Herbicides, Inhibitors of Photosynthesis at PhotosystemII

Abstract Herbicides of photosystem II inhibit the reduction of plastoquinone at the secondary quinone acceptor site ( Q B ‐site) and its subsequent reoxidation at the cytochrome b 6 / f ‐complex. The Q B ‐site is located at the photosystem II reaction center protein called D1. When the reduction of plastoquinone is blocked by the herbicide, light‐induced charge separation leads to recombination processes that via a chlorophyll triplet state generate reactive oxygen species. These will cause extensive damage in photosystem II and eventually kill the plant. Amino acids involved in herbicide binding can be identified in three ways: 1) by comparison with the well‐known X‐ray structure of the bacterial photosynthetic reaction center, 2) by photoaffinity labeling with photolabile radioactive analogs of herbicides, and 3) by analysis of the herbicide binding in herbicide‐resistant mutants of plants, algae, and cyanobacteria with known mutations in the D1 protein. Herbicides of photosystem II belong to the following chemical classes: s ‐triazines, triazinones, uracils, ureas, phenylcarbamates, anilides, cyanophenols, dinitrophenols, and some chemicals that do not belong to these classes, like bentazon, fluoromidine, pyrazon, and pyridate.