Lipidomic analysis reveals differential defense responses of Taxus cuspidata cells to two elicitors, methyl jasmonate and cerium (Ce4+).
Methyl jasmonate (MeJA) and cerium (Ce(4+)) elicitation share common features of increasing taxol accumulation of Taxus cuspidata cells. Interestingly, Ce(4+) induces programmed cell death (PCD), but this phenomenon is not observed with MeJA elicitation. Here, using a lipidomic approach to measure more than 100 membrane glycerophospholipids of T. cuspidata cells quantitatively, we discovered that lysophosphatidylcholine (LysoPC), phosphatidic acid (PA) and phosphatidylcholine were three potential lipid markers that were responsible for the differences between Ce(4+)-induced cells and MeJA-induced cells. Compared with MeJA elicitation, marked increase of phospholipase D (PLD) activity was observed following Ce(4+) elicitation, suggesting that the PLD activation and high concentrations of PA production might mediate the PCD. Rapid increase of phospholipase A(2) (PLA(2)) activity caused the release of fatty acids and LysoPC following Ce(4+) elicitation, which enhanced endogenous jasmonic acid (JA) accumulation. In contrast, PLA(2) activity was poorly induced following MeJA elicitation. PLA(2) inhibitor suppressed not only JA accumulation but also taxol production, suggesting that the PLA(2) activation mediated Ce(4+)-induced taxol production partially through a JA-dependent signaling pathway. These results demonstrate that differential alternation of glycerolphospholipids caused by phospholipases constitutes an important step in cell death response to Ce(4+) and increasing taxol production.
Yang
Song
S
Department of Pharmaceutical Engineering, School of Chemical Engineering and Technology, Tianjin University, Tianjin 300072, PR China.
Lu
Shu-Huan
SH
Yuan
Ying-Jin
YJ
D000085:Acetates / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D002563:Cerium / Q000494:pharmacology*; D002853:Chromatography, Liquid; D003517:Cyclopentanes / Q000494:pharmacology*; D004789:Enzyme Activation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D020404:Glycerophospholipids / Q000032:analysis / Q000737:chemistry; D050356:Lipid Metabolism / Q000187:drug effects*; D008954:Models, Biological; D015999:Multivariate Analysis; D054883:Oxylipins / Q000494:pharmacology*; D017239:Paclitaxel / Q000096:biosynthesis; D064801:Phospholipase A2 Inhibitors; D010739:Phospholipase D / Q000378:metabolism; D054467:Phospholipases A2 / Q000378:metabolism; D021241:Spectrometry, Mass, Electrospray Ionization; D020946:Taxus / Q000166:cytology* / Q000187:drug effects* / Q000201:enzymology
D000085:Acetates; D003517:Cyclopentanes; D004791:Enzyme Inhibitors; D020404:Glycerophospholipids; D054883:Oxylipins; D064801:Phospholipase A2 Inhibitors; D002563:Cerium; C072239:methyl jasmonate; D054467:Phospholipases A2; D010739:Phospholipase D; D017239:Paclitaxel