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Ascorbic acid accumulates as a defense response to Turnip mosaic virus in resistant Brassica rapa cultivars

We initially observed that Brassica rapa cultivars containing the Turnip mosaic virus (TuMV) resistance gene, Rnt1-1, accumulated a high level of endogenous ascorbic acid (AS) and dehydroascobic acid (DHA) when infected with TuMV. We here hypothesized a possible contribution of an elevated level of...

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Autores principales: Fujiwara, Ayaka, Togawa, Satoko, Hikawa, Takahiro, Matsuura, Hideyuki, Masuta, Chikara, Inukai, Tsuyoshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5301938/
https://www.ncbi.nlm.nih.gov/pubmed/27255930
http://dx.doi.org/10.1093/jxb/erw223
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author Fujiwara, Ayaka
Togawa, Satoko
Hikawa, Takahiro
Matsuura, Hideyuki
Masuta, Chikara
Inukai, Tsuyoshi
author_facet Fujiwara, Ayaka
Togawa, Satoko
Hikawa, Takahiro
Matsuura, Hideyuki
Masuta, Chikara
Inukai, Tsuyoshi
author_sort Fujiwara, Ayaka
collection PubMed
description We initially observed that Brassica rapa cultivars containing the Turnip mosaic virus (TuMV) resistance gene, Rnt1-1, accumulated a high level of endogenous ascorbic acid (AS) and dehydroascobic acid (DHA) when infected with TuMV. We here hypothesized a possible contribution of an elevated level of AS+DHA (TAA) to the Rnt1-1-mediated resistance, and conducted a series of experiments using B. rapa and Arabidopsis plants. The application of l-galactose (the key substrate in AS synthesis) to a susceptible cultivar could increase the TAA level ~2-fold, and simultaneously lead to some degree of enhanced viral resistance. To confirm some positive correlation between TAA levels and viral resistance, we analyzed two Arabidopsis knockout mutants (ao and vtc1) in the AS pathways; the TAA levels were significantly increased and decreased in ao and vtc1 plants, respectively. While the ao plants showed enhanced resistance to TuMV, vtc1 plants were more susceptible than the control, supporting our hypothesis. When we analyzed the expression profiles of the genes involved in the AS pathways upon TuMV infection, we found that the observed TAA increase was mainly brought about by the reduction of AS oxidation and activation of AS recycling. We then investigated the secondary signals that regulate endogenous TAA levels in response to viral infection, and found that jasmonic acid (JA) might play an important role in TAA accumulation. In conclusion, we reason that the elevated TAA accumulation in B. rapa plants would be at least partly mediated by the JA-dependent signaling pathway and may significantly contribute to viral resistance.
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spelling pubmed-53019382017-02-16 Ascorbic acid accumulates as a defense response to Turnip mosaic virus in resistant Brassica rapa cultivars Fujiwara, Ayaka Togawa, Satoko Hikawa, Takahiro Matsuura, Hideyuki Masuta, Chikara Inukai, Tsuyoshi J Exp Bot Research Paper We initially observed that Brassica rapa cultivars containing the Turnip mosaic virus (TuMV) resistance gene, Rnt1-1, accumulated a high level of endogenous ascorbic acid (AS) and dehydroascobic acid (DHA) when infected with TuMV. We here hypothesized a possible contribution of an elevated level of AS+DHA (TAA) to the Rnt1-1-mediated resistance, and conducted a series of experiments using B. rapa and Arabidopsis plants. The application of l-galactose (the key substrate in AS synthesis) to a susceptible cultivar could increase the TAA level ~2-fold, and simultaneously lead to some degree of enhanced viral resistance. To confirm some positive correlation between TAA levels and viral resistance, we analyzed two Arabidopsis knockout mutants (ao and vtc1) in the AS pathways; the TAA levels were significantly increased and decreased in ao and vtc1 plants, respectively. While the ao plants showed enhanced resistance to TuMV, vtc1 plants were more susceptible than the control, supporting our hypothesis. When we analyzed the expression profiles of the genes involved in the AS pathways upon TuMV infection, we found that the observed TAA increase was mainly brought about by the reduction of AS oxidation and activation of AS recycling. We then investigated the secondary signals that regulate endogenous TAA levels in response to viral infection, and found that jasmonic acid (JA) might play an important role in TAA accumulation. In conclusion, we reason that the elevated TAA accumulation in B. rapa plants would be at least partly mediated by the JA-dependent signaling pathway and may significantly contribute to viral resistance. Oxford University Press 2016-07 2016-06-02 /pmc/articles/PMC5301938/ /pubmed/27255930 http://dx.doi.org/10.1093/jxb/erw223 Text en © The Author 2016. Published by Oxford University Press on behalf of the Society for Experimental Biology. http://creativecommons.org/licenses/by/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Fujiwara, Ayaka
Togawa, Satoko
Hikawa, Takahiro
Matsuura, Hideyuki
Masuta, Chikara
Inukai, Tsuyoshi
Ascorbic acid accumulates as a defense response to Turnip mosaic virus in resistant Brassica rapa cultivars
title Ascorbic acid accumulates as a defense response to Turnip mosaic virus in resistant Brassica rapa cultivars
title_full Ascorbic acid accumulates as a defense response to Turnip mosaic virus in resistant Brassica rapa cultivars
title_fullStr Ascorbic acid accumulates as a defense response to Turnip mosaic virus in resistant Brassica rapa cultivars
title_full_unstemmed Ascorbic acid accumulates as a defense response to Turnip mosaic virus in resistant Brassica rapa cultivars
title_short Ascorbic acid accumulates as a defense response to Turnip mosaic virus in resistant Brassica rapa cultivars
title_sort ascorbic acid accumulates as a defense response to turnip mosaic virus in resistant brassica rapa cultivars
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5301938/
https://www.ncbi.nlm.nih.gov/pubmed/27255930
http://dx.doi.org/10.1093/jxb/erw223
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