Wound- and mechanostimulated electrical signals control hormone responses

Plants in nature are constantly exposed to organisms that touch them and wound them.A highly conserved response to these stimuli is a rapid collapse of membrane potential (i.e. a decrease of electrical field strength across membranes). This can be coupled to the production and/or action of jasmonate...

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Veröffentlicht in:The New phytologist 2020-08, Vol.227 (4), p.1037-1050
Hauptverfasser: Farmer, Edward E., Gao, Yong-Qiang, Lenzoni, Gioia, Wolfender, Jean-Luc, Wu, Qian
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Sprache:eng
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Zusammenfassung:Plants in nature are constantly exposed to organisms that touch them and wound them.A highly conserved response to these stimuli is a rapid collapse of membrane potential (i.e. a decrease of electrical field strength across membranes). This can be coupled to the production and/or action of jasmonate or ethylene. Here, the various types of electrical signals in plants are discussed in the context of hormone responses. Genetic approaches are revealing genes involved in wound-induced electrical signalling. These include clade 3 GLUTAMATE RECEPTOR-LIKE (GLR) genes, Arabidopsis H⁺-ATPases (AHAs), RESPIRATORY BURST OXIDASE HOMOLOGUEs (RBOHs), and genes that determine cell wall properties. We briefly review touch- and wound-induced increases in cytosolic Ca2+ concentrations and their temporal relationship to electrical activities. We then look at the questions that need addressing to link mechanostimulation and wound-induced electrical activity to hormone responses. Utilizing recently published results, we also present a hypothesis for wound-response leaf-to-leaf electrical signalling. This model is based on rapid electro-osmotic coupling between the phloem and xylem. The model suggests that the depolarization of membranes within the vascular matrix triggered by physical stimuli and/or chemical elicitors is linked to changes in phloem turgor and that this plays vital roles in leaf-to-leaf electrical signal propagation.
ISSN:0028-646X
1469-8137
DOI:10.1111/nph.16646