Cerium elicitor-induced phosphatidic acid triggers apoptotic signaling development in Taxus cuspidata cell suspension cultures.

Degradation of membrane phospholipids is associated with apoptotic responses, but the signaling development of this degradation is not well understood. Cerium (Ce(4+)), an important rare earth element, induces cellular apoptosis and taxol biosynthesis in Taxus cuspidata suspension cultures. Here, using mass spectrometry and biochemical technique, we demonstrated that the phospholipase D (PLD) was rapidly activated by Ce(4+) and hydrolyzed structural phospholipids to generate lipid signal molecule, phosphatidic acid (PA). 1-Butanol, an antagonist of PLD-dependent PA production, blocked the biphasic burst of superoxide anions (O2(*-)) and thus mitigated cellular apoptosis. The time-course analysis of PA accumulation and ERK-like mitogen-activated protein kinase (MAPK) regulation indicated PA generation preceded MAPK activation, suggesting that the rapid accumulation of PA might be required for the initial MAPK activity. After 2h of Ce(4+) elicitation, however, PA-induced O2(*-) burst, forming a negative regulation to MAPK activity, which in turn led to apoptotic signaling development.