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<p>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 has 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 deactivation shunt of JA turnover. Using chemically synthesized (3 <i>R</i>,7<i>S</i>)−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 <i>Arabidopsis thaliana</i>. In vitro enzymatic assays, in silico docking, and metabolite analyses in the <i>jox</i> quadruple mutant (<i>joxQ</i>) reveals that JOX1/2/3/4 exclusively converted JA to 11-OH-JA, whereas 12-OH-JA arose from distinct pathway. 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. This study provides 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 <i>A. thaliana</i>.</p>

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

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  • 发表日期：

    2026年5月21日

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  • Kotaro Matsumoto,
  • Maria Mitsui,
  • Takuya Kaji,
  • Naoki Kitaoka,
  • Ruiqi Gao,
  • Taketomo Otaki,
  • Yuho Nishizato,
  • Hideyuki Matsuura,
  • Minoru Ueda

摘要

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 has 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 deactivation shunt of JA turnover. Using chemically synthesized (3 R,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, in silico docking, and metabolite analyses in the jox quadruple mutant (joxQ) reveals that JOX1/2/3/4 exclusively converted JA to 11-OH-JA, whereas 12-OH-JA arose from distinct pathway. 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. This study provides 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.