BnACBP1-like in regulating JA-dependent leaf senescence via lipid remodeling and interaction with PLA2β in Brassica napus

• BnACBP1-like regulates JA-dependent leaf senescence via lipid remodeling . This study identifies BnACBP1-like, an acyl-CoA-binding protein, as a key regulator of jasmonic acid (JA)-dependent leaf senescence in Brassica napus . Overexpression of BnACBP1-like induces premature senescence through lipid remodeling, while CRISPR/Cas9 knockout lines suppress these phenotypes, highlighting its central role in senescence regulation. • BnACBP1-like interacts with PLA2β to mediate phospholipid hydrolysis . BnACBP1-like interacts with PLA2β, a phospholipase, promoting phospholipid hydrolysis. This interaction increases lysophospholipid and free fatty acid levels, which drive JA biosynthesis and promote leaf senescence, linking lipid metabolism to hormonal regulation of senescence. • Integrated multi-omics reveals novel lipid signaling pathways . Using genetic, molecular, biochemical, and multi-omics approaches, the study uncovers a novel lipid signaling module involving BnACBP1-like and PLA2β. These findings advance our understanding of lipid signaling in leaf senescence and offers potential strategies to enhance photosynthetic product reutilization in rapeseed. Leaf senescence in rapeseed ( Brassica napus ), a globally important oilseed crop, is essential for yield optimization through nutrient remobilization. This study investigates the role of lipid signaling in rapeseed leaf senescence, focusing on the acyl-CoA-binding protein BnACBP1-like. Upregulation of BnACBP1-like induced premature leaf senescence, as evidenced by chlorophyll degradation, increased ion leakage, and jasmonic acid (JA) accumulation (other phytohormones showed no significant differences). Genetic analyses confirmed that this phenotype was dependent on the JA pathway. In contrast, CRISPR/Cas9 knockout lines resembled wild-type plants. Integrated multi-omics analysis revealed that BnACBP1-like overexpression triggered extensive lipid remodeling, characterized by decreased glycerophospholipid levels -including phosphatidic acid, phosphatidylcholine and phosphatidylethanolamine, and increased lysophospholipid levels, such as lysophosphatidylcholine, lysophosphatidylethanolamine, and free fatty acids (FFAs). Transcriptome profiling showed upregulation of lipoxygenases ( LOX3, LOX3-like, LOX4 and LOX5 ) and phospholipase A2β ( PLA2β ), contributing to JA biosynthesis. Protein interaction assays confirmed direct binding between BnACBP1-like and PLA2β, while pharmacological inhibition of PLA2β activity suppressed senescence. These results suggest that their interactions may promote phospholipid hydrolysis and the release of FFA substrates for JA synthesis. Thus, the study reveals a critical role for lipid signaling in leaf senescence and elucidates the molecular mechanism by which BnACBP1-like regulates lipid metabolism, offering potential strategies to enhance photosynthetic product reutilization by controlling leaf senescence.