lysophosphatidylethanolamine and ethylene

Lyso-phosphatidylethanolamine (LPE) is a natural phospholipid that functions in the early stages of plant senescence. Plant innate immunity and early leaf senescence share molecular components. To reveal conserved mechanisms that link-up both processes, we tried to unravel to what extent LPE coordinates defense response and by what mode of action.. We found that LPE-treatment induces signaling and biosynthesis gene expression of the defensive hormone salicylic acid (SA). However, jasmonic acid and ethylene triggered gene induction levels are indistinguishable from the control. In accordance with gene induction for SA, oxidative stress, and reactive oxygen species (ROS) production, we detected raised in-situ hydrogen peroxide levels following LPE-application. Yet, ROS-burst assays of LPE-pretreated plants revealed a reduced release of ROS after PAMP-administration suggesting that LPE interferes with an oxidative burst. Our data refer to a priming effect of LPE on SA/ROS-associated genomic loci that encode pivotal factors in early senescence and considerably improve plant basal immunity. Thus, we challenged Arabidopsis thaliana with the hemibiotrophic pathogen Pseudomonas syringae. Consistently, we found an increased resistance in the LPE-pretreated Arabidopsis plants compared to the mock-pretreated control.. Our results underscore a beneficial effect of LPE on plant innate immunity against hemibiotrophs. Given the resistance-promoting effect of exogenously applied LPE, this bio-agent bears the potential of being applied as a valuable tool for the genetic activation of defense-associated traits.

Topics: Arabidopsis; Arabidopsis Proteins; Cyclopentanes; Ethylenes; Gene Expression Regulation, Plant; Genes, Plant; Lysophospholipids; Oxylipins; Plant Diseases; Plant Immunity; Pseudomonas syringae; Salicylic Acid; Signal Transduction

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.

Topics: Abscisic Acid; Acyltransferases; Amino Acids, Cyclic; beta-Fructofuranosidase; Carboxylic Ester Hydrolases; Carotenoids; Chlorophyll; Ethylenes; Lipid Peroxidation; Lysophospholipids; Malondialdehyde; Philodendron; Phosphatidic Acids; Plant Growth Regulators; Plant Leaves; Signal Transduction