Endoplasmic reticulum stress-induced programmed cell death in soybean cells.

In animal cells, the endoplasmic reticulum may participate in programmed cell death by sensing and transducing apoptotic signals. In an attempt to analyze the role of the endoplasmic reticulum in plant programmed cell death we investigated the effect of cyclopiazonic acid, a specific blocker of plant endoplasmic reticulum-type IIA Ca2+-pumps, in soybean cells. Cyclopiazonic acid treatment elicited endoplasmic reticulum stress and a biphasic increase in cytosolic Ca2+ concentration, followed by the induction of a cell death program. Cyclopiazonic acid-induced programmed cell death occurred with accumulation of H2O2, cytochrome c release from mitochondria, caspase 9- and caspase 3-like protease activation, cytoplasmic shrinkage and chromatin condensation. Chelation of cytosolic Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (acetoxymethil ester) failed to inhibit cyclopiazonic acid-induced cell death. Taken together, our results provide evidence for a role of the endoplasmic reticulum and mitochondria in regulating cyclopiazonic acid-induced programmed cell death in soybean cells, probably via a cross-talk between the two organelles.