<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li J</submitter><funding>Natural Science Foundation of Shandong Province</funding><funding>National Natural Science Foundation of China</funding><pagination>e112401</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10106984</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>42(8)</volume><pubmed_abstract>The maintenance of sodium/potassium (Na&lt;sup>+&lt;/sup> /K&lt;sup>+&lt;/sup> ) homeostasis in plant cells is essential for salt tolerance. Plants export excess Na&lt;sup>+&lt;/sup> 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&lt;sup>+&lt;/sup> 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&lt;sup>+&lt;/sup> /H&lt;sup>+&lt;/sup> antiporter SOS1 to promote the Na&lt;s</pubmed_abstract><journal>The EMBO journal</journal><pubmed_title>Phosphatidic acid-regulated SOS2 controls sodium and potassium homeostasis in Arabidopsis under salt stress.</pubmed_title><pmcid>PMC10106984</pmcid><funding_grant_id>32171956</funding_grant_id><funding_grant_id>32100234</funding_grant_id><funding_grant_id>ZR2020MC021</funding_grant_id><funding_grant_id>32270268</funding_grant_id><funding_grant_id>32000219</funding_grant_id><funding_grant_id>31921001</funding_grant_id><pubmed_authors>Shen L</pubmed_authors><pubmed_authors>Fan W</pubmed_authors><pubmed_authors>Jin W</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Guo Y</pubmed_authors><pubmed_authors>He G</pubmed_authors><pubmed_authors>Han X</pubmed_authors><pubmed_authors>Zhang W</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Yang S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Phosphatidic acid-regulated SOS2 controls sodium and potassium homeostasis in Arabidopsis under salt stress.</name><description>The maintenance of sodium/potassium (Na&lt;sup>+&lt;/sup> /K&lt;sup>+&lt;/sup> ) homeostasis in plant cells is essential for salt tolerance. Plants export excess Na&lt;sup>+&lt;/sup> 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&lt;sup>+&lt;/sup> 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&lt;sup>+&lt;/sup> /H&lt;sup>+&lt;/sup> antiporter SOS1 to promote the Na&lt;s</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2026-07-14T16:26:43.989Z</modification><creation>2025-04-05T00:30:10.922Z</creation></dates><accession>S-EPMC10106984</accession><cross_references><pubmed>36811145</pubmed><doi>10.15252/embj.2022112401</doi></cross_references></HashMap>