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Glutaredoxin GRXS16 mediates brassinosteroid-induced apoplastic H2O2 production to promote pesticide metabolism in tomato.

Identifieur interne : 000260 ( Main/Exploration ); précédent : 000259; suivant : 000261

Glutaredoxin GRXS16 mediates brassinosteroid-induced apoplastic H2O2 production to promote pesticide metabolism in tomato.

Auteurs : Jiayin Hou [République populaire de Chine] ; Qihao Zhang [République populaire de Chine] ; Yue Zhou [République populaire de Chine] ; Golam Jalal Ahammed [République populaire de Chine] ; Yanhong Zhou [République populaire de Chine] ; Jingquan Yu [République populaire de Chine] ; Hua Fang [République populaire de Chine] ; Xiaojian Xia [République populaire de Chine]

Source :

RBID : pubmed:29747107

Descripteurs français

English descriptors

Abstract

Brassinosteroids (BRs), a group of steroid phytohormones, are involved in multiple aspects of plant growth, development and stress responses. Despite recent studies on BRs-promoted pesticide metabolism in plants, the underlying mechanisms remain poorly understood. Here, we showed that 24-epibrassinolide (EBR) significantly enhanced the expression of RESPIRATORY BURST OXIDASE HOMOLOG1 (RBOH1) and H2O2 accumulation in the apoplast of chlorothalonil (CHT, a broad spectrum nonsystemic fungicide)-treated tomato plants. Silencing of RBOH1 significantly decreased the efficiency of EBR-induced CHT metabolism. Moreover, the EBR-induced upregulation in the transcripts of glutaredoxin gene GRXS16 was suppressed in RBOH1-silenced plants. Further studies indicated that silencing of GRXS16 compromised EBR-induced increases in glutathione content, activity of glutathione S-transferase (GST) and transcript of GST1, leading to an increase in CHT residue. By contrast, overexpression of tomato GRXS16 enhanced the basal levels of glutathione content and GST activity that eventually decreased CHT residues in transgenic plants. Our results reveal that BR-mediated induction of a modest oxidative burst is essential for the acceleration of glutathione-dependent pesticide metabolism via redox modulators, such as GRXS16. These findings shed new light on the mechanisms of BR-induced pesticide metabolism and thus have important implication in reducing pesticide residues in agricultural products.

DOI: 10.1016/j.envpol.2018.04.120
PubMed: 29747107


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<term>Brassinosteroids (toxicity)</term>
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<term>Gene Expression Regulation, Plant (drug effects)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Glutathione (metabolism)</term>
<term>Hydrogen Peroxide (metabolism)</term>
<term>Lycopersicon esculentum (drug effects)</term>
<term>Lycopersicon esculentum (metabolism)</term>
<term>NADPH Oxidases (MeSH)</term>
<term>Nitriles (MeSH)</term>
<term>Oxidation-Reduction (MeSH)</term>
<term>Pesticides (metabolism)</term>
<term>Steroids, Heterocyclic (MeSH)</term>
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<term>Brassinostéroïdes (toxicité)</term>
<term>Fongicides industriels (métabolisme)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Glutathion (métabolisme)</term>
<term>Lycopersicon esculentum (effets des médicaments et des substances chimiques)</term>
<term>Lycopersicon esculentum (métabolisme)</term>
<term>NADPH oxidase (MeSH)</term>
<term>Nitriles (MeSH)</term>
<term>Oxydoréduction (MeSH)</term>
<term>Peroxyde d'hydrogène (métabolisme)</term>
<term>Pesticides (métabolisme)</term>
<term>Régulation de l'expression des gènes végétaux (effets des médicaments et des substances chimiques)</term>
<term>Stéroïdes hétérocycliques (MeSH)</term>
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<term>Fungicides, Industrial</term>
<term>Glutaredoxins</term>
<term>Glutathione</term>
<term>Hydrogen Peroxide</term>
<term>Pesticides</term>
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<term>Brassinosteroids</term>
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<term>Gene Expression Regulation, Plant</term>
<term>Lycopersicon esculentum</term>
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<term>Régulation de l'expression des gènes végétaux</term>
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<term>Glutarédoxines</term>
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<term>Peroxyde d'hydrogène</term>
<term>Pesticides</term>
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<term>Brassinostéroïdes</term>
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<term>Nitriles</term>
<term>Oxidation-Reduction</term>
<term>Steroids, Heterocyclic</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr">
<term>NADPH oxidase</term>
<term>Nitriles</term>
<term>Oxydoréduction</term>
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<div type="abstract" xml:lang="en">Brassinosteroids (BRs), a group of steroid phytohormones, are involved in multiple aspects of plant growth, development and stress responses. Despite recent studies on BRs-promoted pesticide metabolism in plants, the underlying mechanisms remain poorly understood. Here, we showed that 24-epibrassinolide (EBR) significantly enhanced the expression of RESPIRATORY BURST OXIDASE HOMOLOG1 (RBOH1) and H
<sub>2</sub>
O
<sub>2</sub>
accumulation in the apoplast of chlorothalonil (CHT, a broad spectrum nonsystemic fungicide)-treated tomato plants. Silencing of RBOH1 significantly decreased the efficiency of EBR-induced CHT metabolism. Moreover, the EBR-induced upregulation in the transcripts of glutaredoxin gene GRXS16 was suppressed in RBOH1-silenced plants. Further studies indicated that silencing of GRXS16 compromised EBR-induced increases in glutathione content, activity of glutathione S-transferase (GST) and transcript of GST1, leading to an increase in CHT residue. By contrast, overexpression of tomato GRXS16 enhanced the basal levels of glutathione content and GST activity that eventually decreased CHT residues in transgenic plants. Our results reveal that BR-mediated induction of a modest oxidative burst is essential for the acceleration of glutathione-dependent pesticide metabolism via redox modulators, such as GRXS16. These findings shed new light on the mechanisms of BR-induced pesticide metabolism and thus have important implication in reducing pesticide residues in agricultural products.</div>
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O
<sub>2</sub>
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<AbstractText>Brassinosteroids (BRs), a group of steroid phytohormones, are involved in multiple aspects of plant growth, development and stress responses. Despite recent studies on BRs-promoted pesticide metabolism in plants, the underlying mechanisms remain poorly understood. Here, we showed that 24-epibrassinolide (EBR) significantly enhanced the expression of RESPIRATORY BURST OXIDASE HOMOLOG1 (RBOH1) and H
<sub>2</sub>
O
<sub>2</sub>
accumulation in the apoplast of chlorothalonil (CHT, a broad spectrum nonsystemic fungicide)-treated tomato plants. Silencing of RBOH1 significantly decreased the efficiency of EBR-induced CHT metabolism. Moreover, the EBR-induced upregulation in the transcripts of glutaredoxin gene GRXS16 was suppressed in RBOH1-silenced plants. Further studies indicated that silencing of GRXS16 compromised EBR-induced increases in glutathione content, activity of glutathione S-transferase (GST) and transcript of GST1, leading to an increase in CHT residue. By contrast, overexpression of tomato GRXS16 enhanced the basal levels of glutathione content and GST activity that eventually decreased CHT residues in transgenic plants. Our results reveal that BR-mediated induction of a modest oxidative burst is essential for the acceleration of glutathione-dependent pesticide metabolism via redox modulators, such as GRXS16. These findings shed new light on the mechanisms of BR-induced pesticide metabolism and thus have important implication in reducing pesticide residues in agricultural products.</AbstractText>
<CopyrightInformation>Copyright © 2018 Elsevier Ltd. All rights reserved.</CopyrightInformation>
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<Affiliation>College of Forestry, Henan University of Science and Technology, 263 Kaiyuan Avenue, Luoyang, PR China. Electronic address: ahammed@haust.edu.cn.</Affiliation>
</AffiliationInfo>
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<Affiliation>Department of Horticulture, Zijingang Campus, Zhejiang University, 866 Yuhangtang Road, Hangzhou, 310058, PR China.</Affiliation>
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<Affiliation>Department of Horticulture, Zijingang Campus, Zhejiang University, 866 Yuhangtang Road, Hangzhou, 310058, PR China; Zhejiang Provincial Key Laboratory of Horticultural Plant Integrative Biology, 866 Yuhangtang Road, Hangzhou, 310058, PR China.</Affiliation>
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<Affiliation>Institute of Pesticide & Environmental Toxicology, Zijingang Campus, Zhejiang University, Hangzhou, 310058, China.</Affiliation>
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</Author>
<Author ValidYN="Y">
<LastName>Xia</LastName>
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<Initials>X</Initials>
<AffiliationInfo>
<Affiliation>Department of Horticulture, Zijingang Campus, Zhejiang University, 866 Yuhangtang Road, Hangzhou, 310058, PR China. Electronic address: xiaojianxia@zju.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
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<Month>05</Month>
<Day>07</Day>
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<Country>England</Country>
<MedlineTA>Environ Pollut</MedlineTA>
<NlmUniqueID>8804476</NlmUniqueID>
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<NameOfSubstance UI="D060406">Brassinosteroids</NameOfSubstance>
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<RegistryNumber>0</RegistryNumber>
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<Chemical>
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<NameOfSubstance UI="C022709">superoxide-forming enzyme</NameOfSubstance>
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<NameOfSubstance UI="C005806">tetrachloroisophthalonitrile</NameOfSubstance>
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<Chemical>
<RegistryNumber>Y9IQ1L53OX</RegistryNumber>
<NameOfSubstance UI="C023623">brassinolide</NameOfSubstance>
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</MeshHeading>
<MeshHeading>
<DescriptorName UI="D018551" MajorTopicYN="N">Lycopersicon esculentum</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D019255" MajorTopicYN="N">NADPH Oxidases</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D009570" MajorTopicYN="N">Nitriles</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D010575" MajorTopicYN="N">Pesticides</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D013260" MajorTopicYN="N">Steroids, Heterocyclic</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">Brassinosteroid</Keyword>
<Keyword MajorTopicYN="N">Detoxification</Keyword>
<Keyword MajorTopicYN="N">Glutathione</Keyword>
<Keyword MajorTopicYN="N">Hydrogen peroxide</Keyword>
<Keyword MajorTopicYN="N">Pesticide</Keyword>
<Keyword MajorTopicYN="N">Redox</Keyword>
</KeywordList>
</MedlineCitation>
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<Year>2018</Year>
<Month>01</Month>
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<PubMedPubDate PubStatus="revised">
<Year>2018</Year>
<Month>04</Month>
<Day>25</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted">
<Year>2018</Year>
<Month>04</Month>
<Day>25</Day>
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<Month>5</Month>
<Day>11</Day>
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<Minute>0</Minute>
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<ArticleIdList>
<ArticleId IdType="pubmed">29747107</ArticleId>
<ArticleId IdType="pii">S0269-7491(18)30458-5</ArticleId>
<ArticleId IdType="doi">10.1016/j.envpol.2018.04.120</ArticleId>
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<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
<region>
<li>Zhejiang</li>
</region>
<settlement>
<li>Hangzhou</li>
</settlement>
<orgName>
<li>Université de Zhejiang</li>
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<country name="République populaire de Chine">
<region name="Zhejiang">
<name sortKey="Hou, Jiayin" sort="Hou, Jiayin" uniqKey="Hou J" first="Jiayin" last="Hou">Jiayin Hou</name>
</region>
<name sortKey="Ahammed, Golam Jalal" sort="Ahammed, Golam Jalal" uniqKey="Ahammed G" first="Golam Jalal" last="Ahammed">Golam Jalal Ahammed</name>
<name sortKey="Fang, Hua" sort="Fang, Hua" uniqKey="Fang H" first="Hua" last="Fang">Hua Fang</name>
<name sortKey="Xia, Xiaojian" sort="Xia, Xiaojian" uniqKey="Xia X" first="Xiaojian" last="Xia">Xiaojian Xia</name>
<name sortKey="Yu, Jingquan" sort="Yu, Jingquan" uniqKey="Yu J" first="Jingquan" last="Yu">Jingquan Yu</name>
<name sortKey="Zhang, Qihao" sort="Zhang, Qihao" uniqKey="Zhang Q" first="Qihao" last="Zhang">Qihao Zhang</name>
<name sortKey="Zhou, Yanhong" sort="Zhou, Yanhong" uniqKey="Zhou Y" first="Yanhong" last="Zhou">Yanhong Zhou</name>
<name sortKey="Zhou, Yue" sort="Zhou, Yue" uniqKey="Zhou Y" first="Yue" last="Zhou">Yue Zhou</name>
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</record>

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