Cysteine and glutathione improve mercury tolerance in rice by modulating cell wall binding, transport, and detoxification pathways

Mercury (Hg), a highly toxic element, poses significant risks to plant growth and human health. This study investigated the mechanisms of Hg accumulation and tolerance by exogenous cysteine (Cys) and glutathione (GSH) in rice. Here, we showed that exogenous Cys and GSH significantly enhanced Hg tolerance in rice but exhibited contrasting effects on Hg accumulation. Exogenous Cys significantly increased Hg accumulation in rice roots, primarily in the cell wall, while exogenous GSH decreased root Hg accumulation. Exogenous Cys significantly increased the expression of cell wall biosynthesis genes, particularly those involved in lignin synthesis, resulting in greater lignin accumulation in epidermis, exodermis, and stele, which correlated with increased Hg binding to the cell wall. In addition, exogenous Cys significantly upregulated several ABC transporters, particularly OsABCGs and OsABCCs, suggesting their possible involvement in Hg transport and vacuolar sequestration. In the process of cellular Hg detoxification, GSH upregulated aquaporin to maintain membrane function and water balance, Cys primarily activated peroxidase-mediated H₂O₂ scavenging. Taken together, these findings highlight novel candidate genes involved in Hg cell wall binding, transport, and detoxification, regulated by Cys and GSH, offering insights for enhancing our understanding of the molecular mechanisms underlying Hg accumulation and tolerance. Furthermore, this study provides new insights into thiol-mediated Hg tolerance and offers potential strategies for reducing Hg accumulation in crops. • Exogenous Cys and GSH enhance Hg tolerance in rice via distinct mechanisms. • Cys increases Hg retention in root cell walls by promoting lignin biosynthesis. • GSH reduces Hg uptake and activates mitochondria synthesis. • Cys induces several ABC transporters potentially involved in Hg transport. • Cys and GSH reduce Hg-induced oxidative damage, but through different antioxidant pathways.