Misexpression of FATTY ACID ELONGATION1 in theArabidopsisEpidermis Induces Cell Death and Suggests a Critical Role for Phospholipase A2 in This Process

Lipids produced by the epidermis serve a number of protective functions, and also act as messengers which activate plant defense responses. The fatty acid elongases which catalyze the formation of very long-chain fatty acids, may be instrumental in the remodeling of the various classes of epidermal lipids, and they also provide a means with which to further investigate the defense mechanisms. In a recent publication, we reported that the epidermal mis-expression of FATTY ACID ELONGASE1 (FAE1) in the Arabidopsis plant both increased the levels of very long-chain fatty acids in various lipid classes, and unexpectedly induced a cell-type specific cell death program in trichome cells, giving the plants a glabrous appearance. Using these plants as a model system for a fatty acid-induced cell death (lipoapoptosis), and a platform for the chemical genetic screen, we identified trichome death inhibitors in the glycerophospholipid fatty acyl remodeling pathway: phospholipase A2 inhibitors, aristolochic acid and bromoenol lactone, as well as the putative lysophospholipid acyltransferase inhibitor, clofibrate. Herein, and due to space limitations, we will briefly discuss these results and the different ways in which the appearance of increasing chain-length fatty acids is likely to regulate the cellular life-or-death switch. The death receptor hypothesis implies the existence of a bioactive lipid ligand(s), the functionality of which is determined by phosphorylation, acyl chain length and saturation.