The salt stress-induced LPA response in Chlamydomonas is produced via PLA2 hydrolysis of DGK-generated phosphatidic acid[S]

The unicellular green alga Chlamydomonas has frequently been used as a eukaryotic model system to study intracellular phospholipid signaling pathways in response to environmental stresses. Earlier, we found that hypersalinity induced a rapid increase in the putative lipid second messenger, phosphati...

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Main Authors: Steven A. Arisz, Teun Munnik
Format: Article
Language:English
Published: Elsevier 2011-11-01
Series:Journal of Lipid Research
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520350914
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author Steven A. Arisz
Teun Munnik
author_facet Steven A. Arisz
Teun Munnik
author_sort Steven A. Arisz
collection DOAJ
description The unicellular green alga Chlamydomonas has frequently been used as a eukaryotic model system to study intracellular phospholipid signaling pathways in response to environmental stresses. Earlier, we found that hypersalinity induced a rapid increase in the putative lipid second messenger, phosphatidic acid (PA), which was suggested to be generated via activation of a phospholipase D (PLD) pathway and the combined action of a phospholipase C/diacylglycerol kinase (PLC/DGK) pathway. Lysophosphatidic acid (LPA) was also increased and was suggested to reflect a phospholipase A2 (PLA2) activity based on pharmacological evidence. The question of PA’s and LPA’s origin is, however, more complicated, especially as both function as precursors in the biosynthesis of phospho- and galactolipids. To address this complexity, a combination of fatty acid-molecular species analysis and in vivo 32P-radiolabeling was performed. Evidence is provided that LPA is formed from a distinct pool of PA characterized by a high α-linolenic acid (18:3n-3) content. This molecular species was highly enriched in the polyphosphoinositide fraction, which is the substrate for PLC to form diacylglycerol. Together with differential 32P-radiolabeling studies and earlier PLD-transphosphatidylation and PLA2-inhibitor assays, the data were consistent with the hypothesis that the salt-induced LPA response is primarily generated through PLA2-mediated hydrolysis of DGK-generated PA and that PLD or de novo synthesis [via endoplasmic reticulum - or plastid-localized routes] is not a major contributor.
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spelling doaj.art-bcf03ef326904b02b2d83aa588d81eca2022-12-21T21:48:27ZengElsevierJournal of Lipid Research0022-22752011-11-01521120122020The salt stress-induced LPA response in Chlamydomonas is produced via PLA2 hydrolysis of DGK-generated phosphatidic acid[S]Steven A. Arisz0Teun Munnik1Section Plant Physiology, Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The NetherlandsTo whom correspondence should be addressed.; Section Plant Physiology, Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The NetherlandsThe unicellular green alga Chlamydomonas has frequently been used as a eukaryotic model system to study intracellular phospholipid signaling pathways in response to environmental stresses. Earlier, we found that hypersalinity induced a rapid increase in the putative lipid second messenger, phosphatidic acid (PA), which was suggested to be generated via activation of a phospholipase D (PLD) pathway and the combined action of a phospholipase C/diacylglycerol kinase (PLC/DGK) pathway. Lysophosphatidic acid (LPA) was also increased and was suggested to reflect a phospholipase A2 (PLA2) activity based on pharmacological evidence. The question of PA’s and LPA’s origin is, however, more complicated, especially as both function as precursors in the biosynthesis of phospho- and galactolipids. To address this complexity, a combination of fatty acid-molecular species analysis and in vivo 32P-radiolabeling was performed. Evidence is provided that LPA is formed from a distinct pool of PA characterized by a high α-linolenic acid (18:3n-3) content. This molecular species was highly enriched in the polyphosphoinositide fraction, which is the substrate for PLC to form diacylglycerol. Together with differential 32P-radiolabeling studies and earlier PLD-transphosphatidylation and PLA2-inhibitor assays, the data were consistent with the hypothesis that the salt-induced LPA response is primarily generated through PLA2-mediated hydrolysis of DGK-generated PA and that PLD or de novo synthesis [via endoplasmic reticulum - or plastid-localized routes] is not a major contributor.http://www.sciencedirect.com/science/article/pii/S0022227520350914diacylglycerollysophosphatidic acidphospholipase A2signal transduction Chlamydomonas32P-radiolabelingα-linolenic acid
spellingShingle Steven A. Arisz
Teun Munnik
The salt stress-induced LPA response in Chlamydomonas is produced via PLA2 hydrolysis of DGK-generated phosphatidic acid[S]
Journal of Lipid Research
diacylglycerol
lysophosphatidic acid
phospholipase A2
signal transduction Chlamydomonas
32P-radiolabeling
α-linolenic acid
title The salt stress-induced LPA response in Chlamydomonas is produced via PLA2 hydrolysis of DGK-generated phosphatidic acid[S]
title_full The salt stress-induced LPA response in Chlamydomonas is produced via PLA2 hydrolysis of DGK-generated phosphatidic acid[S]
title_fullStr The salt stress-induced LPA response in Chlamydomonas is produced via PLA2 hydrolysis of DGK-generated phosphatidic acid[S]
title_full_unstemmed The salt stress-induced LPA response in Chlamydomonas is produced via PLA2 hydrolysis of DGK-generated phosphatidic acid[S]
title_short The salt stress-induced LPA response in Chlamydomonas is produced via PLA2 hydrolysis of DGK-generated phosphatidic acid[S]
title_sort salt stress induced lpa response in chlamydomonas is produced via pla2 hydrolysis of dgk generated phosphatidic acid s
topic diacylglycerol
lysophosphatidic acid
phospholipase A2
signal transduction Chlamydomonas
32P-radiolabeling
α-linolenic acid
url http://www.sciencedirect.com/science/article/pii/S0022227520350914
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