Photosystem II Inhibitors
HRAC Group: C1, C2, C3
WSSA Group: 5, 6, 7
Photosynthetic Inhibitors control many broadleaf and some grass weeds. In general, these herbicides inhibit photosynthesis by binding to D1 proteins of the photosystem II complex in chloroplast thylakoid membranes. Herbicide binding at this protein blocks electron transport and stops CO2 fixation and production of energy needed for plant growth. The death of plants, however, does not occur primarily from photosynthates depletion but rather from an indirect effect on other processes. Blocking electron transport in PSII systems promotes the formation of highly reactive molecules that initiate a chain of reactions causing lipid and protein membrane destruction that results in membrane leakage allowing cells and cell organelles to dry and rapidly disintegrate. In addition, some PSII Inhibitors affect other plant processes such as carotenoid biosynthesis and synthesis of anthocyanin, RNA, and proteins.
PSII Inhibitors used in the United States belong to ten different chemistries with products registered on field crops, orchards, and vegetation management. Although all PSII Inhibitors bind to the D1 protein, the binding occurs at three different attachment sites. PSII Inhibitors are classified based on their attachment site. For example, the C1 group includes herbicides belonging to pyridazinone, triazine, triazinone, and uracil chemistries; C2 group includes ureas and amides; and C3 group includes benzothiadiazinone, nitrile, and phenylpyridazine.
The triazines, triazinones, uracils, pyridazinones, and ureas are soil-applied or early postemergent herbicides in crops and noncropland sites. These herbicides are absorbed by both shoots and roots but are translocated only in the xylem. Phenylcarbamate, amides, benzothiadiazinone, nitrile, and phenylpyridazine are used primarily as early postemergence treatments. They are contact herbicides that are not translocated in the plant.
Injury symptoms: Injury symptoms from soil-applied treatments will not appear until after photosynthesis begins. Susceptible broadleaf plants will exhibit interveinal or veinal chlorosis, depending on the herbicide. Necrosis begins around the leaf margins and progresses toward the center of the leaves. Susceptible grasses will become chlorotic and necrotic beginning at the leaf tips and progressing toward the base of the leaves. Injury symptoms from foliar applications will appear as leaf burn as cell membranes are destroyed. Leaf burn symptoms generally occur most rapidly with hot and humid conditions. It is not unusual to observe symptoms from foliar applied PSII Inhibitors within 72 hours after application.
Chemistry Group and Common Names of PS II Inhibitors
Used in the United States