Senescence‐inducible LEC2 enhances triacylglycerol accumulation in leaves without negatively affecting plant growth

The synthesis of fatty acids and glycerolipids in wild‐type Arabidopsis leaves does not typically lead to strong triacylglycerol (TAG) accumulation. LEAFY COTYLEDON2 (LEC2) is a master regulator of seed maturation and oil accumulation in seeds. Constitutive ectopic LEC2 expression causes somatic embryogenesis and defects in seedling growth. Here, we report that senescence‐inducible LEC2 expression caused a threefold increase in TAG levels in transgenic leaves compared with that in the leaves of wild‐type plants. Plant growth was not severely affected by the accumulation the TAG in response to LEC2 expression. The levels of plastid‐synthesized lipids, mono‐ and di‐galactosyldiacylglycerol and phosphatidylglycerol were reduced more in senescence‐induced LEC2 than in endoplasmic reticulum‐synthesized lipids, including phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol. Senescence‐induced LEC2 up‐regulated the expression of many genes involved in fatty acid and TAG biosynthesis at precise times in senescent leaves, including WRINKLED1 (WRI1), which encodes a fatty acid transcription factor. The expressions of glycerol‐3‐phosphate dehydrogenase 1 and phospholipid:diacylglycerol 2 were increased in the transgenic leaves. Five seed‐type oleosin‐encoding genes, expressed during oil‐body formation, and the seed‐specific FAE1 gene, which encodes the enzyme responsible for the synthesis of C20:1 and C22:1 fatty acids, were also expressed at higher levels in senescing transgenic leaves than in wild‐type leaves. Senescence‐inducible LEC2 triggers the key metabolic steps that increase TAG accumulation in vegetative tissues.