Binding to plastoquinone B site leading to decreased population growth rate via photosystem II inhibition

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 can competitively bind to this QB site, blocking electron flow and suppressing the production of ATP and NADPH in chloroplasts. This disruption constrains downstream processes at different biological levels and consequently result in growth inhibition. PSII inhibitors are frequently detected in surface and ground waters, especially in agricultural regions. Their prolonged mobility results in chronic exposure of non-target organisms, particularly primary producers such as algae, aquatic macrophytes, and terrestrial plants that share conserved QB binding sites with target weeds. To improve mechanistic understanding and strengthen ecological risk assessment of PSII-inhibitor, such as herbicides, AOP #567 was developed. This AOP delineates a linear cascade of key events, beginning with the binding of PSII inhibitors to the QB site on the D1 protein, leading through successive reductions in PSII efficiency, photosynthesis, mitochondrial OXPHOS, and ATP production, and culminating in decreased growth rates of primary producer populations. By systematically linking molecular interactions to population-level outcomes, AOP #567 provides a transparent and biologically plausible framework to assess the environmental hazards posed by PSII inhibitors.

The present AOPdescribes the potential causal events initiated by the binding of photosystem II (PSII) inhibitors to the plastoquinone B (QB) site of the D1 protein within the PSII complex (MIE, event 1975), leading to a decrease in population growth rate in primary producers (adverse outcome, event 2181) via a cascade of intermediate key events (KEs), including inhibition of PSII electron transport (event 1976), decrease in PSII efficiency (event 1977), and ultimately, decrease in growth rate (event 2031). The Table 1 provides a summary of  the KEs that constitute the AOP and the representative methods for measurement of each KE. 

The MIE constitutes the competitive binding of PSII inhibitors to the QB site, which disrupts the transfer of electrons between QA and QB. This blockage has a direct inhibitory impact on the functioning of the PSII complex and causes the first downstream KE: the inhibition of PSII efficiency, which is typically reported as Fv/Fm ratio or ΦPSII. The lower PSII efficiency is an indication of reduced energy conversion in the light-dependent components of photosynthesis. As a logical physiological consequence, this leads to a decrease in carbon fixation and the availability of ATP and NADPH, both of which are essential for cellular growth. here is a consequent decrease in the rate of organismal growth, particularly on the taxa that grows fast like phytoplankton and aquatic plants.

This series of KEs represents the minimal essential path of causally linked events required to describe how a molecular-level interaction with a chemical stressor produces an ecologically relevant adverse outcome. Each KE and its connection to the adjacent events are evidenced by the mechanistic and empirical evidence, dose-response relationships, as well as taxonomic concordance, as it is elaborated in the section “Summary of scientific evidence assessment” below. Although the subsequent secondary effects, such as oxidative stress and thylakoid membrane damage, also can happen after the PSII disruption, they do not constitute a necessary part of this AOP but rather play a modifying role. The mechanisms of the reactions discussed are very well conserved and the events are consequently found in very wide range of photosynthetic organisms i.e. algae, cyanobacteria, and aquatic vascular plants. This linear AOP can be included in a network of herbicide-related inhibition of photosynthesis and downstream effects at the population level that can occur across primary producers.