The molecular mechanism of the α-linolenic acid metabolism pathway in rice in response to Cd stress

BACKGROUND: Cadmium (Cd) toxicity induces changes in gene expression and metabolite profiles, thereby affecting plant growth. However, the molecular basis of Cd toxicity in rice remains unclear. This study investigated the responses of rice leaves and roots to Cd stress using integrated transcriptomic and metabolomic analyses. RESULT: Cd stress significantly inhibited rice growth, impaired antioxidant enzyme systems in leaves and roots, and altered nutrient uptake. Under Cd stress (10 µM Cd), compared with the control group (0 µM Cd), activities of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX) in leaves increased by 47.9%, 156.9%, 104.8%, and 233.0%, respectively; proline, soluble sugar, and soluble protein increased by 205.6%, 296.4%, and 30.4%, respectively. Under the same conditions, soluble sugar and soluble protein in roots increased by 29.1% and 23.2%, respectively, while SOD, POD, CAT, and APX activities increased by 28.2%, 95.4%, 39.9%, and 133.8%, respectively. Cd stress increased soluble sugar and soluble protein in both leaves and roots and reduced chlorophyll content. Transcriptomic analysis identified 4,366 differentially expressed genes (DEGs) in leaves and 4,971 DEGs in roots, associated with antioxidant enzyme expression, ion transport, and hormone-related pathways. Metabolomic analysis detected 1,054 differentially expressed metabolites (DEMs) in leaves and 882 DEMs in roots. Under Cd stress, both tissues showed significant enrichment of the α-linolenic acid metabolism pathway. Genes encoding lipoxygenase (LOX; including LOX2S) and allene oxide synthase (AOS) were differentially expressed, which mitigated oxidative stress. CONCLUSION: This study clarifies physiological and molecular responses of rice to Cd stress and highlights the role of α-linolenic acid metabolism in tolerance to Cd toxicity. These findings advance understanding of Cd effects on rice development and identify candidate molecular targets for genetic approaches to improve Cd stress resistance.