Long-distance turgor pressure changes induce local activation of plant glutamate receptor-like channels.

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 At GLR3.3 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 At GLR3.3 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. [Display omitted] • Plant glutamate receptor-like channel At GLR3.3 is gated by exogenous amino acids • At GLR3.3 ligand-binding domain is essential for channel activation • Leaf injury and osmotic stress induce L-Glu systemic elevation activating At GLR3.3 • Local activation of GLRs does not trigger long-distance Ca2+ waves In Arabidopsis thaliana , mechanical stresses induce long-distance Ca2+ signals mediated by the glutamate receptor-like 3.3 channel. Grenzi et al. show that the stress-induced systemic increase of apoplastic L-glutamate, in a submillimolar range of concentrations, gates the At GLR3.3 through its ligand-binding domain. [ABSTRACT FROM AUTHOR]