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A cadmium stress-responsive gene AtFC1 confers plant tolerance to cadmium toxicity

文献类型： 外文期刊

作者： Song, Jun 1 ; Feng, Sheng Jun 1 ; Chen, Jian 2 ; Zhao, Wen Ting 3 ; Yang, Zhi Min 1 ;

作者机构： 1.Nanjing Agr Univ, Dept Biochem & Mol Biol, Coll Life Sci, Nanjing 210095, Jiangsu, Peoples R China

2.Jiangsu Acad Agr Sci, Inst Food Qual & Safety, Nanjing 210014, Jiangsu, Peoples R China

3.Justus Liebig Univ, Inst Plant Nutr IFZ, Heinrich Buff Ring 26-32, D-35392 Giessen, Germany

关键词： Ferrochelatase-1;Arabidopsis;Cadmium;Glutathione;Phytochelatins

期刊名称：BMC PLANT BIOLOGY （ 影响因子：4.215； 五年影响因子：4.96 ）

ISSN： 1471-2229

年卷期： 2017 年 17 卷

页码：

收录情况： SCI

摘要： Background: Non-essential trance metal such as cadmium (Cd) is toxic to plants. Although some plants have developed elaborate strategies to deal with absorbed Cd through multiple pathways, the regulatory mechanisms behind the Cd tolerance are not fully understood. Ferrochelatase-1 (FC1, EC4.99.1.1) is the terminal enzyme of heme biosynthesis, catalyzing insertion of ferrous ion into protoporphyrin IX. Recent studies have shown that FC1 is involved in several physiological processes. However, its biological function associated with plant abiotic stress response is poorly understood. Results: In this study, we showed that AtFC1 was transcriptionally activated by Cd exposure. AtFC1 overexpression (35S::FC1) lines accumulated more Cd and non-protein thiol compounds than wild-type, and conferred plant tolerance to Cd stress, with improved primary root elongation, biomass and chlorophyll (Chl) content, and low degree of oxidation associated with reduced H2O2, O.2- and peroxides. In contrast, the AtFC1 loss of functional mutant fc1 showed sensitivity to Cd stress. Exogenous provision of heme, the product of AtFC1, partially rescued the Cd-induced toxic phenotype of fc1 mutants by improving the growth of seedlings, generation of glutathione (GSH) and phytochelatins (PCs), and GSH/PCs-synthesized gene expression (e.g. GSH1, GSH2, PCS1, and PCS2). To investigate the mechanism leading to the AtFC1 regulating Cd stress response in Arabidopsis, a transcriptome of fc1 mutant plants under Cd stress was profiled. Our data showed that disfunction of AtFC1 led to 913 genes specifically up-regulated and 522 genes down-regulated in fc1 mutants exposed to Cd. Some of the genes are involved in metal transporters, Cd-induced oxidative stress response, and detoxification. Conclusion: These results indicate that AtFC1 would act as a positive regulator of plant tolerance to Cd stress. Our study will broaden our understanding of the role of FC1 in mediating plant response to Cd stress and provide a basis for further exploration of its downstream genes.

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