(3R, 7S)-11-hydroxy-jasmonic acid is a major oxidative shunt product of jasmonic acid catabolism in Arabidopsis thaliana | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Article (3R, 7S)-11-hydroxy-jasmonic acid is a major oxidative shunt product of jasmonic acid catabolism in Arabidopsis thaliana Minoru Ueda, Kotaro Matsumoto, Maria Mitsui, Takuya Kaji, Naoki Kitaoka, and 4 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7856590/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted You are reading this latest preprint version Abstract 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. Biological sciences/Plant sciences/Plant hormones/Jasmonic acid Physical sciences/Chemistry/Chemical biology/Natural products Full Text Additional Declarations There is NO Competing Interest. Supplementary Files 14Oct2025SI11OHJA.pdf Supplementary Materials Cite Share Download PDF Status: Under Review Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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