The WRKY33 transcription factor was reported for resistance to the necrotrophic fungus Botrytis cinerea. Using microarray-based analysis, we compared Arabidopsis WRKY33 overexpressing lines and wrky33 mutant that showed altered susceptibility to B. cinerea with their corresponding wild-type plants. In the wild-type, about 1660 genes (7% of the transcriptome) were induced and 1054 genes (5% of the transcriptome) were repressed at least twofold at early stages of inoculation with B. cinerea, confirming previous data of the contribution of these genes in B. cinerea resistance. In Arabidopsis wild-type plant infected with B. cinerea, the expressions of the differentially expressed genes encoding for proteins and metabolites involved in pathogen defense and non-defense responses, seem to be dependent on a functional WRKY33 gene. The expression profile of 12-oxo-phytodienoic acidand phytoprostane A 1 -treated Arabidopsis plants in response to B. cinerea revealed that cyclopentenones can also modulate WRKY33 regulation upon inoculation with B. cinerea. These results support the role of electrophilic oxylipins in mediating plant responses to B. cinerea infection through the TGA transcription factor. Future directions toward the identification of the molecular components in cyclopentenone signaling will elucidate the novel oxylipin signal transduction pathways in plant defense.cinerea induces host cell death by producing toxins, cell wall degrading enzymes and reactive oxygen intermediates (ROIs) [1,4,5]. Although cell death and accumulation of ROIs are associated with plant resistance to biotrophic pathogens [6], the ROIs can also increase plant susceptibility to necrotrophs [7]. In addition, the plant polygalacturonase-inhibiting proteins counteract polygalacturonase which are important host colonizing factors for some fungal pathogens [8]. Although the cell wall and cuticle protect plants against pathogen penetration or infection, Arabidopsis mutants defective in components of the cell wall and cuticle were resistant to B. cinerea [9][10][11]. In fact, the cell wall and cuticle are primary barriers against pathogen attacks that may decrease or enhance plant resistance to pathogens. For instance, a lossof-function of the HISTONE MONOUBIQUITINATION1 (HUB1) gene, encoding an E3 ligase required for histone H2B ubiquitination, reduces the cell wall thickness and increases the susceptibility to B. cinerea and Alternaria brassicicola [12].Similarly to animals, plants recognize elicitors derived from pathogens to activate innate immune defense responses [13]. In contrast to race-specific elicitors or resistance genes described for biotroph-plant interactions, plants recognize a pathogen -regardless of its lifestyle-via MAMP that serve as general elicitors [14,15]. Chitins and glucans are fungal MAMPs that plants can recognize by pattern recognition receptors. The Arabidopsis receptor kinases, FLS2 (flagellin sensing 2) and EFR (elongation factor Tu receptor), independently recognize the bacterial flagellin (flg22) and elongati...