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GsMAS1 Encoding a MADS-box Transcription Factor Enhances the Tolerance to Aluminum Stress in Arabidopsis thaliana
The MADS-box transcription factors (TFs) are essential in regulating plant growth and development, and conferring abiotic and metal stress resistance. This study aims to investigate GsMAS1 function in conferring tolerance to aluminum stress in Arabidopsis. The GsMAS1 from the wild soybean BW69 line...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139582/ https://www.ncbi.nlm.nih.gov/pubmed/32183485 http://dx.doi.org/10.3390/ijms21062004 |
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author | Zhang, Xiao Li, Lu Yang, Ce Cheng, Yanbo Han, Zhenzhen Cai, Zhandong Nian, Hai Ma, Qibin |
author_facet | Zhang, Xiao Li, Lu Yang, Ce Cheng, Yanbo Han, Zhenzhen Cai, Zhandong Nian, Hai Ma, Qibin |
author_sort | Zhang, Xiao |
collection | PubMed |
description | The MADS-box transcription factors (TFs) are essential in regulating plant growth and development, and conferring abiotic and metal stress resistance. This study aims to investigate GsMAS1 function in conferring tolerance to aluminum stress in Arabidopsis. The GsMAS1 from the wild soybean BW69 line encodes a MADS-box transcription factor in Glycine soja by bioinformatics analysis. The putative GsMAS1 protein was localized in the nucleus. The GsMAS1 gene was rich in soybean roots presenting a constitutive expression pattern and induced by aluminum stress with a concentration-time specific pattern. The analysis of phenotypic observation demonstrated that overexpression of GsMAS1 enhanced the tolerance of Arabidopsis plants to aluminum (Al) stress with larger values of relative root length and higher proline accumulation compared to those of wild type at the AlCl(3) treatments. The genes and/or pathways regulated by GsMAS1 were further investigated under Al stress by qRT-PCR. The results indicated that six genes resistant to Al stress were upregulated, whereas AtALMT1 and STOP2 were significantly activated by Al stress and GsMAS1 overexpression. After treatment of 50 μM AlCl(3), the RNA abundance of AtALMT1 and STOP2 went up to 17-fold and 37-fold than those in wild type, respectively. Whereas the RNA transcripts of AtALMT1 and STOP2 were much higher than those in wild type with over 82% and 67% of relative expression in GsMAS1 transgenic plants, respectively. In short, the results suggest that GsMAS1 may increase resistance to Al toxicity through certain pathways related to Al stress in Arabidopsis. |
format | Online Article Text |
id | pubmed-7139582 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-71395822020-04-10 GsMAS1 Encoding a MADS-box Transcription Factor Enhances the Tolerance to Aluminum Stress in Arabidopsis thaliana Zhang, Xiao Li, Lu Yang, Ce Cheng, Yanbo Han, Zhenzhen Cai, Zhandong Nian, Hai Ma, Qibin Int J Mol Sci Article The MADS-box transcription factors (TFs) are essential in regulating plant growth and development, and conferring abiotic and metal stress resistance. This study aims to investigate GsMAS1 function in conferring tolerance to aluminum stress in Arabidopsis. The GsMAS1 from the wild soybean BW69 line encodes a MADS-box transcription factor in Glycine soja by bioinformatics analysis. The putative GsMAS1 protein was localized in the nucleus. The GsMAS1 gene was rich in soybean roots presenting a constitutive expression pattern and induced by aluminum stress with a concentration-time specific pattern. The analysis of phenotypic observation demonstrated that overexpression of GsMAS1 enhanced the tolerance of Arabidopsis plants to aluminum (Al) stress with larger values of relative root length and higher proline accumulation compared to those of wild type at the AlCl(3) treatments. The genes and/or pathways regulated by GsMAS1 were further investigated under Al stress by qRT-PCR. The results indicated that six genes resistant to Al stress were upregulated, whereas AtALMT1 and STOP2 were significantly activated by Al stress and GsMAS1 overexpression. After treatment of 50 μM AlCl(3), the RNA abundance of AtALMT1 and STOP2 went up to 17-fold and 37-fold than those in wild type, respectively. Whereas the RNA transcripts of AtALMT1 and STOP2 were much higher than those in wild type with over 82% and 67% of relative expression in GsMAS1 transgenic plants, respectively. In short, the results suggest that GsMAS1 may increase resistance to Al toxicity through certain pathways related to Al stress in Arabidopsis. MDPI 2020-03-15 /pmc/articles/PMC7139582/ /pubmed/32183485 http://dx.doi.org/10.3390/ijms21062004 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Zhang, Xiao Li, Lu Yang, Ce Cheng, Yanbo Han, Zhenzhen Cai, Zhandong Nian, Hai Ma, Qibin GsMAS1 Encoding a MADS-box Transcription Factor Enhances the Tolerance to Aluminum Stress in Arabidopsis thaliana |
title | GsMAS1 Encoding a MADS-box Transcription Factor Enhances the Tolerance to Aluminum Stress in Arabidopsis thaliana |
title_full | GsMAS1 Encoding a MADS-box Transcription Factor Enhances the Tolerance to Aluminum Stress in Arabidopsis thaliana |
title_fullStr | GsMAS1 Encoding a MADS-box Transcription Factor Enhances the Tolerance to Aluminum Stress in Arabidopsis thaliana |
title_full_unstemmed | GsMAS1 Encoding a MADS-box Transcription Factor Enhances the Tolerance to Aluminum Stress in Arabidopsis thaliana |
title_short | GsMAS1 Encoding a MADS-box Transcription Factor Enhances the Tolerance to Aluminum Stress in Arabidopsis thaliana |
title_sort | gsmas1 encoding a mads-box transcription factor enhances the tolerance to aluminum stress in arabidopsis thaliana |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139582/ https://www.ncbi.nlm.nih.gov/pubmed/32183485 http://dx.doi.org/10.3390/ijms21062004 |
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