Priming is a physiological state for protection of plants against a broad range of pathogens, and is achievedthrough stimulation of the plant immune system. Various stimuli, such as beneficial microbes and chemicalinduction, activate defense priming. In the present study, we demonstrate that impairment of the high-affinity nitrate transporter 2.1 (encoded by NRT2.1) enables Arabidopsis to respond more quickly andstrongly to Plectosphaerella cucumerina attack, leading to enhanced resistance. The Arabidopsis thalianamutant lin1 (affected in NRT2.1) is a priming mutant that displays constitutive resistance to this necrotroph,with no associated developmental or growth costs. Chemically induced priming by b–aminobutyric acidtreatment, the constitutive priming mutant ocp3 and the constitutive priming present in the lin1 mutantresult in a common metabolic profile within the same plant–pathogen interactions. The defense priming sig-nificantly affects sugar metabolism, cell-wall remodeling and shikimic acid derivatives levels, and results inspecific changes in the amino acid profile and three specific branches of Trp metabolism, particularly accu-mulation of indole acetic acid, indole-3–carboxaldehyde and camalexin, but not the indolic glucosinolates.Metabolomic analysis facilitated identification of three metabolites in the priming fingerprint: galacturonicacid, indole-3–carboxylic acid and hypoxanthine. Treatment of plants with the latter two metabolites by soildrenching induced resistance against P. cucumerina, demonstrating that these compounds are key compo-nents of defense priming against this necrotrophic fungus. Here we demonstrate that indole-3–carboxylicacid induces resistance by promoting papillae deposition and H2O2production, and that this is independentof PR1, VSP2 and PDF1.2 priming