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 woundinduced 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 Ca 2+ concentrations and their temporal relationship to electrical activities. We then look at the questions that need addressing to link mechanostimulation and woundinduced 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.

Calcium plays a key role in determining the specificity of a vast array of signalling pathways in plants. Cellular calcium elevations with different characteristics (calcium signatures) carry information on the identity of the primary stimulus, ensuring appropriate downstream responses. However, the mechanism for decoding calcium signatures is unknown. To determine this, decoding of the salicylic acid (SA)-mediated plant immunity signalling network controlling gene expression was examined. A dynamic mathematical model of the SA-mediated plant immunity network was developed. This model was used to predict responses to different calcium signatures; these were validated empirically using quantitative real-time PCR to measure gene expression. The mechanism for decoding calcium signatures to control expression of plant immunity genes enhanced disease susceptibility 1 (EDS1) and isochorismate synthase 1 (ICS1) was identified. Calcium, calmodulin, calmodulin-binding transcription activators (CAMTA)3 and calmodulin binding protein 60g (CBP60g) together amplify each calcium signature into three active signals, simultaneously regulating expression. The time required for calcium to return to steady-state level also quantitatively regulates gene expression. Decoding of calcium signatures occurs via nonlinear interactions between these active signals, producing a unique response in each case. Key properties of the calcium signatures are not intuitive, exemplifying the importance of mathematical modelling approaches. This approach can be applied to identifying the decoding mechanisms of other plant calcium signalling pathways.

Plants need to sense increases in temperature to be able to adapt their physiology and development to survive; however, the mechanisms of heat perception are currently relatively poorly understood. Here we demonstrate that in response to elevated temperature the free calcium concentration of the stroma of chloroplasts increases. This response is specific to the chloroplast, as no corresponding increase in calcium is seen in the cytosol. The chloroplast calcium response is dose-dependent above a threshold. The magnitude of this calcium response is dependent upon absolute temperature, not rate of heating. This response is dynamic: repeated stimulation leads to rapid attenuation of the response, which can be overcome by sensitisation at a higher temperature. More long-term acclimation to different temperatures resets the basal sensitivity of the system, such that plants acclimated to lower temperatures are more sensitive than those acclimated to higher temperatures. The heat-induced chloroplast calcium response was partially dependent upon the calcium-sensing receptor CAS which has been shown previously to regulate other chloroplast calcium signalling responses. Taken together our data demonstrate the ability of chloroplasts to sense absolute high temperature and produce commensurately quantitative stromal calcium response, the magnitude of which is a function of both current temperature and stress history.

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