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

The 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.