Cell death signaling and morphology in chemical-treated tobacco BY-2 suspension cultured cells

Abstract

This study addressed the role of lipid-derived factors together with ethylene and ROS in programmed cell death (PCD) signaling in tobacco BY-2 suspension cultured cells. The cells were exposed to the chemical stress agents mastoparan (MP) and ethanol (EtOH). MP is an activator of membrane-associated heterotrimeric G-proteins and downstream phospholipids-dependent processes; EtOH is suggested to affect lipid-associated pathways. The effects of MP and EtOH were compared to cell death in response to CdSO4. All applied chemicals appeared potent cell death inducers. Ethylene and lipid signaling were found instrumental in chemical-induced cell death, presumably in conjunction with ROS. Cadmium and MP induced cell death of apoptotic-like phenotype. Lower EtOH concentrations (1–2%) induced vacuolar cell death associated with autophagy-associated formation of lysosome-like acidic organelles in part of the cells; in other cells in the same suspension apoptotic-like features were observed. At higher EtOH concentration (3%) the dead cells expressed exclusively apoptotic-like morphology. The results suggest that phospholipase D- and phospholipase C-derived phosphatidic acid triggers ROS generation that is responsible for the observed apoptotic-like PCD. Vacuolar cell death in EtOH-treated cells appeared dependent on phospholipase C - phosphatidylinositol-3-kinase-related pathway. The obtained results indicate that depending on the inducer and stress severity, similar or distinct regulatory pathways can be activated, and the signals may interact in the transmission of the cell death message.