Tohoku University and Hokkaido University discover new inactivation pathway for jasmonic acid

When plants are damaged, they produce the plant hormone jasmonic acid to initiate a defense response. The concentration of jasmonic acid in the living body is strictly controlled through metabolic inactivation, and its molecular mechanism is important for appropriately controlling the timing of the start and end of the plant's defense response. Until now, it was believed that the ending of the defense response through the inactivation of jasmonic acid is triggered by hydroxylation at the 12-position, that is, the production of 12-hydroxyjasmonic acid (12-OH-JA).

A research group including Professor Minoru Ueda and Graduate Student Kotaro Matsumoto of the Graduate School of Science at Tohoku University, in collaboration with Professor Hideyuki Matsuura of the Research Faculty of Agriculture at Hokkaido University and others, discovered that the main inactivation product in Arabidopsis thaliana is not 12-OH-JA, but 11-OH-JA. This updates the understanding of jasmonic acid metabolism that has been believed for many years. The results were published in the online edition of Nature Communications.

The research group chemically synthesized 11-OH-JA with natural stereochemistry at high purity. The structures of 11-OH-JA and 12-OH-JA are very similar, and it was difficult to clearly distinguish between the two under conventional analysis conditions. However, by using standard substances, they established analysis conditions that can clearly separate and quantify 11-OH-JA and 12-OH-JA.

Using this analysis method, they measured the jasmonic acid metabolites over time in the damaged leaves of A. thaliana. As a result, they found that 11-OH-JA accumulated greatly after damage, and at 300 minutes after damage, it became the main hydroxylation metabolite, surpassing 12-OH-JA.

Furthermore, when they performed an in vitro reaction using the JOX enzyme, they confirmed that the JOX enzyme converts jasmonic acid to 11-OH-JA and produces almost no 12-OH-JA. In addition, in a mutant where the plant's JOX gene was disrupted, the accumulation of 11-OH-JA decreased greatly.

From these results, they clarified that, contrary to the conventional theory, the JOX enzyme is an enzyme that mainly produces 11-OH-JA, rather than making 12-OH-JA. They also showed that 11-OH-JA does not form a COI1-JAZ receptor complex and is an inactive metabolite that does not activate jasmonic acid signaling.

In gene expression analysis, it was suggested that while the CYP94 enzyme pathway is involved in regulating the early jasmonic acid response after damage, the 11-OH-JA production pathway by the JOX enzyme is involved in controlling the later response. It is thought that plants precisely control the strength and duration of the defense response by using multiple metabolic pathways at different times.

Conventionally, it was thought that jasmonic acid is converted to 12-OH-JA by the JOX enzyme, but this time the team clarified that JOX enzymes 1 to 4 mainly convert jasmonic acid to 11-OH-JA. On the other hand, 12-OH-JA is thought to be produced mainly when JA-Ile is oxidized by the CYP94 enzyme group and then hydrolyzed.

In the future, by investigating how it works under different environmental stresses such as pathogen infection, drought, and salt stress, it is expected to clarify the universal mechanism of plant stress response control. If the mechanism for ending the jasmonic acid signal can be artificially controlled, it could lead to new plant protection technologies and agricultural applications that strengthen the defense response of crops while suppressing growth inhibition.

Journal Information
Publication: Nature Communications
Title: (3R, 7S)-11-hydroxy-jasmonic acid is a major oxidative shunt product of jasmonic acid catabolism in Arabidopsis thaliana
DOI: 10.1038/s41467-026-73528-9