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H(2) Enhances Arabidopsis Salt Tolerance by Manipulating ZAT10/12-Mediated Antioxidant Defence and Controlling Sodium Exclusion

BACKGROUND: The metabolism of hydrogen gas (H(2)) in bacteria and algae has been extensively studied for the interesting of developing H(2)-based fuel. Recently, H(2) is recognized as a therapeutic antioxidant and activates several signalling pathways in clinical trials. However, underlying physiolo...

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Detalles Bibliográficos
Autores principales: Xie, Yanjie, Mao, Yu, Lai, Diwen, Zhang, Wei, Shen, Wenbiao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504229/
https://www.ncbi.nlm.nih.gov/pubmed/23185443
http://dx.doi.org/10.1371/journal.pone.0049800
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author Xie, Yanjie
Mao, Yu
Lai, Diwen
Zhang, Wei
Shen, Wenbiao
author_facet Xie, Yanjie
Mao, Yu
Lai, Diwen
Zhang, Wei
Shen, Wenbiao
author_sort Xie, Yanjie
collection PubMed
description BACKGROUND: The metabolism of hydrogen gas (H(2)) in bacteria and algae has been extensively studied for the interesting of developing H(2)-based fuel. Recently, H(2) is recognized as a therapeutic antioxidant and activates several signalling pathways in clinical trials. However, underlying physiological roles and mechanisms of H(2) in plants as well as its signalling cascade remain unknown. METHODOLOGY/PRINCIPAL FINDINGS: In this report, histochemical, molecular, immunological and genetic approaches were applied to characterize the participation of H(2) in enhancing Arabidopsis salt tolerance. An increase of endogenous H(2) release was observed 6 hr after exposure to 150 mM NaCl. Arabidopsis pretreated with 50% H(2)-saturated liquid medium, mimicking the induction of endogenous H(2) release when subsequently exposed to NaCl, effectively decreased salinity-induced growth inhibition. Further results showed that H(2) pretreatment modulated genes/proteins of zinc-finger transcription factor ZAT10/12 and related antioxidant defence enzymes, thus significantly counteracting the NaCl-induced reactive oxygen species (ROS) overproduction and lipid peroxidation. Additionally, H(2) pretreatment maintained ion homeostasis by regulating the antiporters and H(+) pump responsible for Na(+) exclusion (in particular) and compartmentation. Genetic evidence suggested that SOS1 and cAPX1 might be the target genes of H(2) signalling. CONCLUSIONS: Overall, our findings indicate that H(2) acts as a novel and cytoprotective regulator in coupling ZAT10/12-mediated antioxidant defence and maintenance of ion homeostasis in the improvement of Arabidopsis salt tolerance.
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spelling pubmed-35042292012-11-26 H(2) Enhances Arabidopsis Salt Tolerance by Manipulating ZAT10/12-Mediated Antioxidant Defence and Controlling Sodium Exclusion Xie, Yanjie Mao, Yu Lai, Diwen Zhang, Wei Shen, Wenbiao PLoS One Research Article BACKGROUND: The metabolism of hydrogen gas (H(2)) in bacteria and algae has been extensively studied for the interesting of developing H(2)-based fuel. Recently, H(2) is recognized as a therapeutic antioxidant and activates several signalling pathways in clinical trials. However, underlying physiological roles and mechanisms of H(2) in plants as well as its signalling cascade remain unknown. METHODOLOGY/PRINCIPAL FINDINGS: In this report, histochemical, molecular, immunological and genetic approaches were applied to characterize the participation of H(2) in enhancing Arabidopsis salt tolerance. An increase of endogenous H(2) release was observed 6 hr after exposure to 150 mM NaCl. Arabidopsis pretreated with 50% H(2)-saturated liquid medium, mimicking the induction of endogenous H(2) release when subsequently exposed to NaCl, effectively decreased salinity-induced growth inhibition. Further results showed that H(2) pretreatment modulated genes/proteins of zinc-finger transcription factor ZAT10/12 and related antioxidant defence enzymes, thus significantly counteracting the NaCl-induced reactive oxygen species (ROS) overproduction and lipid peroxidation. Additionally, H(2) pretreatment maintained ion homeostasis by regulating the antiporters and H(+) pump responsible for Na(+) exclusion (in particular) and compartmentation. Genetic evidence suggested that SOS1 and cAPX1 might be the target genes of H(2) signalling. CONCLUSIONS: Overall, our findings indicate that H(2) acts as a novel and cytoprotective regulator in coupling ZAT10/12-mediated antioxidant defence and maintenance of ion homeostasis in the improvement of Arabidopsis salt tolerance. Public Library of Science 2012-11-21 /pmc/articles/PMC3504229/ /pubmed/23185443 http://dx.doi.org/10.1371/journal.pone.0049800 Text en © 2012 Xie et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Xie, Yanjie
Mao, Yu
Lai, Diwen
Zhang, Wei
Shen, Wenbiao
H(2) Enhances Arabidopsis Salt Tolerance by Manipulating ZAT10/12-Mediated Antioxidant Defence and Controlling Sodium Exclusion
title H(2) Enhances Arabidopsis Salt Tolerance by Manipulating ZAT10/12-Mediated Antioxidant Defence and Controlling Sodium Exclusion
title_full H(2) Enhances Arabidopsis Salt Tolerance by Manipulating ZAT10/12-Mediated Antioxidant Defence and Controlling Sodium Exclusion
title_fullStr H(2) Enhances Arabidopsis Salt Tolerance by Manipulating ZAT10/12-Mediated Antioxidant Defence and Controlling Sodium Exclusion
title_full_unstemmed H(2) Enhances Arabidopsis Salt Tolerance by Manipulating ZAT10/12-Mediated Antioxidant Defence and Controlling Sodium Exclusion
title_short H(2) Enhances Arabidopsis Salt Tolerance by Manipulating ZAT10/12-Mediated Antioxidant Defence and Controlling Sodium Exclusion
title_sort h(2) enhances arabidopsis salt tolerance by manipulating zat10/12-mediated antioxidant defence and controlling sodium exclusion
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504229/
https://www.ncbi.nlm.nih.gov/pubmed/23185443
http://dx.doi.org/10.1371/journal.pone.0049800
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