Environmental stress conditions affect the endoplasmic reticulum (ER), cause production of misfolding or non-folding of polypeptides. These peptides lead to a problem called ER stress. There are many ways in the cell to maintain the homeostasis of the ER, and one of the most studied in recent years is ER-phagy, in which the ER is selectively destroyed. ER-phagy is a process triggered by ER stress in the cell exceeding its capacity, especially as a result of expression increases in some genes, and relatively little is known about its mechanism in plants. On the other hand, disulfide bonds are formed in the ER using molecular oxygen for the correct folding of proteins. However, this situation causes the formation of reactive oxygen species (ROS), such as H2O2, in the cell, and the redox balance of the ER is disrupted. Cells have developed various antioxidant defense mechanisms to repair the disrupted redox balance. Mutants that produce more of some of these antioxidants metabolically are in an advantageous position in the fight against stress. Therefore, we used the apx1-2 mutant, which produces more H2O2 cytosolically in our study. There is no information in the literature about the responses of apx mutants to ER stress. The relationship of these mutants with ER-phagy was reported for the first time in this study, and changes in the expressions of related genes in ER stress induced by tunicamycin application were revealed for the first time. |