The plasticity of priming phenomenon activates not only common metabolomic fingerprint but also specific responses against P. cucumerina.

Previously we described that different priming stimuli trigger common metabolomic responses against P. cucumerina. Furthermore we showed that several primed metabolites were present following independent priming inducers such as natural constitutive priming promoted by gene mutations and chemical priming induced by the β-aminobutyric acid (BABA). Despite we found a common metabolomic fingerprint, in the present research we focus our attention in specific metabolites that are primed differentially by a mutation in the NRT2.1 gene (lin1 mutant) and BABA treatments against P. cucumerina. Around eight hundred compounds were overaccumulated in the resistant mutant lin1 and in BABA treated plants upon infection. Among them 404 and 412 were specific of each priming condition while 103 compounds were shared by both. Flavonoids and lignans were specifically accumulated in lin1 in response to the fungal attack, while tyrosine, purine metabolism, and aromatic carbon degradation compounds were only accumulated in BABA primed plants upon infection. However, most metabolites differentially accumulated by the two priming conditions belonged to the same metabolic pathways, suggesting that different priming stimuli, upon a given biotic stress, may stimulate similar pathways but activate specific differences depending on the priming stimulus.