Parsley leaves exhibited incomplete resistance following stomatal inoculation with the broad host range pathogen,Erwinia chrysanthemi, resulting in the development of local lesions in 58% of inoculated leaves. The responses of the same plant material to five mutants generated from the wild type bacterial strain varied from highly susceptible to completely resistant. While the susceptible phenotype was characterized by spreading maceration, hypersensitivelike necrotic lesions were typical for resistant leaves, with both types of symptom becoming visible two days after inoculation. Accumulation of transcripts of an entire set of defense-related genes and of furanocoumarin phytoalexins preceded visible onset of lesion development or maceration in the respective interactions.Escherichia coli did not elicit symptoms, gene activation or phytoalexin accumulation in parsley leaves. No correlation existed between the final extent of plant resistance on the one hand, and the timing or degree gene activation and phytoalexin accumulation on the other hand. Rapid activation of defense-related genes therefore appears to be insufficient, although it may be necessary, to protect parsley from attack byErwinia chrysanthemi.