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ERF-VII transcription factors induce ethanol fermentation in response to amino acid biosynthesis-inhibiting herbicides
Herbicides inhibiting either aromatic or branched-chain amino acid biosynthesis trigger similar physiological responses in plants, despite their different mechanism of action. Both types of herbicides are known to activate ethanol fermentation by inducing the expression of fermentative genes; howeve...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6812701/ https://www.ncbi.nlm.nih.gov/pubmed/31384925 http://dx.doi.org/10.1093/jxb/erz355 |
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author | Gil-Monreal, Miriam Giuntoli, Beatrice Zabalza, Ana Licausi, Francesco Royuela, Mercedes |
author_facet | Gil-Monreal, Miriam Giuntoli, Beatrice Zabalza, Ana Licausi, Francesco Royuela, Mercedes |
author_sort | Gil-Monreal, Miriam |
collection | PubMed |
description | Herbicides inhibiting either aromatic or branched-chain amino acid biosynthesis trigger similar physiological responses in plants, despite their different mechanism of action. Both types of herbicides are known to activate ethanol fermentation by inducing the expression of fermentative genes; however, the mechanism of such transcriptional regulation has not been investigated so far. In plants exposed to low-oxygen conditions, ethanol fermentation is transcriptionally controlled by the ethylene response factors-VII (ERF-VIIs), whose stability is controlled in an oxygen-dependent manner by the Cys-Arg branch of the N-degron pathway. In this study, we investigated the role of ERF-VIIs in the regulation of the ethanol fermentation pathway in herbicide-treated Arabidopsis plants grown under aerobic conditions. Our results demonstrate that these transcriptional regulators are stabilized in response to herbicide treatment and are required for ethanol fermentation in these conditions. We also observed that mutants with reduced fermentative potential exhibit higher sensitivity to herbicide treatments, thus revealing the existence of a mechanism that mimics oxygen deprivation to activate metabolic pathways that enhance herbicide tolerance. We speculate that this signaling pathway may represent a potential target in agriculture to affect tolerance to herbicides that inhibit amino acid biosynthesis. |
format | Online Article Text |
id | pubmed-6812701 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-68127012019-10-28 ERF-VII transcription factors induce ethanol fermentation in response to amino acid biosynthesis-inhibiting herbicides Gil-Monreal, Miriam Giuntoli, Beatrice Zabalza, Ana Licausi, Francesco Royuela, Mercedes J Exp Bot Research Papers Herbicides inhibiting either aromatic or branched-chain amino acid biosynthesis trigger similar physiological responses in plants, despite their different mechanism of action. Both types of herbicides are known to activate ethanol fermentation by inducing the expression of fermentative genes; however, the mechanism of such transcriptional regulation has not been investigated so far. In plants exposed to low-oxygen conditions, ethanol fermentation is transcriptionally controlled by the ethylene response factors-VII (ERF-VIIs), whose stability is controlled in an oxygen-dependent manner by the Cys-Arg branch of the N-degron pathway. In this study, we investigated the role of ERF-VIIs in the regulation of the ethanol fermentation pathway in herbicide-treated Arabidopsis plants grown under aerobic conditions. Our results demonstrate that these transcriptional regulators are stabilized in response to herbicide treatment and are required for ethanol fermentation in these conditions. We also observed that mutants with reduced fermentative potential exhibit higher sensitivity to herbicide treatments, thus revealing the existence of a mechanism that mimics oxygen deprivation to activate metabolic pathways that enhance herbicide tolerance. We speculate that this signaling pathway may represent a potential target in agriculture to affect tolerance to herbicides that inhibit amino acid biosynthesis. Oxford University Press 2019-10-15 2019-08-06 /pmc/articles/PMC6812701/ /pubmed/31384925 http://dx.doi.org/10.1093/jxb/erz355 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 Gil-Monreal, Miriam Giuntoli, Beatrice Zabalza, Ana Licausi, Francesco Royuela, Mercedes ERF-VII transcription factors induce ethanol fermentation in response to amino acid biosynthesis-inhibiting herbicides |
title | ERF-VII transcription factors induce ethanol fermentation in response to amino acid biosynthesis-inhibiting herbicides |
title_full | ERF-VII transcription factors induce ethanol fermentation in response to amino acid biosynthesis-inhibiting herbicides |
title_fullStr | ERF-VII transcription factors induce ethanol fermentation in response to amino acid biosynthesis-inhibiting herbicides |
title_full_unstemmed | ERF-VII transcription factors induce ethanol fermentation in response to amino acid biosynthesis-inhibiting herbicides |
title_short | ERF-VII transcription factors induce ethanol fermentation in response to amino acid biosynthesis-inhibiting herbicides |
title_sort | erf-vii transcription factors induce ethanol fermentation in response to amino acid biosynthesis-inhibiting herbicides |
topic | Research Papers |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6812701/ https://www.ncbi.nlm.nih.gov/pubmed/31384925 http://dx.doi.org/10.1093/jxb/erz355 |
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