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Fusaric acid induced cell death and changes in oxidative metabolism of Solanum lycopersicum L
BACKGROUND: Fusaric acid (FA) has been shown to stimulate the rapid development of disease symptoms, such as necrosis and foliar desiccation. In this study, we have evaluated the phytotoxicity of FA on tomato plants (Solanum lycopersicum L.). FA induced necrotic lesions in detached leaves, which are...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Berlin Heidelberg
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5432760/ https://www.ncbi.nlm.nih.gov/pubmed/28510945 http://dx.doi.org/10.1186/s40529-014-0066-2 |
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author | Singh, Vivek Kumar Upadhyay, Ram Sanmukh |
author_facet | Singh, Vivek Kumar Upadhyay, Ram Sanmukh |
author_sort | Singh, Vivek Kumar |
collection | PubMed |
description | BACKGROUND: Fusaric acid (FA) has been shown to stimulate the rapid development of disease symptoms, such as necrosis and foliar desiccation. In this study, we have evaluated the phytotoxicity of FA on tomato plants (Solanum lycopersicum L.). FA induced necrotic lesions in detached leaves, which are reminiscent of hypersensitive response (HR) lesions induced by plant-pathogen interactions and other abiotic stress factors. RESULTS: FA-treated tomato leaves exhibited visible necrotic lesion as a result of cell death which was evident by Evans blue staining, enhanced reactive oxygen species (ROS) levels and DNA degradation. Changes in the generation of O(2)(.-) and H(2)O(2) as well as the activities of superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) were examined in FA-treated tomato leaves. It was observed that FA exposure stimulated oxidative burst in the leaves, resulting in a lasting activation of O(2)(.-) and H(2)O(2) production. After first day of FA application, the H(2)O(2) scavenging enzymes CAT and APX showed a strong activity decrease followed by gradual recovery to the control level after 2 and 3 days. CONCLUSION: A concomitant increase in ROS production, the down regulation of antioxidative enzymes activities and upregulation of lipid peroxidation were crucial for the onset of cell death. These results suggested that FA-induced damage might result from ROS pathways. Thus, our experiments provide a useful model plant system for research on FA-induced plant cell death. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s40529-014-0066-2) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5432760 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-54327602017-05-31 Fusaric acid induced cell death and changes in oxidative metabolism of Solanum lycopersicum L Singh, Vivek Kumar Upadhyay, Ram Sanmukh Bot Stud Research BACKGROUND: Fusaric acid (FA) has been shown to stimulate the rapid development of disease symptoms, such as necrosis and foliar desiccation. In this study, we have evaluated the phytotoxicity of FA on tomato plants (Solanum lycopersicum L.). FA induced necrotic lesions in detached leaves, which are reminiscent of hypersensitive response (HR) lesions induced by plant-pathogen interactions and other abiotic stress factors. RESULTS: FA-treated tomato leaves exhibited visible necrotic lesion as a result of cell death which was evident by Evans blue staining, enhanced reactive oxygen species (ROS) levels and DNA degradation. Changes in the generation of O(2)(.-) and H(2)O(2) as well as the activities of superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) were examined in FA-treated tomato leaves. It was observed that FA exposure stimulated oxidative burst in the leaves, resulting in a lasting activation of O(2)(.-) and H(2)O(2) production. After first day of FA application, the H(2)O(2) scavenging enzymes CAT and APX showed a strong activity decrease followed by gradual recovery to the control level after 2 and 3 days. CONCLUSION: A concomitant increase in ROS production, the down regulation of antioxidative enzymes activities and upregulation of lipid peroxidation were crucial for the onset of cell death. These results suggested that FA-induced damage might result from ROS pathways. Thus, our experiments provide a useful model plant system for research on FA-induced plant cell death. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s40529-014-0066-2) contains supplementary material, which is available to authorized users. Springer Berlin Heidelberg 2014-08-27 /pmc/articles/PMC5432760/ /pubmed/28510945 http://dx.doi.org/10.1186/s40529-014-0066-2 Text en © Singh and Upadhyay; licensee Springer 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. |
spellingShingle | Research Singh, Vivek Kumar Upadhyay, Ram Sanmukh Fusaric acid induced cell death and changes in oxidative metabolism of Solanum lycopersicum L |
title | Fusaric acid induced cell death and changes in oxidative metabolism of Solanum lycopersicum L |
title_full | Fusaric acid induced cell death and changes in oxidative metabolism of Solanum lycopersicum L |
title_fullStr | Fusaric acid induced cell death and changes in oxidative metabolism of Solanum lycopersicum L |
title_full_unstemmed | Fusaric acid induced cell death and changes in oxidative metabolism of Solanum lycopersicum L |
title_short | Fusaric acid induced cell death and changes in oxidative metabolism of Solanum lycopersicum L |
title_sort | fusaric acid induced cell death and changes in oxidative metabolism of solanum lycopersicum l |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5432760/ https://www.ncbi.nlm.nih.gov/pubmed/28510945 http://dx.doi.org/10.1186/s40529-014-0066-2 |
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