Inhibitory binding to plastoquinone B site on D1 protein of photosystem II leading to decreased population growth rate via disruption of cellular energy metabolism.

Photosystem II (PSII) is essential for photosynthesis in primary producers, facilitating the primary photochemical reaction to oxidize water and drive the production of ATP and NADPH. A critical interaction within PSII occurs at the plastoquinone B (QB) site on the D1 protein, where electron transfer from QA to QB ensures the continuity of photosynthetic electron flow and energy transduction. PSII-inhibitors, such as diuron, can directly bind to the QB site of the D1 protein, thus hindering the flow of electrons and reducing the synthesis of ATP and other compounds (e.g. NADP) in chloroplasts. Such disruption would constrain downstream processes on multiple biological levels, ultimately leading to growth inhibition. PSII inhibitors are typically used as herbicides that are commonly detected in surface and ground waters, especially in agricultural regions. Their mobility in surface water is associated with acute and chronic effects in non-target organisms and especially primary producers such as plants, algae, and aquatic macrophytes that have conserved QB binding sites similar to target weeds. To improve mechanistic understanding and strengthen ecological risk assessment of PSII-inhibitor (e.g. herbicides), AOP #567 was developed. This AOP outlines a linear cascade of events, beginning with the binding of specific PSII inhibitors to the QB site on the D1 protein, leading to successive reductions in PSII efficiency, photosynthesis, mitochondrial OXPHOS, and ATP production, resulting in reduced growth at the individual level, and culminating in decreased population growth rate in primary producers. By systematically linking molecular interactions to population-level outcomes, AOP #567 provides a transparent and biologically plausible framework to assess hazard and aid environmental risks of PSII-inhibitors.