Catabolism of jasmonoyl-isoleucine modulates maize development and defense responses.

Loss of both maize JA-Ile hydroxylases ZmCYP94B1 and ZmCYP94B12 causes JA-Ile accumulation in unstressed leaves and enhances resistance to Spodoptera frugiperda and fungal pathogens.

• Why it matters: JA-Ile levels must be tightly controlled, yet how its CYP94B-mediated catabolism shapes maize growth-defense trade-offs and defense strength is unclear.
• What they did: The study created single and double loss-of-function mutants of ZmCYP94B1 and ZmCYP94B12 in Zea mays, then combined in vitro enzyme assays with in vivo tests for JA-Ile catabolism, development, and defense.
• The result: Double mutants accumulate JA-Ile without stress and show enhanced resistance to Spodoptera frugiperda, Cochliobolus heterostrophus, and Fusarium verticillioides, while also altering plant height and tassel architecture.

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