Intracellular consequences of SOS1 deficiency during salt stress
A mutation of AtSOS1 (Salt Overly Sensitive 1), a plasma membrane Na +/H+-antiporter in Arabidopsis thaliana, leads to a salt-sensitive phenotype accompanied by the death of root cells under salt stress. Intracellular events and changes in gene expression were compared during a non-lethal salt stress between the wild type and a representative SOS1 mutant, atsos1-1, by confocal microscopy using ion-specific fluorophores and by quantitative RT-PCR. In addition to the higher accumulation of sodium ions, atsos1-1 showed inhibition of endocytosis, abnormalities in vacuolar shape and function, and changes in intracellular pH compared to the wild type in root tip cells under stress. Quantitative RT-PCR revealed a dramatically faster and higher induction of root-specific Ca2+ transporters, including several CAXs and CNGCs, and the drastic down-regulation of genes involved in pH-homeostasis and membrane potential maintenance. Differential regulation of genes for functions in intracellular protein trafficking in atsos1-1 was also observed. The results suggested roles of the SOS1 protein, in addition to its function as a Na+/H+ antiporter, whose disruption affected membrane traffic and vacuolar functions possibly by controlling pH homeostasis in root cells.
Publication Source (Journal or Book title)
Journal of Experimental Botany
Oh, D., Lee, S., Bressan, R., Yun, D., & Bohnert, H. (2010). Intracellular consequences of SOS1 deficiency during salt stress. Journal of Experimental Botany, 61 (4), 1205-1213. https://doi.org/10.1093/jxb/erp391