背景回顾：In Arabidopsis thaliana, local wounding and herbivore feeding provoke leaf-to-leaf propagating Ca2+ waves that are dependent on the activity of members of the glutamate receptor-like channels (GLRs). In systemic tissues, GLRs are needed to sustain the synthesis of jasmonic acid (JA) with the subsequent activation of JA-dependent signaling response required for the plant acclimation to the perceived stress. 

提出问题：Even though the role of GLRs is well established, the mechanism through which they are activated remains unclear. 

主要发现：Here, we report that in vivo, the amino-acid-dependent activation of the AtGLR3.3 channel and systemic responses require a functional ligand-binding domain. 

结果1：By combining imaging and genetics, we show that leaf mechanical injury, such as wounds and burns, as well as hypo-osmotic stress in root cells, induces the systemic apoplastic increase of L-glutamate (L-Glu), which is largely independent of AtGLR3.3 that is instead required for systemic cytosolic Ca2+ elevation.  

结果2：Moreover, by using a bioelectronic approach, we show that the local release of minute concentrations of L-Glu in the leaf lamina fails to induce any long-distance Ca2+ waves. 

在拟南芥中，局部性损伤和食草动物的啃食会引起叶片间的钙离子波的传播，而这这取决于谷氨酸类受体通道（GLRs）成员的活性。在系统性组织中，需要GLR维持茉莉酸（JA）的合成，以及随后JA依赖性信号响应的激活，这对于植物适应感知到的胁迫是必需的。尽管GLR的作用已经研究得很清楚了，但其激活机制仍未可知。本文中，作者报道了在植物体内，AtGLR3.3通道的氨基酸依赖性激活和系统性响应需要一个功能性配体结合域。通过结合成像和遗传学，作者发现创伤或灼伤导致的叶片机械损伤和根细胞的低渗胁迫，会诱导L-谷氨酸的系统性的质外体增加，这在很大程度上独立于AtGLR3.3，而AtGLR3.3确实是系统性胞质钙离子增加所必需的。此外，通过生物电子方法，作者发现在叶片中局部释放微浓度的L-Glu，并不能诱导任何长距离的钙离子波。