Enhanced zinc and cadmium tolerance and accumulation in transgenic Arabidopsis plants constitutively overexpressing a barley gene (HvAPX1) that encodes a peroxisomal ascorbate peroxidase

Ascorbate peroxidase (APX) plays an important role in oxidative stress metabolism in higher plants. To determine the role of APX in protection against excessive-zinc-induced oxidative stress, transgenic Arabidopsis plants constitutively overexpressing a peroxisomal ascorbate peroxidase gene (HvAPX1)...

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Published inBotany Vol. 86; no. 6; pp. 567 - 575
Main Authors Xu, Weifeng, Shi, Weiming, Liu, Feng, Ueda, Akihiro, Takabe, Tetsuko
Format Journal Article
LanguageEnglish
Published NRC Research Press 01.06.2008
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Summary:Ascorbate peroxidase (APX) plays an important role in oxidative stress metabolism in higher plants. To determine the role of APX in protection against excessive-zinc-induced oxidative stress, transgenic Arabidopsis plants constitutively overexpressing a peroxisomal ascorbate peroxidase gene (HvAPX1) from barley were analyzed. In this study, we found that transgenic plants were more tolerant to zinc stress than wild-type plants. Under zinc stress, the concentration of hydrogen peroxide and malondialdehyde accumulation were higher in wild-type plants than in transgenic plants. Therefore, the mechanism of zinc tolerance in transgenic plants may be due to reduced oxidative stress damage. Under zinc stress, the activities of APX were significantly higher in transgenic plants than in wild-type plants. We also found that the zinc accumulation in the shoots were much higher in transgenic plants than in wild-type plants under zinc stress. In addition, we found that compared with wild-type plants, transgenic plants were more tolerant to excessive cadmium stress and accumulated more cadmium in shoots. These results suggest that HvAPX1 plays an important role in zinc and cadmium tolerance, and might be a candidate gene for developing high-biomass tolerant plants for phytoremediation of zinc- and cadmium-polluted environments.
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ISSN:1916-2790
1916-2804
DOI:10.1139/B08-025