Cell Death Signaling From the Endoplasmic Reticulum in Soybean

Abstract

Plants are constantly subjected to adverse environmental conditions, such as extremes of temperature, cold, salinity and drought. As a consequence, plant cells have developed coor‐ dinated and integrated mechanisms that respond to these injuries and are immediately acti‐ vated upon stresses. To cope with the stress, cell signaling pathways are activated and promote up or down regulation of specific genes, which minimize the deleterious effect of stresses within the cell. The endoplasmic reticulum (ER) is a key signaling organelle in‐ volved in the activation of cellular stress responses in eukaryotic cells. One such well-char‐ acterized signaling event is the unfolded protein response (UPR), which is activated to cope with the disruption of ER homeostasis that results in the accumulation of unfolded or mis‐ folded proteins in the lumen of the organelle. Upon disruption of ER homeostasis, plant cells activate at least two branches of the unfolded protein response (UPR) through IRE1like (Inositol-Requiring Enzyme 1) and ATF6-like (Activating Transcription factor 6) trans‐ ducers, resulting in the up-regulation of ER-resident molecular chaperones and the activation of the ER-associated degradation protein system. However, if ER stress is sus‐ tained, an apoptotic pathway is activated. Persistent ER stress has been shown to trigger both ER-stress specific apoptotic pathways and shared PCD (programmed cell death) signal‐ ing pathways elicited by other death stimuli. One plant-specific, ER stress-shared response is the ER and osmotic stress-integrated signaling, which converges on N-rich proteins (NRPs) to transduce a cell death signal. NRP-mediated cell death signaling is a distinct, plant-specific branch of the ER stress pathway that has been shown to integrate the ER and osmotic stress signals into a full response. This ERand osmotic-stress induced cell death signaling pathway has been uncovered in soybean and constitutes the major focus of this chapter. A second cell death pathway induced by ER stress has been shown to be mediated