Overexpression of a bacterial mercury transporter MerT in Arabidopsis enhances mercury tolerance
文献类型: 外文期刊
作者: Xu, Sheng 1 ; Sun, Bin 1 ; Wang, Rong 1 ; He, Jia 1 ; Xia, Bing 1 ; Xue, Yong 3 ; Wang, Ren 1 ;
作者机构: 1.Inst Bot, Nanjing 210014, Jiangsu, Peoples R China
2.Chinese Acad Sci, Nanjing 210014, Peoples R China
3.Shanghai Acad Agr Sci, Ecoenvironm Protect Res Inst, Shanghai 201403, Peoples R China
关键词: Arabidopsis;Pseudomonas alcaligenes;Mercuric transport protein;Mercury tolerance;Reactive oxygen species
期刊名称:BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS ( 影响因子:3.575; 五年影响因子:3.381 )
ISSN:
年卷期:
页码:
收录情况: SCI
摘要: The phytoremediation by using of green plants in the removal of environmental pollutant is an environment friendly, green technology that is cost effective and energetically inexpensive. By using Agrobacterium-mediated gene transfer, we generated transgenic Arabidopsis plants ectopically expressing mercuric transport protein gene (merT) from Pseudomonas alcaligenes. Compared with wild-type (WT) plants, overexpressing PamerT in Arabidopsis enhanced the tolerance to HgCl2. Further results showed that the enhanced total activities or corresponding transcripts of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT) and guaiacol peroxidase (POD) were observed in transgenic Arabidopsis under HgCl2 stress. These results were confirmed by the alleviation of oxidative damage, as indicated by the decrease of thiobarbituric acid reactive substances (TBARS) contents and reactive oxygen species (ROS) accumulation. In addition, localization analysis of PaMerT in Arabidopsis protoplast showed that it is likely to be associated with vacuole. In all, PamerT increased mercury (Hg) tolerance in transgenic Arabidopsis, and decreased production of Hg-induced ROS, thereby protecting plants from oxidative damage. The present study has provided further evidence that bacterial MerT plays an important role in the plant tolerance to HgCl2 and in reducing the production of ROS induced by HgCl2. (C) 2017 Elsevier Inc. All rights reserved.
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