ArticlePlant cell reports2025
GSH1 plays a crucial role in melatonin-mediated cadmium tolerance in Arabidopsis.
Article in Plant cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Single-nucleus RNA-seq and ATAC-seq analyses provide molecular insights into cadmium-stress response in alfalfa roots.Horticulture research · 2026Article
- Exogenous melatonin enhances the tolerance of ground-cover Chrysanthemum morifolium Ramat. to cadmium by improving photosynthetic capacity and reactive oxygen species scavenging.Plant cell reports · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
key messageGSH1 functions the downstream of SNAT-mediated melatonin in Cd tolerance, increasing glutathione and total PCs contents. Melatonin is a multifunctional signaling molecule involved in mitigating the damage caused by cadmium (Cd) stress in plants. Previous studies suggested that the gene encoding serotonin N-acetyltransferase (SNAT) was the key gene in the melatonin biosynthetic pathway. Besides, glutathione (GSH) contributed to plant Cd tolerance, however, the specific role of SNAT-mediated melatonin biosynthesis in regulating GSH-dependent pathway, and whether GSH1 acts as an essential downstream effector, remain undefined. Here, we found that SNAT modulated the endogenous melatonin content and Cd stress response in Arabidopsis. Under Cd stress, SNAT-overexpressing roots accumulated higher melatonin levels and exhibited enhanced Cd tolerance with increased root elongation and fresh weight, whereas the atsnat mutant displayed reduced melatonin and hypersensitivity to Cd compared to wild-type. Furthermore, GSH levels were significantly higher in SNAT-overexpressing plants but not in the atsnat mutant upon Cd stress. Treatment with L-buthionine-(S,R)-sulfoximine (BSO, a GSH biosynthesis inhibitor), significantly decreased GSH levels across all genotypes. Exogenous melatonin failed to rescue Cd hypersensitivity in GSH1 mutant atcad2-1, which was defective in GSH biosynthesis. Genetic and transcriptional analyses further confirmed that GSH1 might be, at least partially, a downstream target of melatonin signaling to mediate Cd tolerance through GSH metabolism. Collectively, these findings highlight the critical role of the GSH1-mediated GSH accumulation in SNAT-dependent melatonin-enhanced plant tolerance to Cd stress. This advances current understanding by identifying GSH1 as a critical node integrating melatonin and heavy metal tolerance pathways.
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