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Jasmonic Acid-Involved OsEDS1 Signaling in Rice-Bacteria Interactions

BACKGROUND: The function of Arabidopsis enhanced disease susceptibility 1 (AtEDS1) and its sequence homologs in other dicots have been extensively studied. However, it is unknown whether rice EDS1 homolog (OsEDS1) plays a role in regulating the rice-pathogen interaction. RESULTS: In this study, a Os...

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Autores principales: Ke, Yinggen, Kang, Yuanrong, Wu, Mengxiao, Liu, Hongbo, Hui, Shugang, Zhang, Qinglu, Li, Xianghua, Xiao, Jinghua, Wang, Shiping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6465387/
https://www.ncbi.nlm.nih.gov/pubmed/30989404
http://dx.doi.org/10.1186/s12284-019-0283-0
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author Ke, Yinggen
Kang, Yuanrong
Wu, Mengxiao
Liu, Hongbo
Hui, Shugang
Zhang, Qinglu
Li, Xianghua
Xiao, Jinghua
Wang, Shiping
author_facet Ke, Yinggen
Kang, Yuanrong
Wu, Mengxiao
Liu, Hongbo
Hui, Shugang
Zhang, Qinglu
Li, Xianghua
Xiao, Jinghua
Wang, Shiping
author_sort Ke, Yinggen
collection PubMed
description BACKGROUND: The function of Arabidopsis enhanced disease susceptibility 1 (AtEDS1) and its sequence homologs in other dicots have been extensively studied. However, it is unknown whether rice EDS1 homolog (OsEDS1) plays a role in regulating the rice-pathogen interaction. RESULTS: In this study, a OsEDS1-knouckout mutant (oseds1) was characterized and shown to have increased susceptibility to Xanthomonas oryzae pv. oryzae (Xoo) and Xanthomonas oryzae pv. oryzicola (Xoc), suggesting the positive role of OsEDS1 in regulating rice disease resistance. However, the following evidence suggests that OsEDS1 shares some differences with AtEDS1 in its way to regulate the host-pathogen interactions. Firstly, OsEDS1 modulates the rice-bacteria interactions involving in jasmonic acid (JA) signaling pathway, while AtEDS1 regulates Arabidopsis disease resistance against biotrophic pathogens depending on salicylic acid (SA) signaling pathway. Secondly, introducing AtEDS1 could reduce oseds1 mutant susceptibility to Xoo rather than to Xoc. Thirdly, exogenous application of JA and SA cannot complement the susceptible phenotype of the oseds1 mutant, while exogenous application of SA is capable of complementing the susceptible phenotype of the ateds1 mutant. Finally, OsEDS1 is not required for R gene mediated resistance, while AtEDS1 is required for disease resistance mediated by TIR-NB-LRR class of R proteins. CONCLUSION: OsEDS1 is a positive regulator in rice-pathogen interactions, and shares both similarities and differences with AtEDS1 in its way to regulate plant-pathogen interactions. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12284-019-0283-0) contains supplementary material, which is available to authorized users.
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spelling pubmed-64653872019-05-03 Jasmonic Acid-Involved OsEDS1 Signaling in Rice-Bacteria Interactions Ke, Yinggen Kang, Yuanrong Wu, Mengxiao Liu, Hongbo Hui, Shugang Zhang, Qinglu Li, Xianghua Xiao, Jinghua Wang, Shiping Rice (N Y) Original Article BACKGROUND: The function of Arabidopsis enhanced disease susceptibility 1 (AtEDS1) and its sequence homologs in other dicots have been extensively studied. However, it is unknown whether rice EDS1 homolog (OsEDS1) plays a role in regulating the rice-pathogen interaction. RESULTS: In this study, a OsEDS1-knouckout mutant (oseds1) was characterized and shown to have increased susceptibility to Xanthomonas oryzae pv. oryzae (Xoo) and Xanthomonas oryzae pv. oryzicola (Xoc), suggesting the positive role of OsEDS1 in regulating rice disease resistance. However, the following evidence suggests that OsEDS1 shares some differences with AtEDS1 in its way to regulate the host-pathogen interactions. Firstly, OsEDS1 modulates the rice-bacteria interactions involving in jasmonic acid (JA) signaling pathway, while AtEDS1 regulates Arabidopsis disease resistance against biotrophic pathogens depending on salicylic acid (SA) signaling pathway. Secondly, introducing AtEDS1 could reduce oseds1 mutant susceptibility to Xoo rather than to Xoc. Thirdly, exogenous application of JA and SA cannot complement the susceptible phenotype of the oseds1 mutant, while exogenous application of SA is capable of complementing the susceptible phenotype of the ateds1 mutant. Finally, OsEDS1 is not required for R gene mediated resistance, while AtEDS1 is required for disease resistance mediated by TIR-NB-LRR class of R proteins. CONCLUSION: OsEDS1 is a positive regulator in rice-pathogen interactions, and shares both similarities and differences with AtEDS1 in its way to regulate plant-pathogen interactions. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12284-019-0283-0) contains supplementary material, which is available to authorized users. Springer US 2019-04-15 /pmc/articles/PMC6465387/ /pubmed/30989404 http://dx.doi.org/10.1186/s12284-019-0283-0 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Original Article
Ke, Yinggen
Kang, Yuanrong
Wu, Mengxiao
Liu, Hongbo
Hui, Shugang
Zhang, Qinglu
Li, Xianghua
Xiao, Jinghua
Wang, Shiping
Jasmonic Acid-Involved OsEDS1 Signaling in Rice-Bacteria Interactions
title Jasmonic Acid-Involved OsEDS1 Signaling in Rice-Bacteria Interactions
title_full Jasmonic Acid-Involved OsEDS1 Signaling in Rice-Bacteria Interactions
title_fullStr Jasmonic Acid-Involved OsEDS1 Signaling in Rice-Bacteria Interactions
title_full_unstemmed Jasmonic Acid-Involved OsEDS1 Signaling in Rice-Bacteria Interactions
title_short Jasmonic Acid-Involved OsEDS1 Signaling in Rice-Bacteria Interactions
title_sort jasmonic acid-involved oseds1 signaling in rice-bacteria interactions
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6465387/
https://www.ncbi.nlm.nih.gov/pubmed/30989404
http://dx.doi.org/10.1186/s12284-019-0283-0
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