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Deciphering the physiological and molecular mechanisms for copper tolerance in autotetraploid Arabidopsis
- Li, Mingjuan, Xu, Guoyun, Xia, Xinjie, Wang, Manling, Yin, Xuming, Zhang, Bin, Zhang, Xin, Cui, Yanchun
- Plant cell reports 2017 v.36 no.10 pp. 1585-1597
- Arabidopsis thaliana, abscisic acid, autotetraploidy, biomass, chelation, copper, death, defense mechanisms, diploidy, gene expression, gene expression regulation, genes, glutathione, hydrogen peroxide, malondialdehyde, peroxidase, plant growth, superoxide anion, superoxide dismutase
- KEY MESSAGE : Autotetraploid Arabidopsis line esd and 4COL exhibit enhanced tolerance to Cu stress by enhancing activation of antioxidative defenses, altering expression of genes related to Cu transport, chelation, and ABA-responsive. Autopolyploidy is ubiquitous among angiosperms and often results in better adaptation to stress conditions. Although copper (Cu) is an essential trace element, excess amounts can inhibit plant growth and even result in death. Here, we report that autotetraploid Arabidopsis thaliana esd and 4COL exhibit higher tolerance to Cu stress. Under such conditions, tetraploid plants had lower Cu contents and significantly more biomass compared with diploid plants. When exposed to excess Cu for 24 h, levels of superoxide anions, hydrogen peroxide, and malondialdehyde were lower in tetraploids than in diploids. Moreover, activities of the antioxidant enzymes superoxide dismutase and peroxidase were stimulated and glutathione content was maintained at a relative higher level in the tetraploids. The expression of genes related to Cu transport and chelation was altered in autotetraploid Arabidopsis under Cu stress, and several key genes involved in the response to abscisic acid (ABA) were significantly up-regulated. Our results indicate that tetraploid Arabidopsis esd and 4COL acquire improved tolerance to Cu stress through enhanced activation of antioxidative defense mechanisms, altered expression of genes related to Cu transport and chelation, and positive regulation of expression for ABA-responsive genes.