The COG3 subunit interacts with SNX1 to enhance salt tolerance in Arabidopsis

Salt stress severely restricts plant growth and agricultural productivity. The Conserved Oligomeric Golgi complex (COG) plays a key role in vesicular trafficking, but its function in plant stress responses remains poorly understood. Here, we demonstrated that the expression of the subunit COG3 of the COG complex in Arabidopsis thaliana was significantly induced under salt stress. The COG3 knockdown mutant (cog3) exhibits severe growth and development defects, as well as high sensitivity to salt stress. Furthermore, genetic complementation with COG3-GFP partially rescued the salt-sensitive phenotype of the cog3 mutant, while overexpression of COG3 enhanced plant salt tolerance. Mechanistically, COG3 physically interacts with the Sorting Nexin 1 (SNX1) on the endosome, and genetic evidence indicates that COG3 acts upstream of SNX1. We propose that under salt stress, COG3 maintains Golgi structural integrity and stabilizes SNX1 protein, thereby facilitating SNX1-mediated recycling of cargo proteins from endosomes to the plasma membrane to maintain cellular ion homeostasis. Loss of COG3 function disrupts this recycling pathway, leading to salt hypersensitivity. Our study reveals a novel COG3-SNX1 regulatory module that mediates protein recycling to enhance salt tolerance, providing new insights into the molecular mechanisms underlying plant adaptation to abiotic stress.