Plants defend against herbivores and nematodes by rapidly sending signals from the wounded sites to the whole plant. We investigated how plants generate and transduce these rapidly moving, long-distance signals referred to as systemic wound signals. We developed a system for measuring systemic responses to root wounding in Arabidopsis thaliana. We found that root wounding or the application of glutamate to wounded roots was sufficient to trigger root-to-shoot Ca²⁺ waves and slow wave potentials (SWPs). Both of these systemic signals were inhibited by either disruption of both GLR3.3 and GLR3.6, which encode glutamate receptor–like proteins (GLRs), or constitutive activation of the P-type H⁺-ATPase AHA1. We further showed that GLR3.3 and GLR3.6 displayed Ca²⁺-permeable channel activities gated by both glutamate and extracellular pH. Together, these results support the hypothesis that wounding inhibits P-type H⁺-ATPase activity, leading to apoplastic alkalization. This, together with glutamate released from damaged phloem, activates GLRs, resulting in depolarization of membranes in the form of SWPs and the generation of cytosolic Ca²⁺ increases to propagate systemic wound signaling.

植物通过从受伤部位向整株植物快速发送信号来抵御食草动物和线虫。我们研究了植物如何产生和转导这些快速移动的长距离信号，称为系统性伤口信号。我们开发了一种用于测量拟南芥根部损伤的系统反应的系统。我们发现根部受伤或将谷氨酸盐应用于受伤的根部足以触发根到芽 Ca ²⁺波和慢波电位 (SWP)。这两种全身信号都被编码谷氨酸受体样蛋白 (GLR) 的GLR3.3和GLR3.6 的破坏或 P 型 H ^{+ 的}组成性激活所抑制。-ATPase AHA1。我们进一步表明 GLR3.3 和 GLR3.6 显示出由谷氨酸盐和细胞外 pH 控制的Ca ²⁺可渗透通道活性。总之，这些结果支持以下假设：创伤抑制 P 型 H ⁺ -ATPase 活性，导致质外体碱化。这与从受损韧皮部释放的谷氨酸盐一起激活 GLR，导致 SWP 形式的膜去极化，并且胞质 Ca ²⁺的产生增加以传播全身伤口信号。