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AtHKT1 gene regulating K(+) state in whole plant improves salt tolerance in transgenic tobacco plants
The status of K(+) is important for plant health. However, little is known about if high-affinity potassium transporter HKTs may help K(+) retention under salt stress. Here, we determined the effect of Arabidopsis thaliana transporter gene (AtHKT1) on the K(+) status, Na(+)-induced toxicity, and sal...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6224463/ https://www.ncbi.nlm.nih.gov/pubmed/30410009 http://dx.doi.org/10.1038/s41598-018-34660-9 |
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author | Wang, Li Liu, Yuhui Feng, Shoujiang Wang, Zhuoyu Zhang, Jinwen Zhang, Junlian Wang, Di Gan, Yantai |
author_facet | Wang, Li Liu, Yuhui Feng, Shoujiang Wang, Zhuoyu Zhang, Jinwen Zhang, Junlian Wang, Di Gan, Yantai |
author_sort | Wang, Li |
collection | PubMed |
description | The status of K(+) is important for plant health. However, little is known about if high-affinity potassium transporter HKTs may help K(+) retention under salt stress. Here, we determined the effect of Arabidopsis thaliana transporter gene (AtHKT1) on the K(+) status, Na(+)-induced toxicity, and salt tolerance in tobacco (Nicotiana tabacum L.). Six AtHKT1 transformed tobacco lines (T1, T2, … T6) were contrasted with a non-transgenic plantlet at the whole-plant and molecule levels. AtHKT1 gene was expressed in the xylems of stem, root and leaf vein in the transgenic tobacco, with the line T3 having highest expression. At Day 15, in the 200 mmol L(−1) NaCl stress treatment, the transgenic plants remained a healthy K(+) status, while the control plants decreased K(+) content by 70% and Na(+) contents in leaves and stems were 1.7 times that in the transgenic line. The AtHKT1 expression enhanced the activities of SOD, CAT and POD, raised chlorophyll and soluble sugar contents and root activity, and decreased MDA and proline contents and electrolyte leakage destruction. The constitutive over-expression of AtHKT1 that helps maintain a healthy K(+) status while reducing Na(+) toxicity may serve as a possible mechanism in maximizing productivity of tobacco under salt stress. |
format | Online Article Text |
id | pubmed-6224463 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-62244632018-11-13 AtHKT1 gene regulating K(+) state in whole plant improves salt tolerance in transgenic tobacco plants Wang, Li Liu, Yuhui Feng, Shoujiang Wang, Zhuoyu Zhang, Jinwen Zhang, Junlian Wang, Di Gan, Yantai Sci Rep Article The status of K(+) is important for plant health. However, little is known about if high-affinity potassium transporter HKTs may help K(+) retention under salt stress. Here, we determined the effect of Arabidopsis thaliana transporter gene (AtHKT1) on the K(+) status, Na(+)-induced toxicity, and salt tolerance in tobacco (Nicotiana tabacum L.). Six AtHKT1 transformed tobacco lines (T1, T2, … T6) were contrasted with a non-transgenic plantlet at the whole-plant and molecule levels. AtHKT1 gene was expressed in the xylems of stem, root and leaf vein in the transgenic tobacco, with the line T3 having highest expression. At Day 15, in the 200 mmol L(−1) NaCl stress treatment, the transgenic plants remained a healthy K(+) status, while the control plants decreased K(+) content by 70% and Na(+) contents in leaves and stems were 1.7 times that in the transgenic line. The AtHKT1 expression enhanced the activities of SOD, CAT and POD, raised chlorophyll and soluble sugar contents and root activity, and decreased MDA and proline contents and electrolyte leakage destruction. The constitutive over-expression of AtHKT1 that helps maintain a healthy K(+) status while reducing Na(+) toxicity may serve as a possible mechanism in maximizing productivity of tobacco under salt stress. Nature Publishing Group UK 2018-11-08 /pmc/articles/PMC6224463/ /pubmed/30410009 http://dx.doi.org/10.1038/s41598-018-34660-9 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Wang, Li Liu, Yuhui Feng, Shoujiang Wang, Zhuoyu Zhang, Jinwen Zhang, Junlian Wang, Di Gan, Yantai AtHKT1 gene regulating K(+) state in whole plant improves salt tolerance in transgenic tobacco plants |
title | AtHKT1 gene regulating K(+) state in whole plant improves salt tolerance in transgenic tobacco plants |
title_full | AtHKT1 gene regulating K(+) state in whole plant improves salt tolerance in transgenic tobacco plants |
title_fullStr | AtHKT1 gene regulating K(+) state in whole plant improves salt tolerance in transgenic tobacco plants |
title_full_unstemmed | AtHKT1 gene regulating K(+) state in whole plant improves salt tolerance in transgenic tobacco plants |
title_short | AtHKT1 gene regulating K(+) state in whole plant improves salt tolerance in transgenic tobacco plants |
title_sort | athkt1 gene regulating k(+) state in whole plant improves salt tolerance in transgenic tobacco plants |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6224463/ https://www.ncbi.nlm.nih.gov/pubmed/30410009 http://dx.doi.org/10.1038/s41598-018-34660-9 |
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