Delayed leaf senescence by exogenous lyso-phosphatidylethanolamine: towards a mechanism of action.

Exogenous application of the lysophospholipid, lyso-phosphatidylethanolamine (LPE) is purported to delay leaf senescence in plants. However, lyso-phospholipids are well known to possess detergent-like activity and application of LPE to plant tissues might be expected to rather elicit a wound-like response and enhance senescence progression. Since phosphatidic acid (PA) accumulation and leaf cell death are a consequence of wounding, PA- and hormone-induced senescence was studied in leaf discs from Philodendron cordatum (Vell.) Kunth plants in the presence or absence of egg-derived 18:0-LPE and senescence progression quantified by monitoring both lipid peroxidation (as the change in malondialdehyde concentration), and by measuring retention of total chlorophyll (Chl(a+b)) and carotenoids (C(c+x)). Only abscisic acid (ABA) stimulated lipid peroxidation whereas ABA, 1-aminocyclopropane-1-carboxylic acid (ACC), the immediate precursor to ethylene (ETH), and 16:0-18:2-PA stimulated loss of chloroplast pigments. Results using primary alcohols as attenuators of the endogenous PA signal confirmed a role for PA as an intermediate in both ABA- and ETH-mediated senescence progression. Exogenous 18:0-LPE did not appear to influence senescence progression and was unable to reverse hormone-induced senescence progression. However, when supplied together with 16:0-18:2-PA at 1:1 (mol:mol), activity of phosphatidylglycerol (PG) hydrolase, chlorophyllase (E.C. 3.1.1.14), and progression of leaf senescence were negated. This apparent anti-senescence activity of exogenous 18:0-LPE was associated with induction of the pathogenesis-related protein, extracellular acid invertase (Ac INV, E.C. 3.2.1.26) suggesting that 18:0-LPE like 16:0-18:2-PA functions as an elicitor.