title: The salt stress-induced LPA response in Chlamydomonas is produced via PLA₂ hydrolysis of DGK-generated phosphatidic acid.
abstract: 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: Section Plant Physiology, Swammerdam Institute for Life Sciences,  University of Amsterdam, Amsterdam,  The Netherlands.
authors: Steven A
authors: SA
authors: Arisz
authors: Teun
authors: T
authors: Munnik
mesh_terms: D000818:Animals; D002696:Chlamydomonas / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism* / Q000502:physiology; D019852:Diacylglycerol Kinase / Q000378:metabolism*; D006868:Hydrolysis / Q000187:drug effects; D008246:Lysophospholipids / Q000096:biosynthesis / Q000378:metabolism*; D054467:Phospholipases A2 / Q000378:metabolism*; D012492:Salts / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects; D013312:Stress, Physiological / Q000187:drug effects*
chemical_list: D008246:Lysophospholipids; D012492:Salts; D019852:Diacylglycerol Kinase; D054467:Phospholipases A2; C032881:lysophosphatidic acid