What causes range limits is a central question in evolutionary ecology. Transplant studies indicate that areas just across range boundaries are often stressful. The recent Defense constraint (DC) hypothesis for plants states that the evolution of tolerance to stressful environments across a range boundary is constrained by allocation to chemical defense because of antagonistic crosstalk between abiotic and biotic stress signaling pathways that otherwise could be co-opted for range expansion. Abscisic acid (ABA) drought stress tolerance and jasmonic acid/ethylene (JA/ET) defense signaling pathways, for example, are known to be antagonistic to one another in Arabidopsis and other species. To test the DC hypothesis, we examined quantitative genetic variation and co-variation among marker-inferred inbred lines and sib-families of Boechera stricta, a close wild relative of Arabidopsis. The dynamics of the defense-stress tolerance tradeoff was examined across 1) years that differed in precipitation, 2) drought and ABA treatments, and 3) a NPK nutrient supply gradient. In support of the DC hypothesis, we observed the tradeoff a) in the dry year, and b) in response to water deficiency, which c) was affected by ABA treatments, but the interaction between ABA and glucosinolate (GS) toxin levels was not significant. In contrast to the effects of water deficiency, d) the effect of lower NPK supply to cause the tradeoff was only marginally significant. Because an ABA-mediated stress response is intrinsic to water deficient conditions and because of the known involvement of JA/ET in GS regulation, we suggest that these results provide circumstantial evidence implicating both of these pathways in the tradeoff and thus in the development of range limits.