Phosphatidic acid–regulated SOS2 controls sodium and potassium homeostasis in Arabidopsis under salt stress

Abstract

AbstractThe maintenance of sodium/potassium (Na+/K+) homeostasis in plant cells is essential for salt tolerance. Plants export excess Na+ out of cells mainly through the Salt Overly Sensitive (SOS) pathway, activated by a calcium signal; however, it is unknown whether other signals regulate the SOS pathway and how K+ uptake is regulated under salt stress. Phosphatidic acid (PA) is emerging as a lipid signaling molecule that modulates cellular processes in development and the response to stimuli. Here, we show that PA binds to the residue Lys57 in SOS2, a core member of the SOS pathway, under salt stress, promoting the activity and plasma membrane localization of SOS2, which activates the Na+/H+ antiporter SOS1 to promote the Na+ efflux. In addition, we reveal that PA promotes the phosphorylation of SOS3‐like calcium‐binding protein 8 (SCaBP8) by SOS2 under salt stress, which attenuates the SCaBP8‐mediated inhibition of Arabidopsis K+ transporter 1 (AKT1), an inward‐rectifying K+ channel. These findings suggest that PA regulates the SOS pathway and AKT1 activity under salt stress, promoting Na+ efflux and K+ influx to maintain Na+/K+ homeostasis.