The RING ‐finger E3 ubiquitin ligase SlMIEL1 interacts with SlNAC35 to regulate JA biosynthesis and mediate saline‐alkali stress responses in tomato

SUMMARY Saline‐alkali stress, as a widely existing abiotic stress, severely restricts plant growth and development. NAC transcription factors play a key role in plants' adaptation to abiotic stresses such as low temperature, drought, and salt damage. This study found that SlNAC35 , a member of the NAC transcription factor family, negatively affects saline‐alkali tolerance in tomato ( Solanum lycopersicum L.) by directly targeting and regulating the allene oxide cyclase (AOC) SlAOC, thereby inhibiting jasmonic acid (JA) biosynthesis. Overexpression of SlAOC significantly increased JA accumulation and reduced the excessive accumulation of reactive oxygen species under saline‐alkali stress, indicating that SlAOC plays a positive role in JA synthesis and saline‐alkali tolerance in tomato. Further studies confirmed that SlNAC35 interacts with the E3 ubiquitin ligase SlMIEL1, which mediates the ubiquitin‐dependent degradation of SlNAC35. This reduces its inhibitory effect on SlAOC , promoting JA accumulation and enhancing the saline‐alkali tolerance of tomato. This study reveals that the SlNAC35‐SlMIEL1 module enhances tomato tolerance to saline‐alkali stress by regulating JA synthesis and accumulation. The findings link E3 ubiquitin ligase‐mediated post‐translational modifications to JA biosynthesis in the tomato's response to saline‐alkali stress, filling a gap in the research field of ubiquitination‐regulated JA synthesis to combat saline‐alkali stress.