and only 4% basipetal, indicating that glufosinate has good xylem translocation but limited phloem mobility. Photosynthetic electron flow and carbon assimilation were completely inhibited, and ammonia accumulated at high levels following GS inhibition by glufosinate. Inhibition of GS caused a massive and rapid light-dependent generation of reactive oxygen species (ROS). The free radical formation led to accumulation of malondialdehyde, a product of lipid peroxidation, supporting the hypothesis that ROS triggers the fast action of glufosinate. Based on these facts, we suggest that inhibition of GS blocks both photorespiration and the Calvin Cycle, two major sinks for the energy generated by the light reactions. Under these circumstances, the excess of electrons is transferred to molecular oxygen, which generates ROS, the causal agent of lipid peroxidation and rapid cell death. We conclude that ROS accumulation and limited phloem mobility form the physiological basis for the observed contact activity of glufosinate.<br/>

Reactive oxygen species trigger the fast action of glufosinate

2019 Fall National Meeting

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