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Modulation of (Homo)Glutathione Metabolism and H(2)O(2) Accumulation during Soybean Cyst Nematode Infections in Susceptible and Resistant Soybean Cultivars

In plant immune responses, reactive oxygen species (ROS) act as signaling molecules that activate defense pathways against pathogens, especially following resistance (R) gene-mediated pathogen recognition. Glutathione (GSH), an antioxidant and redox regulator, participates in the removal of hydrogen...

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Autores principales: Chen, Xi, Li, Shuang, Zhao, Xuebing, Zhu, Xiaofeng, Wang, Yuanyuan, Xuan, Yuanhu, Liu, Xiaoyu, Fan, Haiyan, Chen, Lijie, Duan, Yuxi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7013558/
https://www.ncbi.nlm.nih.gov/pubmed/31936278
http://dx.doi.org/10.3390/ijms21020388
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author Chen, Xi
Li, Shuang
Zhao, Xuebing
Zhu, Xiaofeng
Wang, Yuanyuan
Xuan, Yuanhu
Liu, Xiaoyu
Fan, Haiyan
Chen, Lijie
Duan, Yuxi
author_facet Chen, Xi
Li, Shuang
Zhao, Xuebing
Zhu, Xiaofeng
Wang, Yuanyuan
Xuan, Yuanhu
Liu, Xiaoyu
Fan, Haiyan
Chen, Lijie
Duan, Yuxi
author_sort Chen, Xi
collection PubMed
description In plant immune responses, reactive oxygen species (ROS) act as signaling molecules that activate defense pathways against pathogens, especially following resistance (R) gene-mediated pathogen recognition. Glutathione (GSH), an antioxidant and redox regulator, participates in the removal of hydrogen peroxide (H(2)O(2)). However, the mechanism of GSH-mediated H(2)O(2) generation in soybeans (Glycine max (L.) Merr.) that are resistant to the soybean cyst nematode (SCN; Heterodera glycines Ichinohe) remains unclear. To elucidate this underlying relationship, the feeding of race 3 of H. glycines with resistant cultivars, Peking and PI88788, was compared with that on a susceptible soybean cultivar, Williams 82. After 5, 10, and 15 days of SCN infection, we quantified γ-glutamylcysteine (γ-EC) and (homo)glutathione ((h)GSH), and a gene expression analysis showed that GSH metabolism in resistant cultivars differed from that in susceptible soybean roots. ROS accumulation was examined both in resistant and susceptible roots upon SCN infection. The time of intense ROS generation was related to the differences of resistance mechanisms in Peking and PI88788. ROS accumulation that was caused by the (h)GSH depletion-arrested nematode development in susceptible Williams 82. These results suggest that (h)GSH metabolism in resistant soybeans plays a key role in the regulation of ROS-generated signals, leading to resistance against nematodes.
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spelling pubmed-70135582020-03-09 Modulation of (Homo)Glutathione Metabolism and H(2)O(2) Accumulation during Soybean Cyst Nematode Infections in Susceptible and Resistant Soybean Cultivars Chen, Xi Li, Shuang Zhao, Xuebing Zhu, Xiaofeng Wang, Yuanyuan Xuan, Yuanhu Liu, Xiaoyu Fan, Haiyan Chen, Lijie Duan, Yuxi Int J Mol Sci Article In plant immune responses, reactive oxygen species (ROS) act as signaling molecules that activate defense pathways against pathogens, especially following resistance (R) gene-mediated pathogen recognition. Glutathione (GSH), an antioxidant and redox regulator, participates in the removal of hydrogen peroxide (H(2)O(2)). However, the mechanism of GSH-mediated H(2)O(2) generation in soybeans (Glycine max (L.) Merr.) that are resistant to the soybean cyst nematode (SCN; Heterodera glycines Ichinohe) remains unclear. To elucidate this underlying relationship, the feeding of race 3 of H. glycines with resistant cultivars, Peking and PI88788, was compared with that on a susceptible soybean cultivar, Williams 82. After 5, 10, and 15 days of SCN infection, we quantified γ-glutamylcysteine (γ-EC) and (homo)glutathione ((h)GSH), and a gene expression analysis showed that GSH metabolism in resistant cultivars differed from that in susceptible soybean roots. ROS accumulation was examined both in resistant and susceptible roots upon SCN infection. The time of intense ROS generation was related to the differences of resistance mechanisms in Peking and PI88788. ROS accumulation that was caused by the (h)GSH depletion-arrested nematode development in susceptible Williams 82. These results suggest that (h)GSH metabolism in resistant soybeans plays a key role in the regulation of ROS-generated signals, leading to resistance against nematodes. MDPI 2020-01-08 /pmc/articles/PMC7013558/ /pubmed/31936278 http://dx.doi.org/10.3390/ijms21020388 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Chen, Xi
Li, Shuang
Zhao, Xuebing
Zhu, Xiaofeng
Wang, Yuanyuan
Xuan, Yuanhu
Liu, Xiaoyu
Fan, Haiyan
Chen, Lijie
Duan, Yuxi
Modulation of (Homo)Glutathione Metabolism and H(2)O(2) Accumulation during Soybean Cyst Nematode Infections in Susceptible and Resistant Soybean Cultivars
title Modulation of (Homo)Glutathione Metabolism and H(2)O(2) Accumulation during Soybean Cyst Nematode Infections in Susceptible and Resistant Soybean Cultivars
title_full Modulation of (Homo)Glutathione Metabolism and H(2)O(2) Accumulation during Soybean Cyst Nematode Infections in Susceptible and Resistant Soybean Cultivars
title_fullStr Modulation of (Homo)Glutathione Metabolism and H(2)O(2) Accumulation during Soybean Cyst Nematode Infections in Susceptible and Resistant Soybean Cultivars
title_full_unstemmed Modulation of (Homo)Glutathione Metabolism and H(2)O(2) Accumulation during Soybean Cyst Nematode Infections in Susceptible and Resistant Soybean Cultivars
title_short Modulation of (Homo)Glutathione Metabolism and H(2)O(2) Accumulation during Soybean Cyst Nematode Infections in Susceptible and Resistant Soybean Cultivars
title_sort modulation of (homo)glutathione metabolism and h(2)o(2) accumulation during soybean cyst nematode infections in susceptible and resistant soybean cultivars
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7013558/
https://www.ncbi.nlm.nih.gov/pubmed/31936278
http://dx.doi.org/10.3390/ijms21020388
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