A new mechanism by which environmental hazardous substances enhance their toxicities to plants

The coexistence of hazardous substances enhances their toxicities to plants, but its mechanism is still unclear due to the unknown cytochemical behavior of hazardous substance in plants. In this study, by using interdisciplinary methods, we observed the cytochemical behavior of coexisting hazardous substances {terbium [Tb(III)], benzo(a)pyrene (BaP) and cadmium [Cd(II)] in environments} in plants and thus identified a new mechanism by which coexisting hazardous substances in environments enhance their toxicities to plants. First, Tb(III) at environmental exposure level (1.70 × 10^-10 g/L) breaks the inert rule of clathrin-mediated endocytosis (CME) in leaf cells. Specifically, Tb(III) binds to its receptor [FASCICLIN-like arabinogalactan protein 17 (FLA17)] on the plasma membrane of leaf cells and then docks to an intracellular adaptor protein [adaptor protein 2 (AP2)] to form ternary complex [Tb(III)-FLA17-AP2], which finally initiates CME pathway in leaf cells. Second, coexisting Tb(III), BaP and Cd(II) in environments are simultaneously transported into leaf cells via Tb(III)-initiated CME pathway, leading to the accumulation of them in leaf cells. Finally, these accumulated hazardous substances simultaneously poison plant leaf cells. These results provide theoretical and experimental bases for elucidating the mechanisms of hazardous substances in environments poisoning plants, evaluating their risks, and protecting ecosystems.