Abstract
BACKGROUND: Salt stress significantly suppresses rice growth. Uniconazole (S3307) is recognized for its potential to enhance plant stress tolerance. Nevertheless, the mechanisms through which S3307 induces salt tolerance in rice by modulating the carbon metabolism pathway are not fully understood. In this study, at the one-leaf-one-heart stage, the foliage of rice HD961 and 9311 was treated with 10 mg·L(- 1) S3307, followed by a 0.6% (102.56 mmol·L(- 1)) NaCl treatment 24 h later. RESULTS: The results demonstrated that salt stress markedly suppressed the growth of rice aboveground and underground, reduced the net photosynthetic rate (P(n)), and ultimately led to a decline in yield. However, salt stress increased the activities of peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX) and enhanced sucrose metabolism simultaneously of rice leaves. However, compared to salt stress, foliar spraying of S3307 under salt stress increased rice biomass accumulation, enhanced photosynthetic efficiency, reduced malondialdehyde (MDA) content, and further enhanced the activities of superoxide dismutase (SOD), POD, CAT, and APX. Meanwhile, the application of S3307 effectively further promoted the accumulation of sucrose, glucose, and soluble sugar (SS) in rice leaves under salt stress. It also enhanced the activities of key enzymes in glycolysis, namely hexokinase (HK) and pyruvate kinase (PK), and facilitated the accumulation of α-ketoglutaric acid (α-KG), citric acid (CA), and pyruvate (PA). Meanwhile, it increased the effective panicle number (EPN), grains per panicle, yield per panicle and theoretical yield of rice. CONCLUSION: Therefore, S3307 can mitigate the damage caused by salt stress and enhance yield and rice resistance by improving photosynthetic characteristics, strengthening the antioxidant system, and promoting physiological activities in carbon metabolism pathways such as Carbohydrate, glycolysis (EMP) and the tricarboxylic acid (TCA) cycle.