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Critical Role of COI1-Dependent Jasmonate Pathway in AAL toxin induced PCD in Tomato Revealed by Comparative Proteomics
Alternaria alternata f.sp. Lycopersici (AAL) toxin induces programmed cell death (PCD) in susceptible tomato (Solanum lycopersicum) leaves. Jasmonate (JA) promotes AAL toxin induced PCD in a COI1 (coronatine insensitive 1, JA receptor)-dependent manner by enhancement of reactive oxygen species (ROS)...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4914994/ https://www.ncbi.nlm.nih.gov/pubmed/27324416 http://dx.doi.org/10.1038/srep28451 |
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author | Zhang, Min Koh, Jin Liu, Lihong Shao, Zhiyong Liu, Haoran Hu, Songshen Zhu, Ning Dufresne, Craig P. Chen, Sixue Wang, Qiaomei |
author_facet | Zhang, Min Koh, Jin Liu, Lihong Shao, Zhiyong Liu, Haoran Hu, Songshen Zhu, Ning Dufresne, Craig P. Chen, Sixue Wang, Qiaomei |
author_sort | Zhang, Min |
collection | PubMed |
description | Alternaria alternata f.sp. Lycopersici (AAL) toxin induces programmed cell death (PCD) in susceptible tomato (Solanum lycopersicum) leaves. Jasmonate (JA) promotes AAL toxin induced PCD in a COI1 (coronatine insensitive 1, JA receptor)-dependent manner by enhancement of reactive oxygen species (ROS) production. To further elucidate the underlying mechanisms of this process, we performed a comparative proteomic analysis using tomato jasmonic acid insensitive1 ( jai1), the receptor mutant of JA, and its wild type (WT) after AAL toxin treatment with or without JA treatment. A total of 10367 proteins were identified in tomato leaves using isobaric tags for relative and absolute quantitation (iTRAQ) quantitative proteomics approach. 2670 proteins were determined to be differentially expressed in response to AAL toxin and JA. Comparison between AAL toxin treated jai1 and its WT revealed the COI1-dependent JA pathway regulated proteins, including pathways related to redox response, ceramide synthesis, JA, ethylene (ET), salicylic acid (SA) and abscisic acid (ABA) signaling. Autophagy, PCD and DNA damage related proteins were also identified. Our data suggest that COI1-dependent JA pathway enhances AAL toxin induced PCD through regulating the redox status of the leaves, other phytohormone pathways and/or important PCD components. |
format | Online Article Text |
id | pubmed-4914994 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49149942016-06-27 Critical Role of COI1-Dependent Jasmonate Pathway in AAL toxin induced PCD in Tomato Revealed by Comparative Proteomics Zhang, Min Koh, Jin Liu, Lihong Shao, Zhiyong Liu, Haoran Hu, Songshen Zhu, Ning Dufresne, Craig P. Chen, Sixue Wang, Qiaomei Sci Rep Article Alternaria alternata f.sp. Lycopersici (AAL) toxin induces programmed cell death (PCD) in susceptible tomato (Solanum lycopersicum) leaves. Jasmonate (JA) promotes AAL toxin induced PCD in a COI1 (coronatine insensitive 1, JA receptor)-dependent manner by enhancement of reactive oxygen species (ROS) production. To further elucidate the underlying mechanisms of this process, we performed a comparative proteomic analysis using tomato jasmonic acid insensitive1 ( jai1), the receptor mutant of JA, and its wild type (WT) after AAL toxin treatment with or without JA treatment. A total of 10367 proteins were identified in tomato leaves using isobaric tags for relative and absolute quantitation (iTRAQ) quantitative proteomics approach. 2670 proteins were determined to be differentially expressed in response to AAL toxin and JA. Comparison between AAL toxin treated jai1 and its WT revealed the COI1-dependent JA pathway regulated proteins, including pathways related to redox response, ceramide synthesis, JA, ethylene (ET), salicylic acid (SA) and abscisic acid (ABA) signaling. Autophagy, PCD and DNA damage related proteins were also identified. Our data suggest that COI1-dependent JA pathway enhances AAL toxin induced PCD through regulating the redox status of the leaves, other phytohormone pathways and/or important PCD components. Nature Publishing Group 2016-06-21 /pmc/articles/PMC4914994/ /pubmed/27324416 http://dx.doi.org/10.1038/srep28451 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Zhang, Min Koh, Jin Liu, Lihong Shao, Zhiyong Liu, Haoran Hu, Songshen Zhu, Ning Dufresne, Craig P. Chen, Sixue Wang, Qiaomei Critical Role of COI1-Dependent Jasmonate Pathway in AAL toxin induced PCD in Tomato Revealed by Comparative Proteomics |
title | Critical Role of COI1-Dependent Jasmonate Pathway in AAL toxin induced PCD in Tomato Revealed by Comparative Proteomics |
title_full | Critical Role of COI1-Dependent Jasmonate Pathway in AAL toxin induced PCD in Tomato Revealed by Comparative Proteomics |
title_fullStr | Critical Role of COI1-Dependent Jasmonate Pathway in AAL toxin induced PCD in Tomato Revealed by Comparative Proteomics |
title_full_unstemmed | Critical Role of COI1-Dependent Jasmonate Pathway in AAL toxin induced PCD in Tomato Revealed by Comparative Proteomics |
title_short | Critical Role of COI1-Dependent Jasmonate Pathway in AAL toxin induced PCD in Tomato Revealed by Comparative Proteomics |
title_sort | critical role of coi1-dependent jasmonate pathway in aal toxin induced pcd in tomato revealed by comparative proteomics |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4914994/ https://www.ncbi.nlm.nih.gov/pubmed/27324416 http://dx.doi.org/10.1038/srep28451 |
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