title: Delayed leaf senescence by exogenous lyso-phosphatidylethanolamine: towards a mechanism of action.
abstract: 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.
authors.affiliation: Biotech Institute, Glonet BU, Doosan Corporation, Yongin, South Korea.
authors.forename: Ji Heun
authors.initials: JH
authors.lastname: Hong
authors.forename: Gukhoon
authors.initials: G
authors.lastname: Chung
authors.forename: A Keith
authors.initials: AK
authors.lastname: Cowan
mesh_terms: D000040:Abscisic Acid / Q000378:metabolism; D000217:Acyltransferases / Q000378:metabolism; D000598:Amino Acids, Cyclic / Q000378:metabolism; D002265:Carboxylic Ester Hydrolases / Q000378:metabolism; D002338:Carotenoids / Q000378:metabolism; D002734:Chlorophyll / Q000378:metabolism; D005030:Ethylenes / Q000378:metabolism; D015227:Lipid Peroxidation; D008246:Lysophospholipids / Q000378:metabolism*; D008315:Malondialdehyde / Q000378:metabolism; D031062:Philodendron / Q000378:metabolism* / Q000502:physiology; D010712:Phosphatidic Acids / Q000378:metabolism*; D010937:Plant Growth Regulators / Q000378:metabolism; D018515:Plant Leaves / Q000378:metabolism* / Q000502:physiology; D015398:Signal Transduction; D043324:beta-Fructofuranosidase / Q000378:metabolism
chemical_list: D000598:Amino Acids, Cyclic; D005030:Ethylenes; D008246:Lysophospholipids; D010712:Phosphatidic Acids; D010937:Plant Growth Regulators; C008301:lysophosphatidylethanolamine; D002734:Chlorophyll; D002338:Carotenoids; C023863:1-aminocyclopropane-1-carboxylic acid; D008315:Malondialdehyde; D000040:Abscisic Acid; C036216:ethylene; D000217:Acyltransferases; D002265:Carboxylic Ester Hydrolases; C019875:chlorophyllase; D043324:beta-Fructofuranosidase