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Atmospheric CO(2) Alters Resistance of Arabidopsis to Pseudomonas syringae by Affecting Abscisic Acid Accumulation and Stomatal Responsiveness to Coronatine
Atmospheric CO(2) influences plant growth and stomatal aperture. Effects of high or low CO(2) levels on plant disease resistance are less well understood. Here, resistance of Arabidopsis thaliana against the foliar pathogen Pseudomonas syringae pv. tomato DC3000 (Pst) was investigated at three diffe...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5432532/ https://www.ncbi.nlm.nih.gov/pubmed/28559899 http://dx.doi.org/10.3389/fpls.2017.00700 |
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author | Zhou, Yeling Vroegop-Vos, Irene Schuurink, Robert C. Pieterse, Corné M. J. Van Wees, Saskia C. M. |
author_facet | Zhou, Yeling Vroegop-Vos, Irene Schuurink, Robert C. Pieterse, Corné M. J. Van Wees, Saskia C. M. |
author_sort | Zhou, Yeling |
collection | PubMed |
description | Atmospheric CO(2) influences plant growth and stomatal aperture. Effects of high or low CO(2) levels on plant disease resistance are less well understood. Here, resistance of Arabidopsis thaliana against the foliar pathogen Pseudomonas syringae pv. tomato DC3000 (Pst) was investigated at three different CO(2) levels: high (800 ppm), ambient (450 ppm), and low (150 ppm). Under all conditions tested, infection by Pst resulted in stomatal closure within 1 h after inoculation. However, subsequent stomatal reopening at 4 h, triggered by the virulence factor coronatine (COR), occurred only at ambient and high CO(2), but not at low CO(2). Moreover, infection by Pst was reduced at low CO(2) to the same extent as infection by mutant Pst cor(-). Under all CO(2) conditions, the ABA mutants aba2-1 and abi1-1 were as resistant to Pst as wild-type plants under low CO(2), which contained less ABA. Moreover, stomatal reopening mediated by COR was dependent on ABA. Our results suggest that reduced ABA levels at low CO(2) contribute to the observed enhanced resistance to Pst by deregulation of virulence responses. This implies that enhanced ABA levels at increasing CO(2) levels may have a role in weakening plant defense. |
format | Online Article Text |
id | pubmed-5432532 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-54325322017-05-30 Atmospheric CO(2) Alters Resistance of Arabidopsis to Pseudomonas syringae by Affecting Abscisic Acid Accumulation and Stomatal Responsiveness to Coronatine Zhou, Yeling Vroegop-Vos, Irene Schuurink, Robert C. Pieterse, Corné M. J. Van Wees, Saskia C. M. Front Plant Sci Plant Science Atmospheric CO(2) influences plant growth and stomatal aperture. Effects of high or low CO(2) levels on plant disease resistance are less well understood. Here, resistance of Arabidopsis thaliana against the foliar pathogen Pseudomonas syringae pv. tomato DC3000 (Pst) was investigated at three different CO(2) levels: high (800 ppm), ambient (450 ppm), and low (150 ppm). Under all conditions tested, infection by Pst resulted in stomatal closure within 1 h after inoculation. However, subsequent stomatal reopening at 4 h, triggered by the virulence factor coronatine (COR), occurred only at ambient and high CO(2), but not at low CO(2). Moreover, infection by Pst was reduced at low CO(2) to the same extent as infection by mutant Pst cor(-). Under all CO(2) conditions, the ABA mutants aba2-1 and abi1-1 were as resistant to Pst as wild-type plants under low CO(2), which contained less ABA. Moreover, stomatal reopening mediated by COR was dependent on ABA. Our results suggest that reduced ABA levels at low CO(2) contribute to the observed enhanced resistance to Pst by deregulation of virulence responses. This implies that enhanced ABA levels at increasing CO(2) levels may have a role in weakening plant defense. Frontiers Media S.A. 2017-05-16 /pmc/articles/PMC5432532/ /pubmed/28559899 http://dx.doi.org/10.3389/fpls.2017.00700 Text en Copyright © 2017 Zhou, Vroegop-Vos, Schuurink, Pieterse and Van Wees. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Plant Science Zhou, Yeling Vroegop-Vos, Irene Schuurink, Robert C. Pieterse, Corné M. J. Van Wees, Saskia C. M. Atmospheric CO(2) Alters Resistance of Arabidopsis to Pseudomonas syringae by Affecting Abscisic Acid Accumulation and Stomatal Responsiveness to Coronatine |
title | Atmospheric CO(2) Alters Resistance of Arabidopsis to Pseudomonas syringae by Affecting Abscisic Acid Accumulation and Stomatal Responsiveness to Coronatine |
title_full | Atmospheric CO(2) Alters Resistance of Arabidopsis to Pseudomonas syringae by Affecting Abscisic Acid Accumulation and Stomatal Responsiveness to Coronatine |
title_fullStr | Atmospheric CO(2) Alters Resistance of Arabidopsis to Pseudomonas syringae by Affecting Abscisic Acid Accumulation and Stomatal Responsiveness to Coronatine |
title_full_unstemmed | Atmospheric CO(2) Alters Resistance of Arabidopsis to Pseudomonas syringae by Affecting Abscisic Acid Accumulation and Stomatal Responsiveness to Coronatine |
title_short | Atmospheric CO(2) Alters Resistance of Arabidopsis to Pseudomonas syringae by Affecting Abscisic Acid Accumulation and Stomatal Responsiveness to Coronatine |
title_sort | atmospheric co(2) alters resistance of arabidopsis to pseudomonas syringae by affecting abscisic acid accumulation and stomatal responsiveness to coronatine |
topic | Plant Science |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5432532/ https://www.ncbi.nlm.nih.gov/pubmed/28559899 http://dx.doi.org/10.3389/fpls.2017.00700 |
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