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Glutamate-dependent systemic signaling in plants
Upon wounding, plants generate systemic Ca2+ waves and electrical signals that propagate from the wound site to distal tissues (see the Focus by Fichman et al.). The glutamate receptor–like proteins GLR3.3 and GLR3.6 are required for leaf-to-leaf systemic wound signals in Arabidopsis thaliana. Shao et al. found that wounding or the application of glutamate induced root-to-shoot Ca2+ and electrical signaling in Arabidopsis, which required GLR3.3, GLR3.6, and inhibition of the proton pump AHA1. In cultured mammalian cells, GLR3.3 and GLR3.6 functioned as pH-sensitive, glutamate-gated Ca2+ channels. These findings suggest that wounding induces both the leakage of glutamate from the phloem into the apoplastic space and an increase in the apoplastic pH, leading to the activation of GLRs and the generation of systemic Ca2+ waves and electrical signals.
Abstract
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.
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