Document Detail


The salt stress-induced LPA response in Chlamydomonas is produced via PLA₂ hydrolysis of DGK-generated phosphatidic acid.
MedLine Citation:
PMID:  21900174     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Steven A Arisz; Teun Munnik
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-09-06
Journal Detail:
Title:  Journal of lipid research     Volume:  52     ISSN:  0022-2275     ISO Abbreviation:  J. Lipid Res.     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-10-17     Completed Date:  2012-02-02     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  0376606     Medline TA:  J Lipid Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2012-20     Citation Subset:  IM    
Affiliation:
Section Plant Physiology, Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Animals
Chlamydomonas / cytology,  drug effects*,  metabolism*,  physiology
Diacylglycerol Kinase / metabolism*
Hydrolysis / drug effects
Lysophospholipids / biosynthesis,  metabolism*
Phospholipases A2 / metabolism*
Salts / pharmacology*
Signal Transduction / drug effects
Stress, Physiological / drug effects*
Chemical
Reg. No./Substance:
0/Lysophospholipids; 0/Salts; 22002-87-5/lysophosphatidic acid; EC 2.7.1.107/Diacylglycerol Kinase; EC 3.1.1.4/Phospholipases A2
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