Plants respond differentially to wounding and pathogens using distinct signaling pathways, so that wound signals are transmitted to jasmonic acid (JA) which induces basic pathogenesis-related (PR) proteins, whereas pathogenic signals cause, in addition to JA, accumulation of salicylic acid (SA) which stimulates production of acidic PR proteins. Transgenic tobacco plants expressing a gene for a small GTP binding protein respond abnormally to mechanical wounding to produce SA and consequently acidic PR proteins, suggesting that wound signals cross with pathogen signaling pathways [Sane et al. (1994) Proc. Natl. Acad. Sci. USA 91: 10556]. This unusual signal crossing is associated with a highly sensitive wound-response of transgenic plants which, upon wounding, produce JA at least eighteen hours earlier than wild-type plants. When wildtype plants are wounded in the presence of the synthetic cytokinin, benzylaminopurine, production of JA begins six hours earlier than in untreated samples, and also SA begins to accumulate. The cytokinin antagonist, 2-chloro-4-cyclohexylamino-6-ethylamino-s-triazine, erases these effects. Because transgenic plants constitutively produce four- to six-fold higher amounts of endogenous cytokinins than wild-type plants, it is concluded that cytokinins are indispensable for control of endogenous levels of SA and JA.