Delayed leaf senescence by exogenous lyso-phosphatidylethanolamine: Towards a mechanism of action |
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| Authors: | Ji Heun Hong GukHoon Chung A. Keith Cowan |
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| Affiliation: | 1. Biotech Institute, Glonet BU, Doosan Corporation, Yongin 449-795, South Korea;2. AKConsulting, Grahamstown 6140, South Africa;1. Mass Spectrometry Center, QOPNA, Department of Chemistry, University of Aveiro, 3810-193 Aveiro, Portugal;2. CIAFEL, Faculty of Sport, University of Porto, Portugal;3. CITS, IPSN, CESPU CRL, Famalicão, Portugal;4. CICECO, Department of Chemistry, University of Aveiro, 3810-193 Aveiro, Portugal;1. Department of Immuno-Oncology, Beckman Research Institute at City of Hope, Duarte, CA;;2. Key Laboratory of Medical Molecular Biology, Guizhou Medical University, Guiyang, People''s Republic of China;;3. Hematology and Hematopoietic Cell Transplantation, Beckman Research Institute at City of Hope, Duarte, CA;;4. Department of Transplantation, Jagiellonian University Medical College, Cracow, Poland;;5. Gehr Family Center for Leukemia Research, City of Hope, Duarte, CA; and;6. DNA/RNA Synthesis Core Facility, Beckman Research Institute at City of Hope, Duarte, CA;1. Instituto de la Grasa, CSIC, Avda. Padre Garcia Tejero 4, 41012 Seville, Spain;2. Key Lab of Plant Resource Research and Development, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China;3. Department of Plant Biology, Michigan State University, East Lansing, MI 48824, USA;1. Institute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur, Malaysia;2. Biology Division, Centre for Foundation Studies in Science, University of Malaya, Kuala Lumpur, Malaysia;3. Rimba Ilmu Botanic Garden, Institute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur, Malaysia;4. School of Science, Monash University Malaysia, 47500 Selangor, Malaysia |
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| 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 (Chla+b) and carotenoids (Cc+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. |
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