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A Glycine max sodium/hydrogen exchanger enhances salt tolerance through maintaining higher Na(+) efflux rate and K(+)/Na(+) ratio in Arabidopsis

BACKGROUND: Soybean (Glycine max (L.)) is one the most important oil-yielding cash crops. However, the soybean production has been seriously restricted by salinization. It is therefore crucial to identify salt tolerance-related genes and reveal molecular mechanisms underlying salt tolerance in soybe...

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Autores principales: Sun, Tian-Jie, Fan, Long, Yang, Jun, Cao, Ren-Zhi, Yang, Chun-Yan, Zhang, Jie, Wang, Dong-Mei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6833268/
https://www.ncbi.nlm.nih.gov/pubmed/31690290
http://dx.doi.org/10.1186/s12870-019-2084-4
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author Sun, Tian-Jie
Fan, Long
Yang, Jun
Cao, Ren-Zhi
Yang, Chun-Yan
Zhang, Jie
Wang, Dong-Mei
author_facet Sun, Tian-Jie
Fan, Long
Yang, Jun
Cao, Ren-Zhi
Yang, Chun-Yan
Zhang, Jie
Wang, Dong-Mei
author_sort Sun, Tian-Jie
collection PubMed
description BACKGROUND: Soybean (Glycine max (L.)) is one the most important oil-yielding cash crops. However, the soybean production has been seriously restricted by salinization. It is therefore crucial to identify salt tolerance-related genes and reveal molecular mechanisms underlying salt tolerance in soybean crops. A better understanding of how plants resist salt stress provides insights in improving existing soybean varieties as well as cultivating novel salt tolerant varieties. In this study, the biological function of GmNHX1, a NHX-like gene, and the molecular basis underlying GmNHX1-mediated salt stress resistance have been revealed. RESULTS: We found that the transcription level of GmNHX1 was up-regulated under salt stress condition in soybean, reaching its peak at 24 h after salt treatment. By employing the virus-induced gene silencing technique (VIGS), we also found that soybean plants became more susceptible to salt stress after silencing GmNHX1 than wild-type and more silenced plants wilted than wild-type under salt treatment. Furthermore, Arabidopsis thaliana expressing GmNHX1 grew taller and generated more rosette leaves under salt stress condition compared to wild-type. Exogenous expression of GmNHX1 resulted in an increase of Na(+) transportation to leaves along with a reduction of Na(+) absorption in roots, and the consequent maintenance of a high K(+)/Na(+) ratio under salt stress condition. GmNHX1-GFP-transformed onion bulb endothelium cells showed fluorescent pattern in which GFP fluorescence signals enriched in vacuolar membranes. Using the non-invasive micro-test technique (NMT), we found that the Na(+) efflux rate of both wild-type and transformed plants after salt treatment were significantly higher than that of before salt treatment. Additionally, the Na(+) efflux rate of transformed plants after salt treatment were significantly higher than that of wild-type. Meanwhile, the transcription levels of three osmotic stress-related genes, SKOR, SOS1 and AKT1 were all up-regulated in GmNHX1-expressing plants under salt stress condition. CONCLUSION: Vacuolar membrane-localized GmNHX1 enhances plant salt tolerance through maintaining a high K(+)/Na(+) ratio along with inducing the expression of SKOR, SOS1 and AKT1. Our findings provide molecular insights on the roles of GmNHX1 and similar sodium/hydrogen exchangers in regulating salt tolerance.
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spelling pubmed-68332682019-11-08 A Glycine max sodium/hydrogen exchanger enhances salt tolerance through maintaining higher Na(+) efflux rate and K(+)/Na(+) ratio in Arabidopsis Sun, Tian-Jie Fan, Long Yang, Jun Cao, Ren-Zhi Yang, Chun-Yan Zhang, Jie Wang, Dong-Mei BMC Plant Biol Research Article BACKGROUND: Soybean (Glycine max (L.)) is one the most important oil-yielding cash crops. However, the soybean production has been seriously restricted by salinization. It is therefore crucial to identify salt tolerance-related genes and reveal molecular mechanisms underlying salt tolerance in soybean crops. A better understanding of how plants resist salt stress provides insights in improving existing soybean varieties as well as cultivating novel salt tolerant varieties. In this study, the biological function of GmNHX1, a NHX-like gene, and the molecular basis underlying GmNHX1-mediated salt stress resistance have been revealed. RESULTS: We found that the transcription level of GmNHX1 was up-regulated under salt stress condition in soybean, reaching its peak at 24 h after salt treatment. By employing the virus-induced gene silencing technique (VIGS), we also found that soybean plants became more susceptible to salt stress after silencing GmNHX1 than wild-type and more silenced plants wilted than wild-type under salt treatment. Furthermore, Arabidopsis thaliana expressing GmNHX1 grew taller and generated more rosette leaves under salt stress condition compared to wild-type. Exogenous expression of GmNHX1 resulted in an increase of Na(+) transportation to leaves along with a reduction of Na(+) absorption in roots, and the consequent maintenance of a high K(+)/Na(+) ratio under salt stress condition. GmNHX1-GFP-transformed onion bulb endothelium cells showed fluorescent pattern in which GFP fluorescence signals enriched in vacuolar membranes. Using the non-invasive micro-test technique (NMT), we found that the Na(+) efflux rate of both wild-type and transformed plants after salt treatment were significantly higher than that of before salt treatment. Additionally, the Na(+) efflux rate of transformed plants after salt treatment were significantly higher than that of wild-type. Meanwhile, the transcription levels of three osmotic stress-related genes, SKOR, SOS1 and AKT1 were all up-regulated in GmNHX1-expressing plants under salt stress condition. CONCLUSION: Vacuolar membrane-localized GmNHX1 enhances plant salt tolerance through maintaining a high K(+)/Na(+) ratio along with inducing the expression of SKOR, SOS1 and AKT1. Our findings provide molecular insights on the roles of GmNHX1 and similar sodium/hydrogen exchangers in regulating salt tolerance. BioMed Central 2019-11-05 /pmc/articles/PMC6833268/ /pubmed/31690290 http://dx.doi.org/10.1186/s12870-019-2084-4 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Sun, Tian-Jie
Fan, Long
Yang, Jun
Cao, Ren-Zhi
Yang, Chun-Yan
Zhang, Jie
Wang, Dong-Mei
A Glycine max sodium/hydrogen exchanger enhances salt tolerance through maintaining higher Na(+) efflux rate and K(+)/Na(+) ratio in Arabidopsis
title A Glycine max sodium/hydrogen exchanger enhances salt tolerance through maintaining higher Na(+) efflux rate and K(+)/Na(+) ratio in Arabidopsis
title_full A Glycine max sodium/hydrogen exchanger enhances salt tolerance through maintaining higher Na(+) efflux rate and K(+)/Na(+) ratio in Arabidopsis
title_fullStr A Glycine max sodium/hydrogen exchanger enhances salt tolerance through maintaining higher Na(+) efflux rate and K(+)/Na(+) ratio in Arabidopsis
title_full_unstemmed A Glycine max sodium/hydrogen exchanger enhances salt tolerance through maintaining higher Na(+) efflux rate and K(+)/Na(+) ratio in Arabidopsis
title_short A Glycine max sodium/hydrogen exchanger enhances salt tolerance through maintaining higher Na(+) efflux rate and K(+)/Na(+) ratio in Arabidopsis
title_sort glycine max sodium/hydrogen exchanger enhances salt tolerance through maintaining higher na(+) efflux rate and k(+)/na(+) ratio in arabidopsis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6833268/
https://www.ncbi.nlm.nih.gov/pubmed/31690290
http://dx.doi.org/10.1186/s12870-019-2084-4
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