(3R, 7S)-11-hydroxy-jasmonic acid is a major oxidative shunt product of jasmonic acid catabolism in Arabidopsis thaliana

Jasmonoyl-L-isoleucine (JA-Ile) is a pivotal oxylipin hormone that coordinates growth-defense trade-offs, and its precursor jasmonic acid (JA) is therefore subject to tight metabolic control. For more than a decade, the prevailing dogma held that jasmonate turnover is dominated by C12-hydroxylation, with JOX dioxygenases acting on JA and CYP94 monooxygenases acting on JA-Ile. Here we revise this dogma by showing that hydroxylation at the C11 position constitutes a major receptor-silent deactivation shunt of JA turnover. Using chemically synthesized (3R,7S)-11-hydroxy-JA (11-OH-JA) of naturally occurring stereochemistry as a standard, we unambiguously identify 11-OH-JA as the principal shunt product that accumulates in wounded Arabidopsis thaliana. In vitro enzymatic assays and in silico docking revealed that JOX1/2/3/4 exclusively converted JA to 11-OH-JA, whereas 12-OH-JA arose from distinct pathway. Consistently, the jox quadruple mutant (joxQ) abolished 11-OH-JA accumulation without affecting 12-OH-JA levels. Moreover, 11-OH-JA failed to bind the COI1–JAZ co-receptor, establishing it as a biologically inactive endpoint of JA catabolism. These findings correct a long-standing misattribution of the JOX product to 12-OH-JA and redefine the metabolic framework of jasmonate. Parallel, non-redundant inactivation routes deliver layered signal termination of costly defense signals. This study provides new insights into JA catabolism, highlighting 11-OH-JA as a crucial factor in the attenuation of jasmonate signaling, and thereby redefining the framework of JA turnover in A. thaliana.