SGAM1 orchestrates salt tolerance by balancing mitochondrial translation and ROS homeostasis in Arabidopsis

Salt stress severely hampers plant growth and crop productivity. Defects in Golgi α1,2-mannosidase I MNS1 and MNS2 proteins, essential for N-glycan maturation, lead to severe root growth inhibition and swollen tips in Arabidopsis under salt stress. Here, we reported sgam1, a suppressor of mns1 mns2, exhibiting threshold-dependent suppression of salt sensitivity. SGAM1 encodes a mitochondria-localized pentatricopeptide repeat protein, and sgam1 mutations decreased the abundance and activity of mitochondrial electron transport complex (mETC), potentially by disrupting mitoribosome assembly and protein translation. This, in turn, alleviated the mitochondrial ROS accumulation and activated the AOX-mediated alternative respiratory pathway in mns1 mns2 under salt stress. Overexpression of AOX1a notably reversed the salt-sensitive root phenotype in mns1 mns2. Furthermore, sgam1 also suppressed Other N-glycosylation mutants, suggesting a common mechanism. Our findings highlight the cooperative importance of N-glycosylation and mitochondrial activity in maintaining ROS homeostasis during salt stress.

N‐glycosylation; PPR protein; mitochondria.