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Antioxidant Role of PcGSTd1 in Fenpropathrin Resistant Population of the Citrus Red Mite, Panonychus citri (McGregor)

The citrus red mite, Panonychus citri, a major citrus pest distributed worldwide, has evolved severe resistance to various classes of chemical acaricides/insecticides including pyrethroids. It is well known that the resistance to pyrethroids is mainly caused by point mutations of voltage-gated sodiu...

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Autores principales: Liao, Chong-Yu, Feng, Ying-Cai, Li, Gang, Shen, Xiao-Min, Liu, Shi-Huo, Dou, Wei, Wang, Jin-Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5884870/
https://www.ncbi.nlm.nih.gov/pubmed/29651254
http://dx.doi.org/10.3389/fphys.2018.00314
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author Liao, Chong-Yu
Feng, Ying-Cai
Li, Gang
Shen, Xiao-Min
Liu, Shi-Huo
Dou, Wei
Wang, Jin-Jun
author_facet Liao, Chong-Yu
Feng, Ying-Cai
Li, Gang
Shen, Xiao-Min
Liu, Shi-Huo
Dou, Wei
Wang, Jin-Jun
author_sort Liao, Chong-Yu
collection PubMed
description The citrus red mite, Panonychus citri, a major citrus pest distributed worldwide, has evolved severe resistance to various classes of chemical acaricides/insecticides including pyrethroids. It is well known that the resistance to pyrethroids is mainly caused by point mutations of voltage-gated sodium channel gene in a wide range of pests. However, increasing number of evidences support that pyrethroids resistance might also be resulted from the integrated mechanisms including metabolic mechanisms. In this study, firstly, comparative analysis of RNA-seq data showed that multiple detoxification genes, including a GSTs gene PcGSTd1, were up-regulated in a fenpropathrin-resistant population compared with the susceptible strain (SS). Quantitative real time-PCR results showed that the exposure of fenpropathrin had an induction effect on the transcription of PcGSTd1 in a time-dependent manner. In vitro inhibition and metabolic assay of recombinant PcGSTd1 found that fenpropathrin might not be metabolized directly by this protein. However, its antioxidant role in alleviating the oxidative stress caused by fenpropathrin was demonstrated via the reversely genetic experiment. Our results provide a list of candidate genes which may contribute to a multiple metabolic mechanisms implicated in the evolution of fenpropathrin resistance in the field population of P. citri. Furthermore, during the detoxification process, PcGSTd1 plays an antioxidant role by detoxifying lipid peroxidation products induced by fenpropathrin.
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spelling pubmed-58848702018-04-12 Antioxidant Role of PcGSTd1 in Fenpropathrin Resistant Population of the Citrus Red Mite, Panonychus citri (McGregor) Liao, Chong-Yu Feng, Ying-Cai Li, Gang Shen, Xiao-Min Liu, Shi-Huo Dou, Wei Wang, Jin-Jun Front Physiol Physiology The citrus red mite, Panonychus citri, a major citrus pest distributed worldwide, has evolved severe resistance to various classes of chemical acaricides/insecticides including pyrethroids. It is well known that the resistance to pyrethroids is mainly caused by point mutations of voltage-gated sodium channel gene in a wide range of pests. However, increasing number of evidences support that pyrethroids resistance might also be resulted from the integrated mechanisms including metabolic mechanisms. In this study, firstly, comparative analysis of RNA-seq data showed that multiple detoxification genes, including a GSTs gene PcGSTd1, were up-regulated in a fenpropathrin-resistant population compared with the susceptible strain (SS). Quantitative real time-PCR results showed that the exposure of fenpropathrin had an induction effect on the transcription of PcGSTd1 in a time-dependent manner. In vitro inhibition and metabolic assay of recombinant PcGSTd1 found that fenpropathrin might not be metabolized directly by this protein. However, its antioxidant role in alleviating the oxidative stress caused by fenpropathrin was demonstrated via the reversely genetic experiment. Our results provide a list of candidate genes which may contribute to a multiple metabolic mechanisms implicated in the evolution of fenpropathrin resistance in the field population of P. citri. Furthermore, during the detoxification process, PcGSTd1 plays an antioxidant role by detoxifying lipid peroxidation products induced by fenpropathrin. Frontiers Media S.A. 2018-03-29 /pmc/articles/PMC5884870/ /pubmed/29651254 http://dx.doi.org/10.3389/fphys.2018.00314 Text en Copyright © 2018 Liao, Feng, Li, Shen, Liu, Dou and Wang. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Liao, Chong-Yu
Feng, Ying-Cai
Li, Gang
Shen, Xiao-Min
Liu, Shi-Huo
Dou, Wei
Wang, Jin-Jun
Antioxidant Role of PcGSTd1 in Fenpropathrin Resistant Population of the Citrus Red Mite, Panonychus citri (McGregor)
title Antioxidant Role of PcGSTd1 in Fenpropathrin Resistant Population of the Citrus Red Mite, Panonychus citri (McGregor)
title_full Antioxidant Role of PcGSTd1 in Fenpropathrin Resistant Population of the Citrus Red Mite, Panonychus citri (McGregor)
title_fullStr Antioxidant Role of PcGSTd1 in Fenpropathrin Resistant Population of the Citrus Red Mite, Panonychus citri (McGregor)
title_full_unstemmed Antioxidant Role of PcGSTd1 in Fenpropathrin Resistant Population of the Citrus Red Mite, Panonychus citri (McGregor)
title_short Antioxidant Role of PcGSTd1 in Fenpropathrin Resistant Population of the Citrus Red Mite, Panonychus citri (McGregor)
title_sort antioxidant role of pcgstd1 in fenpropathrin resistant population of the citrus red mite, panonychus citri (mcgregor)
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5884870/
https://www.ncbi.nlm.nih.gov/pubmed/29651254
http://dx.doi.org/10.3389/fphys.2018.00314
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