Abstract：
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. Even though the role of GLRs is well established, the mechanism through which they are activated remains unclear. 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. 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. 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.
摘要：
在拟南芥中，局部受伤和食草动物摄食会引起叶到叶传播的Ca2波，这取决于谷氨酸受体样通道（GLR）成员的活性。在全身组织中，需要GLR来维持茉莉酮酸（JA）的合成，并随后激活植物适应感知的胁迫所需的JA依赖性信号传导反应。尽管GLR的作用已经确立，它们被激活的机制尚不清楚。这里,我们报告说，在体内，AtGLR3.3通道的氨基酸依赖性激活和全身反应需要功能性配体结合域。通过结合成像和遗传学，我们证明了叶片的机械损伤，比如伤口和烧伤，以及根细胞的低渗透胁迫，诱导L-谷氨酸（L-Glu）的全身性质增加，这在很大程度上独立于系统胞质Ca2+升高所需的AtGLR3.3。此外，通过使用生物电子方法，我们表明，叶片中微量L-Glu的局部释放无法诱导任何长距离Ca2波。
