Plant responses to wounding and herbivore attack are orchestrated by complex signaling pathways that link the production of chemical and physical signals at the wound site to activation of gene expression and other cellular processes. The systemic nature of many wound-induced responses provides an attractive opportunity to study intercellular signaling pathways that operate over long distances within the plant. Genetic dissection of the wound-response pathway in tomato indicates that (1) systemin and its precursor protein, prosystemin, are upstream components of an intercellular signaling cascade that requires the biosynthesis and action of jasmonic acid (JA); and (2) physiological processes regulated by this pathway confer host resistance to a broad spectrum of plant invaders. Grafting experiments conducted with mutants defective in systemic wound signaling indicate that systemin functions at or near the wound site to trigger the production of JA, which in turn acts non-cell autonomously to promote systemic defense responses. The location of JA biosynthetic enzymes within the companion cell-sieve element complex of vascular bundles, together with the accumulation of JA in vascular tissues, support a role for jasmonates as phloem-mobile signals. The recent discovery of enzymes involved in the metabolism of JA to volatile methyl-JA and bioactive JA-amino acid conjugates has potential implications for the mechanism by which JA promotes wound signaling. Species-specific differences in the mechanism of wound signaling appear to reflect the way in which the wound-induced jasmonate pathway is regulated by other signals including systemin, cell wall-derived oligosaccharides, ethylene, and insect-derived elicitors. Adding to the complexity of the wound-induced jasmonate cascade are wound-signaling pathways that operate independently of JA.