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

2016-04-14T21:30:20Z (GMT) by Vicenta Salvador-Recatalà
<p>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 g</i>enes. 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.</p>