New roles for the <i>GLUTAMATE RECEPTOR-LIKE 3.3, 3.5</i>, and <i>3.6</i> genes as on/off switches of wound-induced systemic electrical signals

Wounding induces systemic potentials in <i>Arabidopsis thaliana</i> that can be abolished by concomitant suppression of the <i>GLUTAMATE RECEPTOR-LIKE GLR3.3</i> and <i>GLR3.6</i> genes. However, the roles of specific GLR channels to these potentials remain unclear. Here I applied the Electrical Penetration Graph (EPG) to study the contribution of three GLR channels to wound-induced, systemically propagated electrical potentials in <i>Arabidopsis thaliana</i>. In contrast to recordings made with conventional rigs for whole-plant electrophysiology, the EPG allows for the unambiguous distinction of the phloem-propagated action potential (AP) from the electrical activity outside of the phloem. The data reported here suggest that: (a) the transmission of wound-induced, phloem-propagated AP to neighbor leaves, requires expression of <i>GLR3.3</i> or <i>GLR3.6</i>, whereas <i>GLR3.5</i> prevents its transmission to non-neighbor leaves; (b) the generation of wound-induced electrical signals outside the phloem network depends on <i>GLR3.6</i> expression; and (c) wound-induced systemic potentials initiated in the shoot are transmitted to the root in the adult plant, which suggests a role for these electrical signals in coordinating the plant defenses in the shoot and in the root. Here, I propose a model for wound-induced systemic electrical signals at the molecular, cellular and anatomical level. In this model, <i>GLR3.3</i> and <i>GLR3.6</i> function as on switches for the propagation of wound-induced potentials beyond the wounded leaf, while <i>GLR3.5</i> functions as an off switch that prevents the propagation of wound-induced electrical potentials to distal, non-neighbor leaves.机械损伤可在拟南芥（Arabidopsis thaliana）中诱导系统性电位，而同时抑制谷氨酸受体样（GLUTAMATE RECEPTOR-LIKE, GLR）3.3与GLR3.6基因可消除该电位。然而，特定GLR通道在这类电位形成中的具体作用仍不明确。本研究采用电穿透图（Electrical Penetration Graph, EPG）技术，探究三类GLR通道对拟南芥伤口诱导的系统性传播电位的调控贡献。与传统全植株电生理记录装置相比，EPG技术可明确区分韧皮部传播的动作电位（action potential, AP）与韧皮部外的电活动。本研究所得数据表明：(a) 伤口诱导的韧皮部传播型AP向邻近叶片的转运，依赖GLR3.3或GLR3.6的表达，而GLR3.5则会阻断该电位向非邻近叶片的传播；(b) 韧皮部网络外的伤口诱导电信号的产生，依赖GLR3.6的表达；(c) 成株中，由地上部启动的伤口诱导系统性电位可传递至根部，这表明这类电信号在协调地上部与根部的植物防御反应中发挥作用。本研究从分子、细胞及解剖层面，提出了一套伤口诱导系统性电信号的作用模型。该模型中，GLR3.3与GLR3.6作为“开启开关”，介导伤口诱导电位从受伤叶片向外传播；而GLR3.5则作为“关闭开关”，阻断伤口诱导电位向远端非邻近叶片的传播。