Figure 1.

Scheme depicting hypothetical mechanism of action initiated by treatment of plant tissues with LPE. Application of LPE or formation of LPE from PE by PLA₂ increases endogenous LPE concentration. Increased LPE may act to attenuate PLDα activity and reduce formation of PA from structural phospholipids (PL) for PA-CTR1 interaction and/or directly inhibit PA-CTR1 binding to suppress downstream ETH-mediated responses. This coupled with the LPE-induced increase in activity of PR proteins such as Ac INV and PAL acts to delay senescence progression and the further deleterious effects of elevated PA. PA also arises from diacylglycerol kinase (DGK)-catalyzed phosphorylation of diacylglycerol (DG) derived either from monogalactosyl DG (MGDG) or the sequential action of phospholipase C (PLC) and DGK after hydrolysis of phosphastidylinositol-4,5-bisphosphate (PIP₂).