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Potassium affects cadmium resistance in Arabidopsis through facilitating root cell wall Cd retention in a nitric oxide dependent manner

Authors :
Ren Fang Shen
Xusheng Zhao
Qi Wu
Xiaofang Zhu
Source :
Environmental and Experimental Botany. 178:104175
Publication Year :
2020
Publisher :
Elsevier BV, 2020.

Abstract

Potassium (K) plays an important role in plant development and in plant responses to various environmental stresses; however, its involvement in the mitigation of heavy metal stress by altering the binding capacity of the cell wall in Arabidopsis thaliana remains elusive. Here, we examined the effect of K (0–12 mM) in the regulation of cadmium (Cd) resistance in Arabidopsis thaliana. Toxic levels of Cd (50 μM) cause chlorosis in young leaves; however, the application of 3 mM K significantly alleviated this symptom in Arabidopsis thaliana, while other K concentrations did not rescue this phenotype. Moreover, 3 mM K significantly increased cell wall polysaccharide (hemicellulose) content and Cd adsorption in the root cell walls, suggesting that the modification of the cell wall composition is responsible for the Cd retention in the root under 3 mM K application. The 3 mM K treatment significantly reduced the expression of genes related to Cd uptake when plants were exposed to Cd, implying a decrease in Cd entering the cells. Furthermore, endogenous Nitric oxide (NO) was demonstrated to be involved in 3 mM K ameliorated-Cd toxicity as nia1nia2 and noa1 mutants, which are defective in NO biosynthesis, this positive effect of 3 mM K on Cd toxicity was abolished. Taken together, our results indicated that the 3 mM K alleviated deleterious effects of Cd by modifying the cell wall Cd binding capacity, particularly through the regulation of the NO accumulation in Arabidopsis thaliana.

Details

ISSN :
00988472
Volume :
178
Database :
OpenAIRE
Journal :
Environmental and Experimental Botany
Accession number :
edsair.doi...........5f556833ce1f60ac83f335182daa8bcd
Full Text :
https://doi.org/10.1016/j.envexpbot.2020.104175