PoplarV1, Main, Exploration, bibRecord, 003234

H2O2 and cytosolic Ca2+ signals triggered by the PM H-coupled transport system mediate K+/Na+ homeostasis in NaCl-stressed Populus euphratica cells.

Identifieur interne : 003234 ( Main/Exploration ); précédent : 003233; suivant : 003235

H2O2 and cytosolic Ca2+ signals triggered by the PM H-coupled transport system mediate K+/Na+ homeostasis in NaCl-stressed Populus euphratica cells.

Auteurs : Jian Sun [République populaire de Chine] ; Mei-Juan Wang ; Ming-Quan Ding ; Shu-Rong Deng ; Mei-Qin Liu ; Cun-Fu Lu ; Xiao-Yang Zhou ; Xin Shen ; Xiao-Jiang Zheng ; Zeng-Kai Zhang ; Jin Song ; Zan-Min Hu ; Yue Xu ; Shao-Liang Chen

Source :

Plant, cell & environment [ 1365-3040 ] ; 2010.

RBID : pubmed:20082667

Descripteurs français

KwdFr :
- Amiloride (pharmacologie), Chlorure de sodium (pharmacologie), Cytosol (effets des médicaments et des substances chimiques), Cytosol (métabolisme), Homéostasie (effets des médicaments et des substances chimiques), Membrane cellulaire (métabolisme), Peroxyde d'hydrogène (métabolisme), Peroxyde d'hydrogène (pharmacologie), Populus (cytologie), Populus (effets des médicaments et des substances chimiques), Populus (métabolisme), Potassium (métabolisme), Potentiels de membrane (effets des médicaments et des substances chimiques), Protons (MeSH), Protoplastes (cytologie), Protoplastes (effets des médicaments et des substances chimiques), Protoplastes (métabolisme), Signalisation calcique (effets des médicaments et des substances chimiques), Sodium (métabolisme), Stress physiologique (effets des médicaments et des substances chimiques), Transport biologique (effets des médicaments et des substances chimiques), Vanadates (pharmacologie).
MESH :
- cytologie : Populus, Protoplastes.
- effets des médicaments et des substances chimiques : Cytosol, Homéostasie, Populus, Potentiels de membrane, Protoplastes, Signalisation calcique, Stress physiologique, Transport biologique.
- métabolisme : Cytosol, Membrane cellulaire, Peroxyde d'hydrogène, Populus, Potassium, Protoplastes, Sodium.
- pharmacologie : Amiloride, Chlorure de sodium, Peroxyde d'hydrogène, Vanadates.
- Protons.

English descriptors

KwdEn :
- Amiloride (pharmacology), Biological Transport (drug effects), Calcium Signaling (drug effects), Cell Membrane (metabolism), Cytosol (drug effects), Cytosol (metabolism), Homeostasis (drug effects), Hydrogen Peroxide (metabolism), Hydrogen Peroxide (pharmacology), Membrane Potentials (drug effects), Populus (cytology), Populus (drug effects), Populus (metabolism), Potassium (metabolism), Protons (MeSH), Protoplasts (cytology), Protoplasts (drug effects), Protoplasts (metabolism), Sodium (metabolism), Sodium Chloride (pharmacology), Stress, Physiological (drug effects), Vanadates (pharmacology).
MESH :
- chemical , metabolism : Hydrogen Peroxide, Potassium, Sodium.
- chemical , pharmacology : Amiloride, Hydrogen Peroxide, Sodium Chloride, Vanadates.
- cytology : Populus, Protoplasts.
- drug effects : Biological Transport, Calcium Signaling, Cytosol, Homeostasis, Membrane Potentials, Populus, Protoplasts, Stress, Physiological.
- metabolism : Cell Membrane, Cytosol, Populus, Protoplasts.
- chemical : Protons.

Abstract

Using confocal microscopy, X-ray microanalysis and the scanning ion-selective electrode technique, we investigated the signalling of H(2)O(2), cytosolic Ca(2+) ([Ca(2+)](cyt)) and the PM H(+)-coupled transport system in K(+)/Na(+) homeostasis control in NaCl-stressed calluses of Populus euphratica. An obvious Na(+)/H(+) antiport was seen in salinized cells; however, NaCl stress caused a net K(+) efflux, because of the salt-induced membrane depolarization. H(2)O(2) levels, regulated upwards by salinity, contributed to ionic homeostasis, because H(2)O(2) restrictions by DPI or DMTU caused enhanced K(+) efflux and decreased Na(+)/H(+) antiport activity. NaCl induced a net Ca(2+) influx and a subsequent rise of [Ca(2+)](cyt), which is involved in H(2)O(2)-mediated K(+)/Na(+) homeostasis in salinized P. euphratica cells. When callus cells were pretreated with inhibitors of the Na(+)/H(+) antiport system, the NaCl-induced elevation of H(2)O(2) and [Ca(2+)](cyt) was correspondingly restricted, leading to a greater K(+) efflux and a more pronounced reduction in Na(+)/H(+) antiport activity. Results suggest that the PM H(+)-coupled transport system mediates H(+) translocation and triggers the stress signalling of H(2)O(2) and Ca(2+), which results in a K(+)/Na(+) homeostasis via mediations of K(+) channels and the Na(+)/H(+) antiport system in the PM of NaCl-stressed cells. Accordingly, a salt stress signalling pathway of P. euphratica cells is proposed.

DOI: 10.1111/j.1365-3040.2010.02118.x
PubMed: 20082667

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 003329
to stream Main, to step Curation: 003329

Le document en format XML

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<term>Biological Transport (drug effects)</term>
<term>Calcium Signaling (drug effects)</term>
<term>Cell Membrane (metabolism)</term>
<term>Cytosol (drug effects)</term>
<term>Cytosol (metabolism)</term>
<term>Homeostasis (drug effects)</term>
<term>Hydrogen Peroxide (metabolism)</term>
<term>Hydrogen Peroxide (pharmacology)</term>
<term>Membrane Potentials (drug effects)</term>
<term>Populus (cytology)</term>
<term>Populus (drug effects)</term>
<term>Populus (metabolism)</term>
<term>Potassium (metabolism)</term>
<term>Protons (MeSH)</term>
<term>Protoplasts (cytology)</term>
<term>Protoplasts (drug effects)</term>
<term>Protoplasts (metabolism)</term>
<term>Sodium (metabolism)</term>
<term>Sodium Chloride (pharmacology)</term>
<term>Stress, Physiological (drug effects)</term>
<term>Vanadates (pharmacology)</term>
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<term>Chlorure de sodium (pharmacologie)</term>
<term>Cytosol (effets des médicaments et des substances chimiques)</term>
<term>Cytosol (métabolisme)</term>
<term>Homéostasie (effets des médicaments et des substances chimiques)</term>
<term>Membrane cellulaire (métabolisme)</term>
<term>Peroxyde d'hydrogène (métabolisme)</term>
<term>Peroxyde d'hydrogène (pharmacologie)</term>
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<term>Populus (effets des médicaments et des substances chimiques)</term>
<term>Populus (métabolisme)</term>
<term>Potassium (métabolisme)</term>
<term>Potentiels de membrane (effets des médicaments et des substances chimiques)</term>
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<term>Protoplastes (cytologie)</term>
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<term>Protoplastes (métabolisme)</term>
<term>Signalisation calcique (effets des médicaments et des substances chimiques)</term>
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<term>Sodium</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Amiloride</term>
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<term>Vanadates</term>
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<term>Calcium Signaling</term>
<term>Cytosol</term>
<term>Homeostasis</term>
<term>Membrane Potentials</term>
<term>Populus</term>
<term>Protoplasts</term>
<term>Stress, Physiological</term>
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<term>Homéostasie</term>
<term>Populus</term>
<term>Potentiels de membrane</term>
<term>Protoplastes</term>
<term>Signalisation calcique</term>
<term>Stress physiologique</term>
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<term>Vanadates</term>
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<front><div type="abstract" xml:lang="en">Using confocal microscopy, X-ray microanalysis and the scanning ion-selective electrode technique, we investigated the signalling of H(2)O(2), cytosolic Ca(2+) ([Ca(2+)](cyt)) and the PM H(+)-coupled transport system in K(+)/Na(+) homeostasis control in NaCl-stressed calluses of Populus euphratica. An obvious Na(+)/H(+) antiport was seen in salinized cells; however, NaCl stress caused a net K(+) efflux, because of the salt-induced membrane depolarization. H(2)O(2) levels, regulated upwards by salinity, contributed to ionic homeostasis, because H(2)O(2) restrictions by DPI or DMTU caused enhanced K(+) efflux and decreased Na(+)/H(+) antiport activity. NaCl induced a net Ca(2+) influx and a subsequent rise of [Ca(2+)](cyt), which is involved in H(2)O(2)-mediated K(+)/Na(+) homeostasis in salinized P. euphratica cells. When callus cells were pretreated with inhibitors of the Na(+)/H(+) antiport system, the NaCl-induced elevation of H(2)O(2) and [Ca(2+)](cyt) was correspondingly restricted, leading to a greater K(+) efflux and a more pronounced reduction in Na(+)/H(+) antiport activity. Results suggest that the PM H(+)-coupled transport system mediates H(+) translocation and triggers the stress signalling of H(2)O(2) and Ca(2+), which results in a K(+)/Na(+) homeostasis via mediations of K(+) channels and the Na(+)/H(+) antiport system in the PM of NaCl-stressed cells. Accordingly, a salt stress signalling pathway of P. euphratica cells is proposed.</div>
</front>
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<DateCompleted><Year>2010</Year>
<Month>10</Month>
<Day>12</Day>
</DateCompleted>
<DateRevised><Year>2015</Year>
<Month>11</Month>
<Day>19</Day>
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<JournalIssue CitedMedium="Internet"><Volume>33</Volume>
<Issue>6</Issue>
<PubDate><Year>2010</Year>
<Month>Jun</Month>
</PubDate>
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<Title>Plant, cell & environment</Title>
<ISOAbbreviation>Plant Cell Environ</ISOAbbreviation>
</Journal>
<ArticleTitle>H2O2 and cytosolic Ca2+ signals triggered by the PM H-coupled transport system mediate K+/Na+ homeostasis in NaCl-stressed Populus euphratica cells.</ArticleTitle>
<Pagination><MedlinePgn>943-58</MedlinePgn>
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<ELocationID EIdType="doi" ValidYN="Y">10.1111/j.1365-3040.2010.02118.x</ELocationID>
<Abstract><AbstractText>Using confocal microscopy, X-ray microanalysis and the scanning ion-selective electrode technique, we investigated the signalling of H(2)O(2), cytosolic Ca(2+) ([Ca(2+)](cyt)) and the PM H(+)-coupled transport system in K(+)/Na(+) homeostasis control in NaCl-stressed calluses of Populus euphratica. An obvious Na(+)/H(+) antiport was seen in salinized cells; however, NaCl stress caused a net K(+) efflux, because of the salt-induced membrane depolarization. H(2)O(2) levels, regulated upwards by salinity, contributed to ionic homeostasis, because H(2)O(2) restrictions by DPI or DMTU caused enhanced K(+) efflux and decreased Na(+)/H(+) antiport activity. NaCl induced a net Ca(2+) influx and a subsequent rise of [Ca(2+)](cyt), which is involved in H(2)O(2)-mediated K(+)/Na(+) homeostasis in salinized P. euphratica cells. When callus cells were pretreated with inhibitors of the Na(+)/H(+) antiport system, the NaCl-induced elevation of H(2)O(2) and [Ca(2+)](cyt) was correspondingly restricted, leading to a greater K(+) efflux and a more pronounced reduction in Na(+)/H(+) antiport activity. Results suggest that the PM H(+)-coupled transport system mediates H(+) translocation and triggers the stress signalling of H(2)O(2) and Ca(2+), which results in a K(+)/Na(+) homeostasis via mediations of K(+) channels and the Na(+)/H(+) antiport system in the PM of NaCl-stressed cells. Accordingly, a salt stress signalling pathway of P. euphratica cells is proposed.</AbstractText>
</Abstract>
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<ForeName>Jian</ForeName>
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<AffiliationInfo><Affiliation>College of Biological Sciences and Technology, Beijing Forestry University, Beijing 100083, China.</Affiliation>
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<Initials>X</Initials>
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<ForeName>Xiao-Jiang</ForeName>
<Initials>XJ</Initials>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Zeng-Kai</ForeName>
<Initials>ZK</Initials>
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<Author ValidYN="Y"><LastName>Song</LastName>
<ForeName>Jin</ForeName>
<Initials>J</Initials>
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<Author ValidYN="Y"><LastName>Hu</LastName>
<ForeName>Zan-Min</ForeName>
<Initials>ZM</Initials>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Yue</ForeName>
<Initials>Y</Initials>
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<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Shao-Liang</ForeName>
<Initials>SL</Initials>
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H2O2 and cytosolic Ca2+ signals triggered by the PM H-coupled transport system mediate K+/Na+ homeostasis in NaCl-stressed Populus euphratica cells.

H2O2 and cytosolic Ca2+ signals triggered by the PM H-coupled transport system mediate K+/Na+ homeostasis in NaCl-stressed Populus euphratica cells.

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