We have used wound- and jasmonic acid (JA)-responsive genes as molecular markers to elucidate the pathway(s) of wound signal transduction in Arabidopsis thaliana. The JA-responsive (JR) genes JR1, JR2, and JR3 are strongly induced by wounding and by JA, while the wound-responsive (WR) genes WR3 and acyl CoA oxidase (ACO) are induced by wounding only. Accumulation of JR transcripts upon wounding was blocked by indomethacin. However, indomethacin did not affect either induction of these genes by JA or wound-induced expression of WR genes, suggesting that JA synthesis is only needed for wound-dependent induction of JR genes, and also that separate JA-dependent and -independent wound signal transduction pathways exist in Arabidopsis. The two pathways are differentially regulated by Ca2+ and calmodulin. Mobilization of intracellular Ca2+ pools blocked induction of JR genes by both wounding and JA, but not the induction of WR genes by wounding, but this effect could not be reproduced by increasing intracellular Ca2+ levels using ionophores. In addition, calmodulin antagonists blocked the expression of JR genes and up-regulated WR gene expression. Ca2+ and calmodulin seem to act downstream of both JA and the COI1 gene in the JA-dependent pathway, and downstream of reversible phosphorylation events that differentially regulate JA-dependent and JA-independent wound signal transduction pathways.