PoplarV1, Main, Exploration, bibRecord, 001C29

NaCl-elicited, vacuolar Ca(2+) release facilitates prolonged cytosolic Ca(2+) signaling in the salt response of Populus euphratica cells.

Identifieur interne : 001C29 ( Main/Exploration ); précédent : 001C28; suivant : 001C30

NaCl-elicited, vacuolar Ca(2+) release facilitates prolonged cytosolic Ca(2+) signaling in the salt response of Populus euphratica cells.

Source :

Cell calcium [ 1532-1991 ] ; 2015.

RBID : pubmed:25840638

Descripteurs français

KwdFr :
- Calcium (métabolisme), Cellules cultivées (MeSH), Chlorure de sodium (pharmacologie), Homéostasie (effets des médicaments et des substances chimiques), Homéostasie (physiologie), Membranes intracellulaires (effets des médicaments et des substances chimiques), Modèles biologiques (MeSH), Populus (cytologie), Populus (physiologie), Relation dose-effet des médicaments (MeSH), Signalisation calcique (effets des médicaments et des substances chimiques), Signalisation calcique (physiologie), Transduction du signal (effets des médicaments et des substances chimiques), Transduction du signal (physiologie), Vacuoles (métabolisme).
MESH :
- cytologie : Populus.
- effets des médicaments et des substances chimiques : Homéostasie, Membranes intracellulaires, Signalisation calcique, Transduction du signal.
- métabolisme : Calcium, Vacuoles.
- pharmacologie : Chlorure de sodium.
- physiologie : Homéostasie, Populus, Signalisation calcique, Transduction du signal.
- Cellules cultivées, Modèles biologiques, Relation dose-effet des médicaments.

English descriptors

KwdEn :
- Calcium (metabolism), Calcium Signaling (drug effects), Calcium Signaling (physiology), Cells, Cultured (MeSH), Dose-Response Relationship, Drug (MeSH), Homeostasis (drug effects), Homeostasis (physiology), Intracellular Membranes (drug effects), Models, Biological (MeSH), Populus (cytology), Populus (physiology), Signal Transduction (drug effects), Signal Transduction (physiology), Sodium Chloride (pharmacology), Vacuoles (metabolism).
MESH :
- chemical , metabolism : Calcium.
- cytology : Populus.
- drug effects : Calcium Signaling, Homeostasis, Intracellular Membranes, Signal Transduction.
- metabolism : Vacuoles.
- chemical , pharmacology : Sodium Chloride.
- physiology : Calcium Signaling, Homeostasis, Populus, Signal Transduction.
- Cells, Cultured, Dose-Response Relationship, Drug, Models, Biological.

Abstract

High environmental salt elicits an increase in cytosolic Ca(2+) ([Ca(2+)]cyt) in plants, which is generated by extracellular Ca(2+) influx and Ca(2+) release from intracellular stores, such as vacuole and endoplasmic reticulum. This study aimed to determine the physiological mechanisms underlying Ca(2+) release from vacuoles and its role in ionic homeostasis in Populus euphratica. In vivo Ca(2+) imaging showed that NaCl treatment induced a rapid elevation in [Ca(2+)]cyt, which was accompanied by a subsequent release of vacuolar Ca(2+). In cell cultures, NaCl-altered intracellular Ca(2+) mobilization was abolished by antagonists of inositol (1, 4, 5) trisphosphate (IP3) and cyclic adenosine diphosphate ribose (cADPR) signaling pathways, but not by slow vacuolar (SV) channel blockers. Furthermore, the NaCl-induced vacuolar Ca(2+) release was dependent on extracellular ATP, extracellular Ca(2+) influx, H2O2, and NO. In vitro Ca(2+) flux recordings confirmed that IP3, cADPR, and Ca(2+) induced substantial Ca(2+) efflux from intact vacuoles, but this vacuolar Ca(2+) flux did not directly respond to ATP, H2O2, or NO. Moreover, the IP3/cADPR-mediated vacuolar Ca(2+) release enhanced the expression of salt-responsive genes that regulated a wide range of cellular processes required for ion homeostasis, including cytosolic K(+) maintenance, Na(+) and Cl(-) exclusion across the plasma membrane, and Na(+)/H(+) and Cl(-)/H(+) exchanges across the vacuolar membrane.

DOI: 10.1016/j.ceca.2015.03.001
PubMed: 25840638

Affiliations:

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Le document en format XML

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<term>Calcium Signaling (drug effects)</term>
<term>Calcium Signaling (physiology)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Dose-Response Relationship, Drug (MeSH)</term>
<term>Homeostasis (drug effects)</term>
<term>Homeostasis (physiology)</term>
<term>Intracellular Membranes (drug effects)</term>
<term>Models, Biological (MeSH)</term>
<term>Populus (cytology)</term>
<term>Populus (physiology)</term>
<term>Signal Transduction (drug effects)</term>
<term>Signal Transduction (physiology)</term>
<term>Sodium Chloride (pharmacology)</term>
<term>Vacuoles (metabolism)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Calcium (métabolisme)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Chlorure de sodium (pharmacologie)</term>
<term>Homéostasie (effets des médicaments et des substances chimiques)</term>
<term>Homéostasie (physiologie)</term>
<term>Membranes intracellulaires (effets des médicaments et des substances chimiques)</term>
<term>Modèles biologiques (MeSH)</term>
<term>Populus (cytologie)</term>
<term>Populus (physiologie)</term>
<term>Relation dose-effet des médicaments (MeSH)</term>
<term>Signalisation calcique (effets des médicaments et des substances chimiques)</term>
<term>Signalisation calcique (physiologie)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>Transduction du signal (physiologie)</term>
<term>Vacuoles (métabolisme)</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Calcium Signaling</term>
<term>Homeostasis</term>
<term>Intracellular Membranes</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Homéostasie</term>
<term>Membranes intracellulaires</term>
<term>Signalisation calcique</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Vacuoles</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Calcium</term>
<term>Vacuoles</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chlorure de sodium</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Sodium Chloride</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Homéostasie</term>
<term>Populus</term>
<term>Signalisation calcique</term>
<term>Transduction du signal</term>
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<term>Populus</term>
<term>Signal Transduction</term>
</keywords>
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<term>Dose-Response Relationship, Drug</term>
<term>Models, Biological</term>
</keywords>
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<front><div type="abstract" xml:lang="en">High environmental salt elicits an increase in cytosolic Ca(2+) ([Ca(2+)]cyt) in plants, which is generated by extracellular Ca(2+) influx and Ca(2+) release from intracellular stores, such as vacuole and endoplasmic reticulum. This study aimed to determine the physiological mechanisms underlying Ca(2+) release from vacuoles and its role in ionic homeostasis in Populus euphratica. In vivo Ca(2+) imaging showed that NaCl treatment induced a rapid elevation in [Ca(2+)]cyt, which was accompanied by a subsequent release of vacuolar Ca(2+). In cell cultures, NaCl-altered intracellular Ca(2+) mobilization was abolished by antagonists of inositol (1, 4, 5) trisphosphate (IP3) and cyclic adenosine diphosphate ribose (cADPR) signaling pathways, but not by slow vacuolar (SV) channel blockers. Furthermore, the NaCl-induced vacuolar Ca(2+) release was dependent on extracellular ATP, extracellular Ca(2+) influx, H2O2, and NO. In vitro Ca(2+) flux recordings confirmed that IP3, cADPR, and Ca(2+) induced substantial Ca(2+) efflux from intact vacuoles, but this vacuolar Ca(2+) flux did not directly respond to ATP, H2O2, or NO. Moreover, the IP3/cADPR-mediated vacuolar Ca(2+) release enhanced the expression of salt-responsive genes that regulated a wide range of cellular processes required for ion homeostasis, including cytosolic K(+) maintenance, Na(+) and Cl(-) exclusion across the plasma membrane, and Na(+)/H(+) and Cl(-)/H(+) exchanges across the vacuolar membrane.</div>
</front>
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<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ceca.2015.03.001</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S0143-4160(15)00055-X</ELocationID>
<Abstract><AbstractText>High environmental salt elicits an increase in cytosolic Ca(2+) ([Ca(2+)]cyt) in plants, which is generated by extracellular Ca(2+) influx and Ca(2+) release from intracellular stores, such as vacuole and endoplasmic reticulum. This study aimed to determine the physiological mechanisms underlying Ca(2+) release from vacuoles and its role in ionic homeostasis in Populus euphratica. In vivo Ca(2+) imaging showed that NaCl treatment induced a rapid elevation in [Ca(2+)]cyt, which was accompanied by a subsequent release of vacuolar Ca(2+). In cell cultures, NaCl-altered intracellular Ca(2+) mobilization was abolished by antagonists of inositol (1, 4, 5) trisphosphate (IP3) and cyclic adenosine diphosphate ribose (cADPR) signaling pathways, but not by slow vacuolar (SV) channel blockers. Furthermore, the NaCl-induced vacuolar Ca(2+) release was dependent on extracellular ATP, extracellular Ca(2+) influx, H2O2, and NO. In vitro Ca(2+) flux recordings confirmed that IP3, cADPR, and Ca(2+) induced substantial Ca(2+) efflux from intact vacuoles, but this vacuolar Ca(2+) flux did not directly respond to ATP, H2O2, or NO. Moreover, the IP3/cADPR-mediated vacuolar Ca(2+) release enhanced the expression of salt-responsive genes that regulated a wide range of cellular processes required for ion homeostasis, including cytosolic K(+) maintenance, Na(+) and Cl(-) exclusion across the plasma membrane, and Na(+)/H(+) and Cl(-)/H(+) exchanges across the vacuolar membrane.</AbstractText>
<CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Xuan</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>College of Biological Sciences and Technology, Beijing Forestry University (Box 162), Beijing 100083, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shen</LastName>
<ForeName>Zedan</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>College of Biological Sciences and Technology, Beijing Forestry University (Box 162), Beijing 100083, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Jian</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Institute of Integrative Plant Biology, School of Life Science, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province, People's Republic of China. Electronic address: Sunjian@jsnu.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yu</LastName>
<ForeName>Yicheng</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Institute of Integrative Plant Biology, School of Life Science, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Deng</LastName>
<ForeName>Shurong</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>College of Biological Sciences and Technology, Beijing Forestry University (Box 162), Beijing 100083, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Zongyun</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Institute of Integrative Plant Biology, School of Life Science, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Cunhua</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Institute of Integrative Plant Biology, School of Life Science, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Jian</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Institute of Integrative Plant Biology, School of Life Science, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Rui</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>College of Biological Sciences and Technology, Beijing Forestry University (Box 162), Beijing 100083, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shen</LastName>
<ForeName>Xin</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>College of Biological Sciences and Technology, Beijing Forestry University (Box 162), Beijing 100083, People's Republic of China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Shaoliang</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>College of Biological Sciences and Technology, Beijing Forestry University (Box 162), Beijing 100083, People's Republic of China. Electronic address: Lschen@bjfu.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2015</Year>
<Month>03</Month>
<Day>18</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Cell Calcium</MedlineTA>
<NlmUniqueID>8006226</NlmUniqueID>
<ISSNLinking>0143-4160</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>451W47IQ8X</RegistryNumber>
<NameOfSubstance UI="D012965">Sodium Chloride</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber>
<NameOfSubstance UI="D002118">Calcium</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020013" MajorTopicYN="N">Calcium Signaling</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006706" MajorTopicYN="N">Homeostasis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007425" MajorTopicYN="N">Intracellular Membranes</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D032107" MajorTopicYN="N">Populus</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012965" MajorTopicYN="N">Sodium Chloride</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014617" MajorTopicYN="N">Vacuoles</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">IP(3)</Keyword>
<Keyword MajorTopicYN="N">Ion flux</Keyword>
<Keyword MajorTopicYN="N">Poplar</Keyword>
<Keyword MajorTopicYN="N">SV channel</Keyword>
<Keyword MajorTopicYN="N">Salinity</Keyword>
<Keyword MajorTopicYN="N">Vacuolar Ca(2+) signaling</Keyword>
<Keyword MajorTopicYN="N">cADPR</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year>
<Month>10</Month>
<Day>07</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2015</Year>
<Month>02</Month>
<Day>24</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2015</Year>
<Month>03</Month>
<Day>09</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2015</Year>
<Month>4</Month>
<Day>5</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2015</Year>
<Month>4</Month>
<Day>5</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2016</Year>
<Month>1</Month>
<Day>20</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">25840638</ArticleId>
<ArticleId IdType="pii">S0143-4160(15)00055-X</ArticleId>
<ArticleId IdType="doi">10.1016/j.ceca.2015.03.001</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
<settlement><li>Pékin</li>
</settlement>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Xuan" sort="Zhang, Xuan" uniqKey="Zhang X" first="Xuan" last="Zhang">Xuan Zhang</name>
</noRegion>
<name sortKey="Chen, Shaoliang" sort="Chen, Shaoliang" uniqKey="Chen S" first="Shaoliang" last="Chen">Shaoliang Chen</name>
<name sortKey="Deng, Shurong" sort="Deng, Shurong" uniqKey="Deng S" first="Shurong" last="Deng">Shurong Deng</name>
<name sortKey="Li, Zongyun" sort="Li, Zongyun" uniqKey="Li Z" first="Zongyun" last="Li">Zongyun Li</name>
<name sortKey="Shen, Xin" sort="Shen, Xin" uniqKey="Shen X" first="Xin" last="Shen">Xin Shen</name>
<name sortKey="Shen, Zedan" sort="Shen, Zedan" uniqKey="Shen Z" first="Zedan" last="Shen">Zedan Shen</name>
<name sortKey="Sun, Cunhua" sort="Sun, Cunhua" uniqKey="Sun C" first="Cunhua" last="Sun">Cunhua Sun</name>
<name sortKey="Sun, Jian" sort="Sun, Jian" uniqKey="Sun J" first="Jian" last="Sun">Jian Sun</name>
<name sortKey="Yu, Yicheng" sort="Yu, Yicheng" uniqKey="Yu Y" first="Yicheng" last="Yu">Yicheng Yu</name>
<name sortKey="Zhang, Jian" sort="Zhang, Jian" uniqKey="Zhang J" first="Jian" last="Zhang">Jian Zhang</name>
<name sortKey="Zhao, Rui" sort="Zhao, Rui" uniqKey="Zhao R" first="Rui" last="Zhao">Rui Zhao</name>
</country>
</tree>
</affiliations>
</record>

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NaCl-elicited, vacuolar Ca(2+) release facilitates prolonged cytosolic Ca(2+) signaling in the salt response of Populus euphratica cells.

NaCl-elicited, vacuolar Ca(2+) release facilitates prolonged cytosolic Ca(2+) signaling in the salt response of Populus euphratica cells.

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