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The plant defensin gene AtPDF2.1 mediates ammonium metabolism by regulating glutamine synthetase activity in Arabidopsis thaliana
BACKGROUND: In plants, ammonium metabolism is particularly important for converting absorbed nitrogen into amino acids. However, the molecular mechanism underlying this conversion remains largely unknown. RESULTS: Using wild type Arabidopsis thaliana (Col-0) and AtPDF2.1 mutants (pdf2.1–1 and pdf2.1...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6916093/ https://www.ncbi.nlm.nih.gov/pubmed/31842759 http://dx.doi.org/10.1186/s12870-019-2183-2 |
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author | Yao, Junyue Luo, Jin-Song Xiao, Yan Zhang, Zhenhua |
author_facet | Yao, Junyue Luo, Jin-Song Xiao, Yan Zhang, Zhenhua |
author_sort | Yao, Junyue |
collection | PubMed |
description | BACKGROUND: In plants, ammonium metabolism is particularly important for converting absorbed nitrogen into amino acids. However, the molecular mechanism underlying this conversion remains largely unknown. RESULTS: Using wild type Arabidopsis thaliana (Col-0) and AtPDF2.1 mutants (pdf2.1–1 and pdf2.1–2), we found that the small cysteine-rich peptide AtPDF2.1, a plant defensin, is involved in regulating ammonium metabolism in the shoot. Ammonium significantly induced the expression of AtPDF2.1 in the shoot and root, particularly in root xylem vascular bundles, as demonstrated by histochemical analysis. Subcellular localization analysis revealed that AtPDF2.1 was localized to the cell wall. Ammonium concentration was higher in the shoot of mutants than in the shoot of Col-0, but no differences were found for total nitrogen content, root ammonium concentration, and the expression of the ammonium transporter gene AtAMT2.1. The activity of glutamine synthetase was significantly decreased in mutants, and the glutamine synthetase family genes GLN1.3 and GLN1.5 were significantly downregulated in mutants compared to Col-0. The activity of nitrate reductase showed no difference between mutants and Col-0. CONCLUSIONS: Overall, these data suggest that AtPDF2.1 affects ammonium metabolism by regulating the expression of GLN1.3 and GLN1.5 through a yet unidentified mechanism. |
format | Online Article Text |
id | pubmed-6916093 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-69160932019-12-30 The plant defensin gene AtPDF2.1 mediates ammonium metabolism by regulating glutamine synthetase activity in Arabidopsis thaliana Yao, Junyue Luo, Jin-Song Xiao, Yan Zhang, Zhenhua BMC Plant Biol Research Article BACKGROUND: In plants, ammonium metabolism is particularly important for converting absorbed nitrogen into amino acids. However, the molecular mechanism underlying this conversion remains largely unknown. RESULTS: Using wild type Arabidopsis thaliana (Col-0) and AtPDF2.1 mutants (pdf2.1–1 and pdf2.1–2), we found that the small cysteine-rich peptide AtPDF2.1, a plant defensin, is involved in regulating ammonium metabolism in the shoot. Ammonium significantly induced the expression of AtPDF2.1 in the shoot and root, particularly in root xylem vascular bundles, as demonstrated by histochemical analysis. Subcellular localization analysis revealed that AtPDF2.1 was localized to the cell wall. Ammonium concentration was higher in the shoot of mutants than in the shoot of Col-0, but no differences were found for total nitrogen content, root ammonium concentration, and the expression of the ammonium transporter gene AtAMT2.1. The activity of glutamine synthetase was significantly decreased in mutants, and the glutamine synthetase family genes GLN1.3 and GLN1.5 were significantly downregulated in mutants compared to Col-0. The activity of nitrate reductase showed no difference between mutants and Col-0. CONCLUSIONS: Overall, these data suggest that AtPDF2.1 affects ammonium metabolism by regulating the expression of GLN1.3 and GLN1.5 through a yet unidentified mechanism. BioMed Central 2019-12-16 /pmc/articles/PMC6916093/ /pubmed/31842759 http://dx.doi.org/10.1186/s12870-019-2183-2 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 Yao, Junyue Luo, Jin-Song Xiao, Yan Zhang, Zhenhua The plant defensin gene AtPDF2.1 mediates ammonium metabolism by regulating glutamine synthetase activity in Arabidopsis thaliana |
title | The plant defensin gene AtPDF2.1 mediates ammonium metabolism by regulating glutamine synthetase activity in Arabidopsis thaliana |
title_full | The plant defensin gene AtPDF2.1 mediates ammonium metabolism by regulating glutamine synthetase activity in Arabidopsis thaliana |
title_fullStr | The plant defensin gene AtPDF2.1 mediates ammonium metabolism by regulating glutamine synthetase activity in Arabidopsis thaliana |
title_full_unstemmed | The plant defensin gene AtPDF2.1 mediates ammonium metabolism by regulating glutamine synthetase activity in Arabidopsis thaliana |
title_short | The plant defensin gene AtPDF2.1 mediates ammonium metabolism by regulating glutamine synthetase activity in Arabidopsis thaliana |
title_sort | plant defensin gene atpdf2.1 mediates ammonium metabolism by regulating glutamine synthetase activity in arabidopsis thaliana |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6916093/ https://www.ncbi.nlm.nih.gov/pubmed/31842759 http://dx.doi.org/10.1186/s12870-019-2183-2 |
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