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Enhanced accumulation of gibberellins rendered rice seedlings sensitive to ammonium toxicity
Ammonium (NH(4)(+)) phytotoxicity is a worldwide phenomenon, but the primary toxic mechanisms are still controversial. In the present study, we investigated the physiological function of gibberellins (GAs) in the response of rice plants to NH(4)(+) toxicity and polyamine accumulation using GA biosyn...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031073/ https://www.ncbi.nlm.nih.gov/pubmed/31667503 http://dx.doi.org/10.1093/jxb/erz492 |
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author | Wang, Baolan Wei, Haifang Zhang, Hui Zhang, Wen-Hao |
author_facet | Wang, Baolan Wei, Haifang Zhang, Hui Zhang, Wen-Hao |
author_sort | Wang, Baolan |
collection | PubMed |
description | Ammonium (NH(4)(+)) phytotoxicity is a worldwide phenomenon, but the primary toxic mechanisms are still controversial. In the present study, we investigated the physiological function of gibberellins (GAs) in the response of rice plants to NH(4)(+) toxicity and polyamine accumulation using GA biosynthesis-related rice mutants. Exposure to NH(4)(+) significantly decreased GA(4) production in shoots of wild-type (WT) plants. Both exogenous GA application to the WT and increases in endogenous GA levels in eui1 mutants rendered them more sensitive to NH(4)(+) toxicity. In contrast, growth of sd1 GA-deficient mutants was more tolerant to NH(4)(+) toxicity than that of their WT counterparts. The role of polyamines in GA-mediated NH(4)(+) toxicity was evaluated using WT rice plants and their GA-related mutants. The eui1 mutants with GA overproduction displayed a higher endogenous putrescine (Put) accumulation than WT plants, leading to an enhanced Put/[spermidine (Spd)+spermine (Spm)] ratio in their shoots. In contrast, mutation of the SD1 gene encoding a defective enzyme in GA biosynthesis resulted in a significant increase in Spd and Spm production, and reduction in the Put/(Spd+Spm) ratio when exposed to a high NH(4)(+) medium. Exogenous application of Put exacerbated symptoms associated with NH(4)(+) toxicity in rice shoots, while the symptoms were alleviated by an inhibitor of Put biosynthesis. These findings highlight the involvement of GAs in NH(4)(+) toxicity, and that GA-induced Put accumulation is responsible for the increased sensitivity to NH(4)(+) toxicity in rice plants. |
format | Online Article Text |
id | pubmed-7031073 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-70310732020-02-25 Enhanced accumulation of gibberellins rendered rice seedlings sensitive to ammonium toxicity Wang, Baolan Wei, Haifang Zhang, Hui Zhang, Wen-Hao J Exp Bot Research Papers Ammonium (NH(4)(+)) phytotoxicity is a worldwide phenomenon, but the primary toxic mechanisms are still controversial. In the present study, we investigated the physiological function of gibberellins (GAs) in the response of rice plants to NH(4)(+) toxicity and polyamine accumulation using GA biosynthesis-related rice mutants. Exposure to NH(4)(+) significantly decreased GA(4) production in shoots of wild-type (WT) plants. Both exogenous GA application to the WT and increases in endogenous GA levels in eui1 mutants rendered them more sensitive to NH(4)(+) toxicity. In contrast, growth of sd1 GA-deficient mutants was more tolerant to NH(4)(+) toxicity than that of their WT counterparts. The role of polyamines in GA-mediated NH(4)(+) toxicity was evaluated using WT rice plants and their GA-related mutants. The eui1 mutants with GA overproduction displayed a higher endogenous putrescine (Put) accumulation than WT plants, leading to an enhanced Put/[spermidine (Spd)+spermine (Spm)] ratio in their shoots. In contrast, mutation of the SD1 gene encoding a defective enzyme in GA biosynthesis resulted in a significant increase in Spd and Spm production, and reduction in the Put/(Spd+Spm) ratio when exposed to a high NH(4)(+) medium. Exogenous application of Put exacerbated symptoms associated with NH(4)(+) toxicity in rice shoots, while the symptoms were alleviated by an inhibitor of Put biosynthesis. These findings highlight the involvement of GAs in NH(4)(+) toxicity, and that GA-induced Put accumulation is responsible for the increased sensitivity to NH(4)(+) toxicity in rice plants. Oxford University Press 2020-02-07 2019-10-31 /pmc/articles/PMC7031073/ /pubmed/31667503 http://dx.doi.org/10.1093/jxb/erz492 Text en © The Author(s) 2019. Published by Oxford University Press on behalf of the Society for Experimental Biology. http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Research Papers Wang, Baolan Wei, Haifang Zhang, Hui Zhang, Wen-Hao Enhanced accumulation of gibberellins rendered rice seedlings sensitive to ammonium toxicity |
title | Enhanced accumulation of gibberellins rendered rice seedlings sensitive to ammonium toxicity |
title_full | Enhanced accumulation of gibberellins rendered rice seedlings sensitive to ammonium toxicity |
title_fullStr | Enhanced accumulation of gibberellins rendered rice seedlings sensitive to ammonium toxicity |
title_full_unstemmed | Enhanced accumulation of gibberellins rendered rice seedlings sensitive to ammonium toxicity |
title_short | Enhanced accumulation of gibberellins rendered rice seedlings sensitive to ammonium toxicity |
title_sort | enhanced accumulation of gibberellins rendered rice seedlings sensitive to ammonium toxicity |
topic | Research Papers |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031073/ https://www.ncbi.nlm.nih.gov/pubmed/31667503 http://dx.doi.org/10.1093/jxb/erz492 |
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