Ecotoxicology and Environmental Safety (Dec 2021)
Potassium enhances cadmium resistance ability of Panax notoginseng by brassinolide signaling pathway-regulated cell wall pectin metabolism
Abstract
The mechanism of how potassium (K) attenuates cadmium (Cd)-induced demethylation and anabolism of cell wall (CW) pectin through the brassinolide (BR) signaling pathway was verified in Panax notoginseng (Burk.). The P. notoginseng pectin methylesterase gene (PnPME1) was cloned and functionally verified in tobacco. Pectin and BR metabolism, Cd content and the pectin methylation degree (PMD) were detected in response to K, 2,4-epibrassinolide (EBL), and brassinazole treatments of P. notoginseng and tobacco under Cd stress. Activity of the main root pectin methylesterase enzyme (PME) was promoted by 22.29% under the EBL treatment, and Cd content increased by 29.03% under Cd stress. Potassium reduced PME activity and Cd content in main root pectin by 61.03% and 50.73%, respectively, under the EBL and Cd co-treatment. Potassium inhibited the promoting effects of Cd stress on the expression of PnPME1 by 57.04%. Potassium also inhibited expression of BR synthesis genes PnDET2, PnROT3, PnCYP90A1, and PnBR6OX1 by 65.61%, 52.02%, 47.36%, and 55.16%, respectively, and reduced the accumulation of Cd. The PnPME1 was located in the CW. The activity of transgenic tobacco root PME was higher than that of the wild-type, while the PMD was significantly lower. The regulatory effects of K and EBL on tobacco root pectin metabolism were consistent with those in P. notoginseng. In conclusion, K downregulated the expression of BR synthesis genes in P. notoginseng roots under Cd stress and reduced the production of BRs, which inhibited PnPME1 expression. The reduction in PME activity increased the PMD, which reduced the accumulation of Cd.
