Hydrogen Sulfide Mediates K+ and Na+ Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress.
Identifieur interne : 000E41 ( Main/Exploration ); précédent : 000E40; suivant : 000E42Hydrogen Sulfide Mediates K+ and Na+ Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress.
Auteurs : Nan Zhao [République populaire de Chine] ; Huipeng Zhu [République populaire de Chine] ; Huilong Zhang [République populaire de Chine] ; Jian Sun [République populaire de Chine] ; Jinchi Zhou [République populaire de Chine] ; Chen Deng [République populaire de Chine] ; Yuhong Zhang [République populaire de Chine] ; Rui Zhao [République populaire de Chine] ; Xiaoyang Zhou [République populaire de Chine] ; Cunfu Lu [République populaire de Chine] ; Shanzhi Lin [République populaire de Chine] ; Shaoliang Chen [République populaire de Chine]Source :
- Frontiers in plant science [ 1664-462X ] ; 2018.
Abstract
Non-invasive micro-test techniques (NMT) were used to analyze NaCl-altered flux profiles of K+, Na+, and H+ in roots and effects of NaHS (a H2S donor) on root ion fluxes in two contrasting poplar species, Populus euphratica (salt-resistant) and Populus popularis (salt-sensitive). Both poplar species displayed a net K+ efflux after exposure to salt shock (100 mM NaCl), as well as after short-term (24 h), and long-term (LT) (5 days) saline treatment (50 mM NaCl, referred to as salt stress). NaHS (50 μM) restricted NaCl-induced K+ efflux in roots irrespective of the duration of salt exposure, but K+ efflux was not pronounced in data collected from the LT salt stress treatment of P. euphratica. The NaCl-induced K+ efflux was inhibited by a K+ channel blocker, tetraethylammonium chloride (TEA) in P. popularis root samples, but K+ loss increased with a specific inhibitor of plasma membrane (PM) H+-ATPase, sodium orthovanadate, in both poplar species under LT salt stress and NaHS treatment. This indicates that NaCl-induced K+ loss was through depolarization-activated K+ channels. NaHS caused increased Na+ efflux and a corresponding increase in H+ influx for poplar roots subjected to both the short- and LT salt stress. The NaHS-enhanced H+ influx was not significant in P. euphratica samples subjected to short term salt stress. Both sodium orthovanadate and amiloride (a Na+/H+ antiporter inhibitor) effectively inhibited the NaHS-augmented Na+ efflux, indicating that the H2S-enhanced Na+ efflux was due to active Na+ exclusion across the PM. We therefore conclude that the beneficial effects of H2S probably arise from upward regulation of the Na+/H+ antiport system (H+ pumps and Na+/H+ antiporters), which promote exchange of Na+ with H+ across the PM and simultaneously restricted the channel-mediated K+ loss that activated by membrane depolarization.
DOI: 10.3389/fpls.2018.01366
PubMed: 30283479
PubMed Central: PMC6157452
Affiliations:
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and Na<sup>+</sup>
Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress.</title>
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Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress.</title>
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<author><name sortKey="Zhao, Rui" sort="Zhao, Rui" uniqKey="Zhao R" first="Rui" last="Zhao">Rui Zhao</name>
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<front><div type="abstract" xml:lang="en">Non-invasive micro-test techniques (NMT) were used to analyze NaCl-altered flux profiles of K<sup>+</sup>
, Na<sup>+</sup>
, and H<sup>+</sup>
in roots and effects of NaHS (a H<sub>2</sub>
S donor) on root ion fluxes in two contrasting poplar species, <i>Populus euphratica</i>
(salt-resistant) and <i>Populus popularis</i>
(salt-sensitive). Both poplar species displayed a net K<sup>+</sup>
efflux after exposure to salt shock (100 mM NaCl), as well as after short-term (24 h), and long-term (LT) (5 days) saline treatment (50 mM NaCl, referred to as salt stress). NaHS (50 μM) restricted NaCl-induced K<sup>+</sup>
efflux in roots irrespective of the duration of salt exposure, but K<sup>+</sup>
efflux was not pronounced in data collected from the LT salt stress treatment of <i>P. euphratica</i>
. The NaCl-induced K<sup>+</sup>
efflux was inhibited by a K<sup>+</sup>
channel blocker, tetraethylammonium chloride (TEA) in <i>P. popularis</i>
root samples, but K<sup>+</sup>
loss increased with a specific inhibitor of plasma membrane (PM) H<sup>+</sup>
-ATPase, sodium orthovanadate, in both poplar species under LT salt stress and NaHS treatment. This indicates that NaCl-induced K<sup>+</sup>
loss was through depolarization-activated K<sup>+</sup>
channels. NaHS caused increased Na<sup>+</sup>
efflux and a corresponding increase in H<sup>+</sup>
influx for poplar roots subjected to both the short- and LT salt stress. The NaHS-enhanced H<sup>+</sup>
influx was not significant in <i>P. euphratica</i>
samples subjected to short term salt stress. Both sodium orthovanadate and amiloride (a Na<sup>+</sup>
/H<sup>+</sup>
antiporter inhibitor) effectively inhibited the NaHS-augmented Na<sup>+</sup>
efflux, indicating that the H<sub>2</sub>
S-enhanced Na<sup>+</sup>
efflux was due to active Na<sup>+</sup>
exclusion across the PM. We therefore conclude that the beneficial effects of H<sub>2</sub>
S probably arise from upward regulation of the Na<sup>+</sup>
/H<sup>+</sup>
antiport system (H<sup>+</sup>
pumps and Na<sup>+</sup>
/H<sup>+</sup>
antiporters), which promote exchange of Na<sup>+</sup>
with H<sup>+</sup>
across the PM and simultaneously restricted the channel-mediated K<sup>+</sup>
loss that activated by membrane depolarization.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">30283479</PMID>
<DateRevised><Year>2020</Year>
<Month>10</Month>
<Day>01</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-462X</ISSN>
<JournalIssue CitedMedium="Print"><Volume>9</Volume>
<PubDate><Year>2018</Year>
</PubDate>
</JournalIssue>
<Title>Frontiers in plant science</Title>
<ISOAbbreviation>Front Plant Sci</ISOAbbreviation>
</Journal>
<ArticleTitle>Hydrogen Sulfide Mediates K<sup>+</sup>
and Na<sup>+</sup>
Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress.</ArticleTitle>
<Pagination><MedlinePgn>1366</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.3389/fpls.2018.01366</ELocationID>
<Abstract><AbstractText>Non-invasive micro-test techniques (NMT) were used to analyze NaCl-altered flux profiles of K<sup>+</sup>
, Na<sup>+</sup>
, and H<sup>+</sup>
in roots and effects of NaHS (a H<sub>2</sub>
S donor) on root ion fluxes in two contrasting poplar species, <i>Populus euphratica</i>
(salt-resistant) and <i>Populus popularis</i>
(salt-sensitive). Both poplar species displayed a net K<sup>+</sup>
efflux after exposure to salt shock (100 mM NaCl), as well as after short-term (24 h), and long-term (LT) (5 days) saline treatment (50 mM NaCl, referred to as salt stress). NaHS (50 μM) restricted NaCl-induced K<sup>+</sup>
efflux in roots irrespective of the duration of salt exposure, but K<sup>+</sup>
efflux was not pronounced in data collected from the LT salt stress treatment of <i>P. euphratica</i>
. The NaCl-induced K<sup>+</sup>
efflux was inhibited by a K<sup>+</sup>
channel blocker, tetraethylammonium chloride (TEA) in <i>P. popularis</i>
root samples, but K<sup>+</sup>
loss increased with a specific inhibitor of plasma membrane (PM) H<sup>+</sup>
-ATPase, sodium orthovanadate, in both poplar species under LT salt stress and NaHS treatment. This indicates that NaCl-induced K<sup>+</sup>
loss was through depolarization-activated K<sup>+</sup>
channels. NaHS caused increased Na<sup>+</sup>
efflux and a corresponding increase in H<sup>+</sup>
influx for poplar roots subjected to both the short- and LT salt stress. The NaHS-enhanced H<sup>+</sup>
influx was not significant in <i>P. euphratica</i>
samples subjected to short term salt stress. Both sodium orthovanadate and amiloride (a Na<sup>+</sup>
/H<sup>+</sup>
antiporter inhibitor) effectively inhibited the NaHS-augmented Na<sup>+</sup>
efflux, indicating that the H<sub>2</sub>
S-enhanced Na<sup>+</sup>
efflux was due to active Na<sup>+</sup>
exclusion across the PM. We therefore conclude that the beneficial effects of H<sub>2</sub>
S probably arise from upward regulation of the Na<sup>+</sup>
/H<sup>+</sup>
antiport system (H<sup>+</sup>
pumps and Na<sup>+</sup>
/H<sup>+</sup>
antiporters), which promote exchange of Na<sup>+</sup>
with H<sup>+</sup>
across the PM and simultaneously restricted the channel-mediated K<sup>+</sup>
loss that activated by membrane depolarization.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Nan</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Beijing Advanced Innovation Center for Tree Breeding by Molecular Design, College of Biological Sciences and Technology, Beijing Forestry University, Beijing, China.</Affiliation>
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<affiliations><list><country><li>République populaire de Chine</li>
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<name sortKey="Zhang, Yuhong" sort="Zhang, Yuhong" uniqKey="Zhang Y" first="Yuhong" last="Zhang">Yuhong Zhang</name>
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