Constantly exposed to environmental stresses such as extreme temperatures, drought, or attacks by herbivorous or microbial pests, plants rapidly activate adaptive responses through the action of defense hormone networks. Among these, jasmonates (JAs) form a family of compounds derived from jasmonic acid (JA), whose active form, the jasmonoyl-isoleucine conjugate (JA-Ile), regulates a myriad of stress tolerance responses.
JA-Ile levels are themselves regulated by three enzymatic pathways, two of which are oxidative in nature. In the first pathway, cytochromes P450 of the CYP94 family oxidize JA-Ile at carbon 12, and the resulting 12-OH-JA-Ile is cleaved to 12-OH-JA by amidohydrolases. This 12-OH-JA has long been described as also being produced by direct hydroxylation of JA by JA oxidases (JAO), an important metabolic bypass that attenuates basal levels of JA-Ile and defense responses.
In a study published in Nature Communications, Thierry Heitz and his colleagues from Emmanuel Gaquerel’s team and MASS platform at the IBMP, in collaboration with chemists from UMR7177, conducted an in-depth re-examination of these hydroxylation mechanisms. Using new reference compounds obtained from a Japanese team, methodological advances in the structural analysis of compounds via LC-MS and NMR, and the use of numerous genetic resources, the researchers demonstrated that JAOs actually produce 11-OH-JA, isomers distinct from 12-OH-JA derived from the CYP94/AH pathway, and thus define a new branch in the complex catabolism of jasmonates. It appears that wounding (simulating herbivory) and fungal infection produce distinct profiles of OH-JA, as well as of glucosylated or sulfated derivatives, illustrating the preferential activation of one pathway or the other by these two biotic stresses.This research elucidates the previously overlooked biosynthetic pathway of 11-OH-JAs and integrates it into a metabolic sink that attenuates JA-Ile signaling, which is conserved across plant species. It provides a better understanding of the catabolic pathways that regulate responses to JAs, which are central to plants’ stress adaptation strategies.
