Abstract
The activation of defense genes in response to wounding involves the integration of multiple inputs from various signaling molecules produced in different tissues and cellular compartments. In this report, we demonstrate that calcium and magnesium ions enhance systemin activity and that calcium fluxes are necessary for wound gene activation. During wounding, intracellular contents such as calcium, magnesium and the defense peptide systemin, a potent activator of the wound response, are released into the apoplastic space. Our analysis showed that elevated concentrations of calcium or magnesium ions in the apoplast significantly enhanced the biological activity of systemin by decreasing the concentration necessary to induce maximal proteinase inhibitor accumulation by 100-fold. Calcium ionophores disrupt calcium gradients across biological membranes and consequently elevate intracellular calcium levels. Plants treated with the calcium ionophores ionomycin and A23187 induced the accumulation of proteinase inhibitor proteins to levels similar to those produced by wounding. Ionophore-mediated proteinase inhibitor induction was blocked in the jasmonic acid signaling mutant def-1, indicating that increased levels of intracellular calcium activated the octadecanoid pathway leading to wound gene activation. Calcium transport antagonists (nifedipine, verapamil, ruthenium red, and erythrosine-B) were found to inhibit proteinase inhibitor synthesis in response to wounding, whereas extracellular calcium chelators were found to induce the synthesis of proteinase inhibitors in a jasmonic acid-dependent and systemin-independent manner. Taken together, our data show that calcium and potentially magnesium ions play an integral role in mediating the plant's response to wounding.
Published Version
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