The glutamate receptors AtGLR1.2 and AtGLR1.3 increase cold tolerance by regulating jasmonate signaling in Arabidopsis thaliana

被引:63
|
作者
Zheng, Yan [1 ,2 ]
Luo, Landi [3 ]
Wei, Jingjing [1 ]
Chen, Qian [1 ]
Yang, Yongping [1 ]
Hu, Xiangyang [4 ]
Kong, Xiangxiang [1 ]
机构
[1] Chinese Acad Sci, Kunming Inst Bot, Key Lab Plant Divers & Biogeog East Asia, Kunming 650201, Yunnan, Peoples R China
[2] Univ Chinese Acad Sci, Beijing 100049, Peoples R China
[3] Yunnan Univ, Sch Ecol & Environm Sci, Kunming 650504, Yunnan, Peoples R China
[4] Shanghai Univ, Plant Sci Ctr, Sch Life Sci, Shanghai Key Lab Bioenergy Crops, Shanghai 200444, Peoples R China
基金
美国国家科学基金会;
关键词
AtGLR1.2; and; 1.3; Cold; Jasmonate signaling; CBF/DREB1; pathway; FREEZING TOLERANCE; GENES; EXPRESSION; PROTEINS; GROWTH; OVEREXPRESSION; CBF;
D O I
10.1016/j.bbrc.2018.10.153
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Plant glutamate-like receptors (GLRs), which are homologs of mammalian ionotropic glutamate receptors (iGluRs), are thought to be involved in plant growth, development, and environmental stress responses. In this study, we demonstrated that two members of Arabidopsis glutamate-like receptors, AtGLR1.2 and AtGLR1.3, play positive roles in the plant response to cold stress. Genetic and biochemical experiments revealed that exogenous jasmonate could attenuate the cold sensitivity of gir1.2 and glr1.3 mutants, and the overexpression of GLR1.2 or GLR1.3 enhanced cold tolerance by increasing endogenous jasmonate levels under cold stress. In addition, the expression of genes in the CBF/DREB1 signaling pathway was decreased in the glr1.2 and glr1.3 mutants, but was promoted in GLR1.2-OE and GLR1.3-OE transgenic plants compared with the wild-type during cold treatment Further investigation revealed that AtGLR1.2 and AtGLR1.3 independently drove similar functions without directly interacting. Together, our findings suggest that AtGLR1.2 and 1.3 positively enhance cold tolerance in Arabidopsis by activating endogenous jasmonate accumulation and subsequently promoting the downstream CBF/DREBI cold response pathway during cold stress. (C) 2018 Elsevier Inc. All rights reserved.
引用
收藏
页码:895 / 900
页数:6
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