SUMMARY Jasmonic acid and related oxylipin compounds are plant signalling molecules that are involved in the response to pathogens, insects, wounding and ozone. To explore further the role of jasmonates in stress signal transduction, the response of two jasmonate-signalling mutants, jin1 and jin4, to pathogens and ozone was analysed in this study. Upon treatment with the biotrophic bacterial pathogen Pseudomonas syringae, endogenous jasmonate levels increased in jin1 and jin4 similar to wild-type, demonstrating that these mutants are not defective in jasmonate biosynthesis. Jin1 but not jin4 is more resistant to P. syringae and this higher resistance is accompanied by higher levels of salicylic acid. Jin1 is also more resistant to the necrotrophic fungal pathogen Botrytis cinerea and shows wild-type sensitivity to ozone whereas jin4 is more susceptible to B. cinerea and ozone. These results indicate that the mutations in jin1 and jin4 affect different branches of the jasmonate signalling pathway. Additionally, in this combination of phenotypes, jin1 is unique among all other jasmonate-related mutants described thus far. These data also provide support for a crosstalk between the jasmonate and salicylate pathways.

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l-lysine catabolic routes in plants include the saccharopine pathway to α-aminoadipate and decarboxylation of lysine to cadaverine. The current review will cover a third l-lysine metabolic pathway having a major role in plant systemic acquired resistance (SAR) to pathogen infection that was recently discovered in Arabidopsis thaliana. In this pathway, the aminotransferase AGD2-like defense response protein (ALD1) α-transaminates l-lysine and generates cyclic dehydropipecolic (DP) intermediates that are subsequently reduced to pipecolic acid (Pip) by the reductase SAR-deficient 4 (SARD4). l-pipecolic acid, which occurs ubiquitously in the plant kingdom, is further N-hydroxylated to the systemic acquired resistance (SAR)-activating metabolite N-hydroxypipecolic acid (NHP) by flavin-dependent monooxygenase1 (FMO1). N-hydroxypipecolic acid induces the expression of a set of major plant immune genes to enhance defense readiness, amplifies resistance responses, acts synergistically with the defense hormone salicylic acid, promotes the hypersensitive cell death response and primes plants for effective immune mobilization in cases of future pathogen challenge. This pathogen-inducible NHP biosynthetic pathway is activated at the transcriptional level and involves feedback amplification. Apart from FMO1, some cytochrome P450 monooxygenases involved in secondary metabolism catalyze N-hydroxylation reactions in plants. In specific taxa, pipecolic acid might also serve as a precursor in the biosynthesis of specialized natural products, leading to C-hydroxylated and otherwise modified piperidine derivatives, including indolizidine alkaloids. Finally, we show that NHP is glycosylated in Arabidopsis to form a hexose-conjugate, and then discuss open questions in Pip/NHP-related research.