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SlCOMT1-dependent melatonin biosynthesis is required for auxin-mediated alleviation of cadmium toxicity in tomato
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DOI：10.1016/j.jplph.2026.154817.png)
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Abstract
En 中文
Cadmium (Cd) severely inhibits plant growth by disrupting ion homeostasis, impairing redox balance, and inhibiting photosynthesis. Although auxin has been demonstrated to alleviate Cd damage in plants, the downstream signaling mechanisms remain unclear. In this study, tomato (Solanum lycopersicum L.) seedlings were used to investigate the role of melatonin (MT) in IAA-induced alleviation of Cd damage. exogenous IAA mitigated Cd-induced growth inhibition and decreased its accumulation. The alleviating effects of IAA were associated with increased contents of cell wall components and detoxification-related metabolites, including lignin, cellulose, hemicellulose, pectin, glutathione, and phytochelatins. In addition, IAA alleviated oxidative damage and photosynthetic impairment caused by Cd. Further analysis showed that IAA enhanced the Cd-induced expression of SlCOMT1 (caffeic acid O-methyltransferase 1), a key gene involved in MT biosynthesis, and promoted endogenous MT accumulation. Notably, pharmacological inhibition of MT biosynthesis by p-CPA (CPA) weakened the protective effect of IAA. Genetic evidence showed that SlCOMT1 overexpression enhanced the alleviating effect of IAA, whereas the slcomt1 mutant compromised this effect. Exogenous MT restored the responsiveness of slcomt1 plants to IAA. Together, these findings indicate that SlCOMT1-mediated MT biosynthesis is required for IAA to alleviate Cd toxicity, revealing a new mechanism of IAA-mediated Cd detoxification through MT signaling and providing a theoretical basis for reducing Cd accumulation in crops via genetic improvement or exogenous regulation of the MT pathway.
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