Figure 1.

Priming by salicylic acid and benzothiadiazole. Chemical priming by SA and its structural analog BTH is best described in P. crispum L. (parsley) suspension culture and A. thaliana. Primed plants accumulate small amounts of the phytoalexin coumarin, and the secretion increases strongly after Pst infection or elicitor application¹, which is accompanied by augmented PHENYLALANINE AMMONIA-LYASE (PAL) expression. PAL induces SA biosynthesis (dashed line arrow) and thus further enhances disease resistance. Chemical treatment has a limited direct effect on callose deposition, which, however, increases rapidly after pathogen infection. Additionally, SA treatment enhances the oxidative burst after the application of a fungal elicitor. Primed plants accumulate inactive MPK3 and MPK6 and their respective mRNAs. After pathogen infection, accumulated MPKs are activated by phosphorylation allowing for stronger immune responses. The primed plant possesses chromatin modifications at the WRKY transcription factor and PR1 regulatory regions. This allows their augmented expression after flg22 application or stress by water infiltration¹. The transcriptional coregulator NPR1 is the key player in chemical priming required for the majority of the described processes. In O. sativa cv. NB, diterpenoid phytoalexin biosynthesis is augmented upon infection by M. oryzae in a process dependent on WRKY45 and mediated by CK, especially isopentenyladenine. Light grey color, effects are less pronounced in primed plants than in primed-and-infected plants. ¹Water infiltration stress causes cell collapse or a wound stress response in the leaf.