The Arabidopsis defensin gene AtPDF2.5 mediates cadmium tolerance and accumulation

Plant, Cell and Environment - Tập 42 Số 9 - Trang 2681-2695 - 2019
Jin‐Song Luo1,2, Yong Yang1,2, Tianyu Gu3, Zhimin Wu1,2, Zhenhua Zhang1,2
1Hunan Provincial Key Laboratory of Farmland Pollution Control and Agricultural Resources Use, Hunan Provincial Key Laboratory of Nutrition in Common University, National Engineering Laboratory on Soil and Fertilizer Resources Efficient Utilization, Changsha, 410128, China
2Southern Regional Collaborative Innovation Center for Grain and Oil Crops in China, College of Resources and Environmental Sciences, Hunan Agricultural University, Changsha, 410128, China
3National Key Laboratory of Plant Molecular Genetics and CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai 200032, China

Tóm tắt

AbstractAlthough excess cadmium (Cd) accumulation is harmful to plants, the molecular mechanisms underlying Cd detoxification and accumulation in Arabidopsis thaliana remain largely undetermined. In this study, we demonstrated that the A. thaliana PLANT DEFENSIN 2 gene AtPDF2.5 is involved in Cd tolerance and accumulation. In vitro Cd‐binding assays revealed that AtPDF2.5 has Cd‐chelating activity. Site‐directed mutagenesis of AtPDF2.5 identified eight cysteine residues that were essential for mediating Cd tolerance and chelation. Histochemical analysis demonstrated that AtPDF2.5 was mainly expressed in root xylem vascular bundles, and that AtPDF2.5 was significantly induced by Cd. Subcellular localization analysis revealed that AtPDF2.5 was localized to the cell wall. The overexpression of AtPDF2.5 significantly enhanced Cd tolerance and accumulation in Athaliana and its heterologous overexpression in rice increased Cd accumulation; however, the functional disruption of AtPDF2.5 decreased Cd tolerance and accumulation. Physiological analysis suggested that AtPDF2.5 promoted Cd efflux from the protoplast and its subsequent accumulation in the cell wall. These data suggest that AtPDF2.5 promotes cytoplasmic Cd efflux via chelation, thereby enhancing Cd detoxification and apoplastic accumulation.

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