Abolishment of N‐glycan trimming in the early Golgi triggers ferroptosis under salt stress in Arabidopsis root tips

Summary Ferroptosis, a type of regulated necrotic cell death characterized by iron‐dependent accumulation of lipid reactive oxygen species (ROS), has been well documented in animals. Recently, several studies have reported ferroptosis‐like processes in plants. However, the key genes regulating ferroptosis in plants are largely unknown. Our previous research revealed that mutations in Golgi α1,2‐mannosidase (MNS1 and MNS2) render Arabidopsis hypersensitive to salt stress. Trypan blue and Perls/Perls‐DAB staining assessed cell death and iron accumulation, respectively. Lipid ROS accumulation was measured with C11‐BODIPY 581/591, and mitochondrial ultrastructure was examined by transmission electron microscope. We found that mns1 mns2 seedlings underwent ferroptosis in the swollen regions of the root tips under salt stress (NaCl), characterized by the accumulation of iron and lipid ROS, and the presence of ferroptosis‐like mitochondrial morphology. Notably, wild‐type seedlings exhibited an adaptive response to salt stress by depleting iron from root tips. Ferroptosis was observed in the cortex, endodermis and epidermis of the root tips in mns1 mns2 and could be inhibited by iron deprivation, ciclopirox olamine or vitamin E treatment. We uncover a scenario in which N‐glycosylation defects exacerbated ferroptosis in root tips under salt stress, suggesting that ferroptosis involves secretory glycoproteins related to iron, lipid and ROS homeostasis.