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 pat...
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| Veröffentlicht in: | The EMBO journal 2023-04, Vol.42 (8), p.e112401-n/a |
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| creator | Li, Jianfang Shen, Like Han, Xiuli He, Gefeng Fan, Wenxia Li, Yu Yang, Shiping Zhang, Ziding Yang, Yongqing Jin, Weiwei Wang, Yi Zhang, Wenhua Guo, Yan |
| description | 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.
Synopsis
The maintenance of Na
+
/K
+
homeostasis in plant cells is essential for salt tolerance. Here, the lipid signaling molecule phosphatidic acid (PA) is shown to determine the Na
+
/K
+
homeostasis under salt stress via SOS2 protein kinase‐dependent activation of Na
+
efflux via SOS1 and AKT1‐mediated K
+
influx. PA promotes the kinase activity and plasma membrane localization of SOS2 under salt stress.
The residue Lys57 is critical for the PA‐mediated regulation of SOS2.
The PA–SOS2 module activates the Na
+
/H
+
antiporter SOS1 to promote Na
+
efflux.
The PA–SOS2 interaction also relieves the SCaBP8‐mediated inhibition of the inward K
+
channel AKT1 to promote K
+
uptake.
Graphical Abstract
Increased membrane concentration of phosphatidic acid under salt stress protects plant cells by triggering the release of Na
+
and the uptake of K
+
. |
| doi_str_mv | 10.15252/embj.2022112401 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_C6C</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10106984</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2801863820</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4781-304afacfcf92c0bb05abde57adc92e41e58c5991ec6c9f8093ca8a57195d036f3</originalsourceid><addsrcrecordid>eNqFkc1u1DAUhSMEotPCnhWyxIZNyr1OnNgSEipV-VNRkQpry7GdGY-SeOqbgLrrO_CGPAkZprQUCbGyjvydo3t0suwJwiEKLvgL3zfrQw6cI_IS8F62wLKCnEMt7mcL4BXmJUq1l-0TrQFAyBofZntFJRGxFIus_7SKtFmZMbhgmbHB_bj6nvxy6szoHTs_O-fMxmFMsSNG0YWpZ2ZwbBNHQ7RVq9j7SLMKxMLAjpJpgoubrZwG5xMj042MxuSJHmUPWtORf3z9HmRf3px8Pn6Xn569fX98dJrbspaYF1Ca1tjWtopbaBoQpnFe1MZZxX2JXkgrlEJvK6taCaqwRhpRoxIOiqotDrJXu9zN1PTeWT8XMJ3epNCbdKmjCfruzxBWehm_agSESslyTnh-nZDixeRp1H0g67vODD5OpHldq0KghHpGn_2FruOUhrmf5hJQVoXkMFOwo2yKRMm3N9cg6F9j6u2Y-nbM2fL0zxY3ht_rzcDLHfAtdP7yv4H65OPrD3fycWen2Tksfbo9_J83_QSRGL_v</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2801863820</pqid></control><display><type>article</type><title>Phosphatidic acid–regulated SOS2 controls sodium and potassium homeostasis in Arabidopsis under salt stress</title><source>Springer Nature OA Free Journals</source><creator>Li, Jianfang ; Shen, Like ; Han, Xiuli ; He, Gefeng ; Fan, Wenxia ; Li, Yu ; Yang, Shiping ; Zhang, Ziding ; Yang, Yongqing ; Jin, Weiwei ; Wang, Yi ; Zhang, Wenhua ; Guo, Yan</creator><creatorcontrib>Li, Jianfang ; Shen, Like ; Han, Xiuli ; He, Gefeng ; Fan, Wenxia ; Li, Yu ; Yang, Shiping ; Zhang, Ziding ; Yang, Yongqing ; Jin, Weiwei ; Wang, Yi ; Zhang, Wenhua ; Guo, Yan</creatorcontrib><description>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.
Synopsis
The maintenance of Na
+
/K
+
homeostasis in plant cells is essential for salt tolerance. Here, the lipid signaling molecule phosphatidic acid (PA) is shown to determine the Na
+
/K
+
homeostasis under salt stress via SOS2 protein kinase‐dependent activation of Na
+
efflux via SOS1 and AKT1‐mediated K
+
influx. PA promotes the kinase activity and plasma membrane localization of SOS2 under salt stress.
The residue Lys57 is critical for the PA‐mediated regulation of SOS2.
The PA–SOS2 module activates the Na
+
/H
+
antiporter SOS1 to promote Na
+
efflux.
The PA–SOS2 interaction also relieves the SCaBP8‐mediated inhibition of the inward K
+
channel AKT1 to promote K
+
uptake.
Graphical Abstract
Increased membrane concentration of phosphatidic acid under salt stress protects plant cells by triggering the release of Na
+
and the uptake of K
+
.</description><identifier>ISSN: 0261-4189</identifier><identifier>EISSN: 1460-2075</identifier><identifier>DOI: 10.15252/embj.2022112401</identifier><identifier>PMID: 36811145</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Abiotic stress ; AKT ; AKT1 protein ; Arabidopsis ; Arabidopsis - metabolism ; Arabidopsis Proteins - metabolism ; Calcium ; Calcium signalling ; Calcium-binding protein ; Efflux ; EMBO20 ; EMBO30 ; Homeostasis ; Hydrogen ; Kinases ; Life Sciences ; Lipids ; Localization ; Maintenance ; Membranes ; Na+/H+-exchanging ATPase ; Phosphatidic acid ; Phosphatidic Acids - metabolism ; Phosphorylation ; Plant cells ; Potassium ; Potassium - metabolism ; Potassium channels ; Protein Serine-Threonine Kinases - metabolism ; Proteins ; Residues ; Salinity tolerance ; Salt ; salt stress ; Salt Stress - genetics ; Salt tolerance ; Signal transduction ; Signaling ; Sodium ; Sodium - metabolism ; sodium and potassium homeostasis ; SOS pathway</subject><ispartof>The EMBO journal, 2023-04, Vol.42 (8), p.e112401-n/a</ispartof><rights>The Author(s) 2023</rights><rights>2023 The Authors</rights><rights>2023 The Authors.</rights><rights>2023 EMBO</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4781-304afacfcf92c0bb05abde57adc92e41e58c5991ec6c9f8093ca8a57195d036f3</citedby><cites>FETCH-LOGICAL-c4781-304afacfcf92c0bb05abde57adc92e41e58c5991ec6c9f8093ca8a57195d036f3</cites><orcidid>0000-0002-6955-8008 ; 0000-0002-3660-5859 ; 0000-0002-3155-9208 ; 0000-0002-2445-677X ; 0000-0001-8192-7120 ; 0000-0001-5631-3549 ; 0000-0001-8628-8559</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106984/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106984/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,41120,42189,45574,45575,46409,46833,51576,53791,53793</link.rule.ids><linktorsrc>$$Uhttps://doi.org/10.15252/embj.2022112401$$EView_record_in_Springer_Nature$$FView_record_in_$$GSpringer_Nature</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36811145$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Jianfang</creatorcontrib><creatorcontrib>Shen, Like</creatorcontrib><creatorcontrib>Han, Xiuli</creatorcontrib><creatorcontrib>He, Gefeng</creatorcontrib><creatorcontrib>Fan, Wenxia</creatorcontrib><creatorcontrib>Li, Yu</creatorcontrib><creatorcontrib>Yang, Shiping</creatorcontrib><creatorcontrib>Zhang, Ziding</creatorcontrib><creatorcontrib>Yang, Yongqing</creatorcontrib><creatorcontrib>Jin, Weiwei</creatorcontrib><creatorcontrib>Wang, Yi</creatorcontrib><creatorcontrib>Zhang, Wenhua</creatorcontrib><creatorcontrib>Guo, Yan</creatorcontrib><title>Phosphatidic acid–regulated SOS2 controls sodium and potassium homeostasis in Arabidopsis under salt stress</title><title>The EMBO journal</title><addtitle>EMBO J</addtitle><addtitle>EMBO J</addtitle><description>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.
Synopsis
The maintenance of Na
+
/K
+
homeostasis in plant cells is essential for salt tolerance. Here, the lipid signaling molecule phosphatidic acid (PA) is shown to determine the Na
+
/K
+
homeostasis under salt stress via SOS2 protein kinase‐dependent activation of Na
+
efflux via SOS1 and AKT1‐mediated K
+
influx. PA promotes the kinase activity and plasma membrane localization of SOS2 under salt stress.
The residue Lys57 is critical for the PA‐mediated regulation of SOS2.
The PA–SOS2 module activates the Na
+
/H
+
antiporter SOS1 to promote Na
+
efflux.
The PA–SOS2 interaction also relieves the SCaBP8‐mediated inhibition of the inward K
+
channel AKT1 to promote K
+
uptake.
Graphical Abstract
Increased membrane concentration of phosphatidic acid under salt stress protects plant cells by triggering the release of Na
+
and the uptake of K
+
.</description><subject>Abiotic stress</subject><subject>AKT</subject><subject>AKT1 protein</subject><subject>Arabidopsis</subject><subject>Arabidopsis - metabolism</subject><subject>Arabidopsis Proteins - metabolism</subject><subject>Calcium</subject><subject>Calcium signalling</subject><subject>Calcium-binding protein</subject><subject>Efflux</subject><subject>EMBO20</subject><subject>EMBO30</subject><subject>Homeostasis</subject><subject>Hydrogen</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Lipids</subject><subject>Localization</subject><subject>Maintenance</subject><subject>Membranes</subject><subject>Na+/H+-exchanging ATPase</subject><subject>Phosphatidic acid</subject><subject>Phosphatidic Acids - metabolism</subject><subject>Phosphorylation</subject><subject>Plant cells</subject><subject>Potassium</subject><subject>Potassium - metabolism</subject><subject>Potassium channels</subject><subject>Protein Serine-Threonine Kinases - metabolism</subject><subject>Proteins</subject><subject>Residues</subject><subject>Salinity tolerance</subject><subject>Salt</subject><subject>salt stress</subject><subject>Salt Stress - genetics</subject><subject>Salt tolerance</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Sodium</subject><subject>Sodium - metabolism</subject><subject>sodium and potassium homeostasis</subject><subject>SOS pathway</subject><issn>0261-4189</issn><issn>1460-2075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhSMEotPCnhWyxIZNyr1OnNgSEipV-VNRkQpry7GdGY-SeOqbgLrrO_CGPAkZprQUCbGyjvydo3t0suwJwiEKLvgL3zfrQw6cI_IS8F62wLKCnEMt7mcL4BXmJUq1l-0TrQFAyBofZntFJRGxFIus_7SKtFmZMbhgmbHB_bj6nvxy6szoHTs_O-fMxmFMsSNG0YWpZ2ZwbBNHQ7RVq9j7SLMKxMLAjpJpgoubrZwG5xMj042MxuSJHmUPWtORf3z9HmRf3px8Pn6Xn569fX98dJrbspaYF1Ca1tjWtopbaBoQpnFe1MZZxX2JXkgrlEJvK6taCaqwRhpRoxIOiqotDrJXu9zN1PTeWT8XMJ3epNCbdKmjCfruzxBWehm_agSESslyTnh-nZDixeRp1H0g67vODD5OpHldq0KghHpGn_2FruOUhrmf5hJQVoXkMFOwo2yKRMm3N9cg6F9j6u2Y-nbM2fL0zxY3ht_rzcDLHfAtdP7yv4H65OPrD3fycWen2Tksfbo9_J83_QSRGL_v</recordid><startdate>20230417</startdate><enddate>20230417</enddate><creator>Li, Jianfang</creator><creator>Shen, Like</creator><creator>Han, Xiuli</creator><creator>He, Gefeng</creator><creator>Fan, Wenxia</creator><creator>Li, Yu</creator><creator>Yang, Shiping</creator><creator>Zhang, Ziding</creator><creator>Yang, Yongqing</creator><creator>Jin, Weiwei</creator><creator>Wang, Yi</creator><creator>Zhang, Wenhua</creator><creator>Guo, Yan</creator><general>Nature Publishing Group UK</general><general>Blackwell Publishing Ltd</general><general>John Wiley and Sons Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6955-8008</orcidid><orcidid>https://orcid.org/0000-0002-3660-5859</orcidid><orcidid>https://orcid.org/0000-0002-3155-9208</orcidid><orcidid>https://orcid.org/0000-0002-2445-677X</orcidid><orcidid>https://orcid.org/0000-0001-8192-7120</orcidid><orcidid>https://orcid.org/0000-0001-5631-3549</orcidid><orcidid>https://orcid.org/0000-0001-8628-8559</orcidid></search><sort><creationdate>20230417</creationdate><title>Phosphatidic acid–regulated SOS2 controls sodium and potassium homeostasis in Arabidopsis under salt stress</title><author>Li, Jianfang ; Shen, Like ; Han, Xiuli ; He, Gefeng ; Fan, Wenxia ; Li, Yu ; Yang, Shiping ; Zhang, Ziding ; Yang, Yongqing ; Jin, Weiwei ; Wang, Yi ; Zhang, Wenhua ; Guo, Yan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4781-304afacfcf92c0bb05abde57adc92e41e58c5991ec6c9f8093ca8a57195d036f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Abiotic stress</topic><topic>AKT</topic><topic>AKT1 protein</topic><topic>Arabidopsis</topic><topic>Arabidopsis - metabolism</topic><topic>Arabidopsis Proteins - metabolism</topic><topic>Calcium</topic><topic>Calcium signalling</topic><topic>Calcium-binding protein</topic><topic>Efflux</topic><topic>EMBO20</topic><topic>EMBO30</topic><topic>Homeostasis</topic><topic>Hydrogen</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Lipids</topic><topic>Localization</topic><topic>Maintenance</topic><topic>Membranes</topic><topic>Na+/H+-exchanging ATPase</topic><topic>Phosphatidic acid</topic><topic>Phosphatidic Acids - metabolism</topic><topic>Phosphorylation</topic><topic>Plant cells</topic><topic>Potassium</topic><topic>Potassium - metabolism</topic><topic>Potassium channels</topic><topic>Protein Serine-Threonine Kinases - metabolism</topic><topic>Proteins</topic><topic>Residues</topic><topic>Salinity tolerance</topic><topic>Salt</topic><topic>salt stress</topic><topic>Salt Stress - genetics</topic><topic>Salt tolerance</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Sodium</topic><topic>Sodium - metabolism</topic><topic>sodium and potassium homeostasis</topic><topic>SOS pathway</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Jianfang</creatorcontrib><creatorcontrib>Shen, Like</creatorcontrib><creatorcontrib>Han, Xiuli</creatorcontrib><creatorcontrib>He, Gefeng</creatorcontrib><creatorcontrib>Fan, Wenxia</creatorcontrib><creatorcontrib>Li, Yu</creatorcontrib><creatorcontrib>Yang, Shiping</creatorcontrib><creatorcontrib>Zhang, Ziding</creatorcontrib><creatorcontrib>Yang, Yongqing</creatorcontrib><creatorcontrib>Jin, Weiwei</creatorcontrib><creatorcontrib>Wang, Yi</creatorcontrib><creatorcontrib>Zhang, Wenhua</creatorcontrib><creatorcontrib>Guo, Yan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The EMBO journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Li, Jianfang</au><au>Shen, Like</au><au>Han, Xiuli</au><au>He, Gefeng</au><au>Fan, Wenxia</au><au>Li, Yu</au><au>Yang, Shiping</au><au>Zhang, Ziding</au><au>Yang, Yongqing</au><au>Jin, Weiwei</au><au>Wang, Yi</au><au>Zhang, Wenhua</au><au>Guo, Yan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Phosphatidic acid–regulated SOS2 controls sodium and potassium homeostasis in Arabidopsis under salt stress</atitle><jtitle>The EMBO journal</jtitle><stitle>EMBO J</stitle><addtitle>EMBO J</addtitle><date>2023-04-17</date><risdate>2023</risdate><volume>42</volume><issue>8</issue><spage>e112401</spage><epage>n/a</epage><pages>e112401-n/a</pages><issn>0261-4189</issn><eissn>1460-2075</eissn><abstract>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.
Synopsis
The maintenance of Na
+
/K
+
homeostasis in plant cells is essential for salt tolerance. Here, the lipid signaling molecule phosphatidic acid (PA) is shown to determine the Na
+
/K
+
homeostasis under salt stress via SOS2 protein kinase‐dependent activation of Na
+
efflux via SOS1 and AKT1‐mediated K
+
influx. PA promotes the kinase activity and plasma membrane localization of SOS2 under salt stress.
The residue Lys57 is critical for the PA‐mediated regulation of SOS2.
The PA–SOS2 module activates the Na
+
/H
+
antiporter SOS1 to promote Na
+
efflux.
The PA–SOS2 interaction also relieves the SCaBP8‐mediated inhibition of the inward K
+
channel AKT1 to promote K
+
uptake.
Graphical Abstract
Increased membrane concentration of phosphatidic acid under salt stress protects plant cells by triggering the release of Na
+
and the uptake of K
+
.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>36811145</pmid><doi>10.15252/embj.2022112401</doi><tpages>27</tpages><orcidid>https://orcid.org/0000-0002-6955-8008</orcidid><orcidid>https://orcid.org/0000-0002-3660-5859</orcidid><orcidid>https://orcid.org/0000-0002-3155-9208</orcidid><orcidid>https://orcid.org/0000-0002-2445-677X</orcidid><orcidid>https://orcid.org/0000-0001-8192-7120</orcidid><orcidid>https://orcid.org/0000-0001-5631-3549</orcidid><orcidid>https://orcid.org/0000-0001-8628-8559</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext_linktorsrc |
| identifier | ISSN: 0261-4189 |
| ispartof | The EMBO journal, 2023-04, Vol.42 (8), p.e112401-n/a |
| issn | 0261-4189 1460-2075 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10106984 |
| source | Springer Nature OA Free Journals |
| subjects | Abiotic stress AKT AKT1 protein Arabidopsis Arabidopsis - metabolism Arabidopsis Proteins - metabolism Calcium Calcium signalling Calcium-binding protein Efflux EMBO20 EMBO30 Homeostasis Hydrogen Kinases Life Sciences Lipids Localization Maintenance Membranes Na+/H+-exchanging ATPase Phosphatidic acid Phosphatidic Acids - metabolism Phosphorylation Plant cells Potassium Potassium - metabolism Potassium channels Protein Serine-Threonine Kinases - metabolism Proteins Residues Salinity tolerance Salt salt stress Salt Stress - genetics Salt tolerance Signal transduction Signaling Sodium Sodium - metabolism sodium and potassium homeostasis SOS pathway |
| title | Phosphatidic acid–regulated SOS2 controls sodium and potassium homeostasis in Arabidopsis under salt stress |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-19T06%3A06%3A59IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_C6C&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Phosphatidic%20acid%E2%80%93regulated%20SOS2%20controls%20sodium%20and%20potassium%20homeostasis%20in%20Arabidopsis%20under%20salt%20stress&rft.jtitle=The%20EMBO%20journal&rft.au=Li,%20Jianfang&rft.date=2023-04-17&rft.volume=42&rft.issue=8&rft.spage=e112401&rft.epage=n/a&rft.pages=e112401-n/a&rft.issn=0261-4189&rft.eissn=1460-2075&rft_id=info:doi/10.15252/embj.2022112401&rft_dat=%3Cproquest_C6C%3E2801863820%3C/proquest_C6C%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2801863820&rft_id=info:pmid/36811145&rfr_iscdi=true |