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The modulation of acetic acid pathway genes in Arabidopsis improves survival under drought stress

The Arabidopsis histone deacetylase 6 (HDA6) mutant exhibits increased tolerance to drought stress by negatively regulating the expression of ALDH2B7 and PDC1. Therefore, it was logical to determine if transgenic Arabidopsis plants expressing PDC1 or ALDH2B7 using a suitable promoter would also exhi...

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Autores principales: Rasheed, Sultana, Bashir, Khurram, Kim, Jong-Myong, Ando, Marina, Tanaka, Maho, Seki, Motoaki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5959891/
https://www.ncbi.nlm.nih.gov/pubmed/29777132
http://dx.doi.org/10.1038/s41598-018-26103-2
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author Rasheed, Sultana
Bashir, Khurram
Kim, Jong-Myong
Ando, Marina
Tanaka, Maho
Seki, Motoaki
author_facet Rasheed, Sultana
Bashir, Khurram
Kim, Jong-Myong
Ando, Marina
Tanaka, Maho
Seki, Motoaki
author_sort Rasheed, Sultana
collection PubMed
description The Arabidopsis histone deacetylase 6 (HDA6) mutant exhibits increased tolerance to drought stress by negatively regulating the expression of ALDH2B7 and PDC1. Therefore, it was logical to determine if transgenic Arabidopsis plants expressing PDC1 or ALDH2B7 using a suitable promoter would also exhibit tolerance to drought stress. An analysis of published microarray data indicated the up-regulation of the TSPO gene, which encodes an outer membrane tryptophan-rich sensory protein (TSPO), by drought stress. RT-qPCR, as well as GUS analysis of the promoter, confirmed the up-regulation of TSPO by drought stress in Arabidopsis roots and shoots. Thus, the TSPO promoter was used to drive drought-responsive expression of ALDH2B7 and PDC1. RT-qPCR analysis confirmed that the expression of PDC1 and ALDH2B7 was up-regulated, relative to WT plants, by drought stress in homozygous pTSPO-PDC1 and pTSPO-ALDH2B7 plant lines. pTSPO-ALDH2B7 and pTSPO-PDC1 transgenic lines showed prolonged survival under drought stress. Microarray analyses revealed transcriptomic changes related to metabolism in pTSPO-PDC1 plants, indicating that selective regulation of metabolism may occur; resulting in the acquisition of drought stress tolerance. These results confirmed that TSPO promoter can be used to elevate the expression of acetic acid biosynthesis pathway genes; ensuring prolonged survival under drought stress in Arabidopsis.
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spelling pubmed-59598912018-05-24 The modulation of acetic acid pathway genes in Arabidopsis improves survival under drought stress Rasheed, Sultana Bashir, Khurram Kim, Jong-Myong Ando, Marina Tanaka, Maho Seki, Motoaki Sci Rep Article The Arabidopsis histone deacetylase 6 (HDA6) mutant exhibits increased tolerance to drought stress by negatively regulating the expression of ALDH2B7 and PDC1. Therefore, it was logical to determine if transgenic Arabidopsis plants expressing PDC1 or ALDH2B7 using a suitable promoter would also exhibit tolerance to drought stress. An analysis of published microarray data indicated the up-regulation of the TSPO gene, which encodes an outer membrane tryptophan-rich sensory protein (TSPO), by drought stress. RT-qPCR, as well as GUS analysis of the promoter, confirmed the up-regulation of TSPO by drought stress in Arabidopsis roots and shoots. Thus, the TSPO promoter was used to drive drought-responsive expression of ALDH2B7 and PDC1. RT-qPCR analysis confirmed that the expression of PDC1 and ALDH2B7 was up-regulated, relative to WT plants, by drought stress in homozygous pTSPO-PDC1 and pTSPO-ALDH2B7 plant lines. pTSPO-ALDH2B7 and pTSPO-PDC1 transgenic lines showed prolonged survival under drought stress. Microarray analyses revealed transcriptomic changes related to metabolism in pTSPO-PDC1 plants, indicating that selective regulation of metabolism may occur; resulting in the acquisition of drought stress tolerance. These results confirmed that TSPO promoter can be used to elevate the expression of acetic acid biosynthesis pathway genes; ensuring prolonged survival under drought stress in Arabidopsis. Nature Publishing Group UK 2018-05-18 /pmc/articles/PMC5959891/ /pubmed/29777132 http://dx.doi.org/10.1038/s41598-018-26103-2 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
Rasheed, Sultana
Bashir, Khurram
Kim, Jong-Myong
Ando, Marina
Tanaka, Maho
Seki, Motoaki
The modulation of acetic acid pathway genes in Arabidopsis improves survival under drought stress
title The modulation of acetic acid pathway genes in Arabidopsis improves survival under drought stress
title_full The modulation of acetic acid pathway genes in Arabidopsis improves survival under drought stress
title_fullStr The modulation of acetic acid pathway genes in Arabidopsis improves survival under drought stress
title_full_unstemmed The modulation of acetic acid pathway genes in Arabidopsis improves survival under drought stress
title_short The modulation of acetic acid pathway genes in Arabidopsis improves survival under drought stress
title_sort modulation of acetic acid pathway genes in arabidopsis improves survival under drought stress
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5959891/
https://www.ncbi.nlm.nih.gov/pubmed/29777132
http://dx.doi.org/10.1038/s41598-018-26103-2
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