Lipidomic analysis reveals differential defense responses of Taxus cuspidata cells to two elicitors, methyl jasmonate and cerium (Ce4+)

Methyl jasmonate (MeJA) and cerium (Ce4+) elicitation share common features of increasing taxol accumulation of Taxus cuspidata cells. Interestingly, Ce4+ 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 Ce4+-induced cells and MeJA-induced cells. Compared with MeJA elicitation, marked increase of phospholipase D (PLD) activity was observed following Ce4+ elicitation, suggesting that the PLD activation and high concentrations of PA production might mediate the PCD. Rapid increase of phospholipase A2 (PLA2) activity caused the release of fatty acids and LysoPC following Ce4+ elicitation, which enhanced endogenous jasmonic acid (JA) accumulation. In contrast, PLA2 activity was poorly induced following MeJA elicitation. PLA2 inhibitor suppressed not only JA accumulation but also taxol production, suggesting that the PLA2 activation mediated Ce4+-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 Ce4+ and increasing taxol production.