Elicitation of Suspension-Cultured Tomato Cells Triggers the Formation of Phosphatidic Acid and Diacylglycerol Pyrophosphate1

Phosphatidic acid (PA) and its phosphorylated derivative diacylglycerol pyrophosphate (DGPP) are lipid molecules that have been implicated in plant cell signaling. In this study we report the rapid but transient accumulation of PA and DGPP in suspension-cultured tomato ( Lycopersicon esculentum ) ce...

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Published inPlant physiology (Bethesda) Vol. 123; no. 4; pp. 1507 - 1516
Main Authors van der Luit, Arnold H., Piatti, Titus, van Doorn, Aveline, Musgrave, Alan, Felix, Georg, Boller, Thomas, Munnik, Teun
Format Journal Article
LanguageEnglish
Published American Society of Plant Physiologists 01.08.2000
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Summary:Phosphatidic acid (PA) and its phosphorylated derivative diacylglycerol pyrophosphate (DGPP) are lipid molecules that have been implicated in plant cell signaling. In this study we report the rapid but transient accumulation of PA and DGPP in suspension-cultured tomato ( Lycopersicon esculentum ) cells treated with the general elicitors, N , N ′, N ", N ‴-tetraacetylchitotetraose, xylanase, and the flagellin-derived peptide flg22. To determine whether PA originated from the activation of phospholipase D or from the phosphorylation of diacylglycerol (DAG) by DAG kinase, a strategy involving differential radiolabeling with [ 32 P]orthophosphate was used. DAG kinase was found to be the dominant producer of PA that was subsequently metabolized to DGPP. A minor but significant role for phospholipase D could only be detected when xylanase was used as elicitor. Since PA formation was correlated with the high turnover of polyphosphoinositides, we hypothesize that elicitor treatment activates phospholipase C to produce DAG, which in turn acts as substrate for DAG kinase. The potential roles of PA and DGPP in plant defense signaling are discussed.
Bibliography:Corresponding author; e-mail munnik@bio.uva.nl; fax 31–20–5257934.
Present Address: Division of Cellular Biochemistry, The Netherlands Cancer Institute, Plesmanlaan 121, NL–1066 CX, Amsterdam, The Netherlands.
This manuscript is dedicated to the memory of Titus Piatti, who died prior to the publication of this paper.
ISSN:0032-0889
1532-2548