The glutamate receptors AtGLR1.2 and AtGLR1.3 increase cold tolerance by regulating jasmonate signaling in Arabidopsis thaliana
The glutamate receptors AtGLR1.2 and AtGLR1.3 increase cold tolerance by regulating jasmonate signaling in Arabidopsis thaliana
复制标题
拟南芥谷氨酸受体 AtGLR1.2 和 AtGLR1.3 通过调节茉莉酸信号传导提高耐冷性
DOI：
10.1016/j.bbrc.2018.10.153
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发表时间：
2018-12-02
影响因子：
3.1
通讯作者：
Kong, Xiangxiang
中科院分区：
文献类型：
--
作者：
Zheng, Yan;Luo, Landi;Kong, Xiangxiang
植物谷氨酸样受体（GLRs）是哺乳动物嗜离子谷氨酸受体（iGluRs）的同源物，被认为参与植物的生长发育和环境胁迫反应。在本研究中，我们发现拟南芥谷氨酸样受体AtGLR1.2和AtGLR1.3在植物对冷胁迫的响应中发挥积极作用。遗传和生化实验表明，外源茉莉酸可以减弱gir1.2和glr1.3突变体的冷敏感性，GLR1.2和glr1.3的过表达通过增加内源茉莉酸水平来增强冷胁迫下的耐寒性。此外，与野生型相比，glr1.2 - oe和glr1.3转基因植株在冷处理过程中CBF/DREB1信号通路基因的表达降低，而在glr1.2 - oe和glr1.3 - oe转基因植株中表达上调。进一步研究发现，AtGLR1.2和AtGLR1.3各自独立驱动类似的功能，并不直接相互作用。总之，我们的研究结果表明，AtGLR1.2和1.3通过激活内源茉莉酸积累，进而促进下游CBF/DREBI冷响应途径，在冷胁迫下正向增强拟南芥的耐寒性。(C) 2018爱思唯尔公司版权所有。
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.