Abstract
Salt stress seriously affects plant growth and development. Through genetic screening, we identified and characterized an Arabidopsis (Arabidopsis thaliana) sensitive to salt1 (ses1) mutant. SES1 was ubiquitously expressed and induced by salt treatment. The salt-sensitive phenotype of ses1 was due neither to the overaccumulation of Na+ nor to the suppression of salt tolerance-associated genes. SES1 encoded an uncharacterized endoplasmic reticulum (ER)-localized protein. Coinciding with its subcellular distribution, ses1 exhibited overactivation of unfolded protein response genes and was largely influenced by severe ER stress. Biochemical evidence revealed that SES1 functions as an important molecular chaperone to alleviate salt-induced ER stress. Furthermore, the ER stress sensor basic leucine zipper factor17 transactivated SES1 by binding directly to its promoter region. These results provide insights into salt stress responses and ER homeostasis and shed light on the mechanism by which SES1 modulates salt resistance.