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Differential proteomic analysis of replanted Rehmannia glutinosa roots by iTRAQ reveals molecular mechanisms for formation of replant disease

BACKGROUND: The normal growth of Rehmannia glutinosa, a widely used medicinal plant in China, is severely disturbed by replant disease. The formation of replant disease commonly involves interactions among plants, allelochemicals and microbes; however, these relationships remain largely unclear. As...

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Autores principales: Li, Mingjie, Yang, Yanhui, Feng, Fajie, Zhang, Bao, Chen, Shuqiang, Yang, Chuyun, Gu, Li, Wang, Fengqing, Zhang, Junyi, Chen, Aiguo, Lin, Wenxiong, Chen, Xinjian, Zhang, Zhongyi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5504617/
https://www.ncbi.nlm.nih.gov/pubmed/28693420
http://dx.doi.org/10.1186/s12870-017-1060-0
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author Li, Mingjie
Yang, Yanhui
Feng, Fajie
Zhang, Bao
Chen, Shuqiang
Yang, Chuyun
Gu, Li
Wang, Fengqing
Zhang, Junyi
Chen, Aiguo
Lin, Wenxiong
Chen, Xinjian
Zhang, Zhongyi
author_facet Li, Mingjie
Yang, Yanhui
Feng, Fajie
Zhang, Bao
Chen, Shuqiang
Yang, Chuyun
Gu, Li
Wang, Fengqing
Zhang, Junyi
Chen, Aiguo
Lin, Wenxiong
Chen, Xinjian
Zhang, Zhongyi
author_sort Li, Mingjie
collection PubMed
description BACKGROUND: The normal growth of Rehmannia glutinosa, a widely used medicinal plant in China, is severely disturbed by replant disease. The formation of replant disease commonly involves interactions among plants, allelochemicals and microbes; however, these relationships remain largely unclear. As a result, no effective measures are currently available to treat replant disease. RESULTS: In this study, an integrated R. glutinosa transcriptome was constructed, from which an R. glutinosa protein library was obtained. iTRAQ technology was then used to investigate changes in the proteins in replanted R. glutinosa roots, and the proteins that were expressed in response to replant disease were identified. An integrated R. glutinosa transcriptome from different developmental stages of replanted and normal-growth R. glutinosa produced 65,659 transcripts, which were accurately translated into 47,818 proteins. Using this resource, a set of 189 proteins was found to be significantly differentially expressed between normal-growth and replanted R. glutinosa. Of the proteins that were significantly upregulated in replanted R. glutinosa, most were related to metabolism, immune responses, ROS generation, programmed cell death, ER stress, and lignin synthesis. CONCLUSIONS: By integrating these key events and the results of previous studies on replant disease formation, a new picture of the damaging mechanisms that cause replant disease stress emerged. Replant disease altered the metabolic balance of R. glutinosa, activated immune defence systems, increased levels of ROS and antioxidant enzymes, and initiated the processes of cell death and senescence in replanted R. glutinosa. Additionally, lignin deposition in R. glutinosa roots that was caused by replanting significantly inhibited tuberous root formation. These key processes provide important insights into the underlying mechanisms leading to the formation of replant disease and also for the subsequent development of new control measures to improve production and quality of replanted plants. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12870-017-1060-0) contains supplementary material, which is available to authorized users.
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spelling pubmed-55046172017-07-12 Differential proteomic analysis of replanted Rehmannia glutinosa roots by iTRAQ reveals molecular mechanisms for formation of replant disease Li, Mingjie Yang, Yanhui Feng, Fajie Zhang, Bao Chen, Shuqiang Yang, Chuyun Gu, Li Wang, Fengqing Zhang, Junyi Chen, Aiguo Lin, Wenxiong Chen, Xinjian Zhang, Zhongyi BMC Plant Biol Research Article BACKGROUND: The normal growth of Rehmannia glutinosa, a widely used medicinal plant in China, is severely disturbed by replant disease. The formation of replant disease commonly involves interactions among plants, allelochemicals and microbes; however, these relationships remain largely unclear. As a result, no effective measures are currently available to treat replant disease. RESULTS: In this study, an integrated R. glutinosa transcriptome was constructed, from which an R. glutinosa protein library was obtained. iTRAQ technology was then used to investigate changes in the proteins in replanted R. glutinosa roots, and the proteins that were expressed in response to replant disease were identified. An integrated R. glutinosa transcriptome from different developmental stages of replanted and normal-growth R. glutinosa produced 65,659 transcripts, which were accurately translated into 47,818 proteins. Using this resource, a set of 189 proteins was found to be significantly differentially expressed between normal-growth and replanted R. glutinosa. Of the proteins that were significantly upregulated in replanted R. glutinosa, most were related to metabolism, immune responses, ROS generation, programmed cell death, ER stress, and lignin synthesis. CONCLUSIONS: By integrating these key events and the results of previous studies on replant disease formation, a new picture of the damaging mechanisms that cause replant disease stress emerged. Replant disease altered the metabolic balance of R. glutinosa, activated immune defence systems, increased levels of ROS and antioxidant enzymes, and initiated the processes of cell death and senescence in replanted R. glutinosa. Additionally, lignin deposition in R. glutinosa roots that was caused by replanting significantly inhibited tuberous root formation. These key processes provide important insights into the underlying mechanisms leading to the formation of replant disease and also for the subsequent development of new control measures to improve production and quality of replanted plants. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12870-017-1060-0) contains supplementary material, which is available to authorized users. BioMed Central 2017-07-10 /pmc/articles/PMC5504617/ /pubmed/28693420 http://dx.doi.org/10.1186/s12870-017-1060-0 Text en © The Author(s). 2017 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. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Li, Mingjie
Yang, Yanhui
Feng, Fajie
Zhang, Bao
Chen, Shuqiang
Yang, Chuyun
Gu, Li
Wang, Fengqing
Zhang, Junyi
Chen, Aiguo
Lin, Wenxiong
Chen, Xinjian
Zhang, Zhongyi
Differential proteomic analysis of replanted Rehmannia glutinosa roots by iTRAQ reveals molecular mechanisms for formation of replant disease
title Differential proteomic analysis of replanted Rehmannia glutinosa roots by iTRAQ reveals molecular mechanisms for formation of replant disease
title_full Differential proteomic analysis of replanted Rehmannia glutinosa roots by iTRAQ reveals molecular mechanisms for formation of replant disease
title_fullStr Differential proteomic analysis of replanted Rehmannia glutinosa roots by iTRAQ reveals molecular mechanisms for formation of replant disease
title_full_unstemmed Differential proteomic analysis of replanted Rehmannia glutinosa roots by iTRAQ reveals molecular mechanisms for formation of replant disease
title_short Differential proteomic analysis of replanted Rehmannia glutinosa roots by iTRAQ reveals molecular mechanisms for formation of replant disease
title_sort differential proteomic analysis of replanted rehmannia glutinosa roots by itraq reveals molecular mechanisms for formation of replant disease
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5504617/
https://www.ncbi.nlm.nih.gov/pubmed/28693420
http://dx.doi.org/10.1186/s12870-017-1060-0
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