Jasmonate biosynthesis in Arabidopsis thaliana requires peroxisomal β-oxidation enzymes – Additional proof by properties of pex6 and aim1

Jasmonic acid (JA) is an important regulator of plant development and stress responses. Several enzymes involved in the biosynthesis of JA from α-linolenic acid have been characterized. The final biosynthesis steps are the β-oxidation of 12-oxo-phytoenoic acid. We analyzed JA biosynthesis in the Arabidopsis mutants  pex6 , affected in peroxisome biogenesis, and  aim1 , disrupted in fatty acid β-oxidation. Upon wounding, these mutants exhibit reduced JA levels compared to wild type.  pex6  accumulated the precursor OPDA. Feeding experiments with deuterated OPDA substantiate this accumulation pattern, suggesting the mutants are impaired in the β-oxidation of JA biosynthesis at different steps. Decreased expression of JA-responsive genes, such as  VSP1 ,  VSP2 ,  AtJRG21  and  LOX2 , following wounding in the mutants compared to the wild type reflects the reduced JA levels of the mutants. By use of these additional mutants in combination with feeding experiments, the necessity of functional peroxisomes for JA-biosynthesis is confirmed. Furthermore an essential function of one of the two multifunctional proteins of fatty acid β-oxidation (AIM1) for wound-induced JA formation is demonstrated for the first time. These data confirm that JA biosynthesis occurs  via  peroxisomal fatty acid β-oxidation machinery.