Overexpression of AtGolS3 and CsRFS in poplar enhances ROS tolerance and represses defense response to leaf rust disease.
Identifieur interne : 000022 ( Main/Corpus ); précédent : 000021; suivant : 000023Overexpression of AtGolS3 and CsRFS in poplar enhances ROS tolerance and represses defense response to leaf rust disease.
Auteurs : Jonathan La Mantia ; Faride Unda ; Carl J. Douglas ; Shawn D. Mansfield ; Richard HamelinSource :
- Tree physiology [ 1758-4469 ] ; 2018.
English descriptors
- KwdEn :
- Arabidopsis (genetics), Basidiomycota (physiology), Cucumis sativus (genetics), Disease Resistance (genetics), Gene Expression Regulation, Plant (MeSH), Plant Diseases (microbiology), Plants, Genetically Modified (genetics), Plants, Genetically Modified (immunology), Plants, Genetically Modified (microbiology), Populus (genetics), Populus (immunology), Populus (microbiology), Reactive Oxygen Species (metabolism).
- MESH :
- chemical , metabolism : Reactive Oxygen Species.
- genetics : Arabidopsis, Cucumis sativus, Disease Resistance, Plants, Genetically Modified, Populus.
- immunology : Plants, Genetically Modified, Populus.
- microbiology : Plant Diseases, Plants, Genetically Modified, Populus.
- physiology : Basidiomycota.
- Gene Expression Regulation, Plant.
Abstract
Plants respond to pathogens through an orchestration of signaling events that coordinate modifications to transcriptional profiles and physiological processes. Resistance to necrotrophic pathogens often requires jasmonic acid, which antagonizes the salicylic acid dependent biotrophic defense response. Recently, myo-inositol has been shown to negatively impact salicylic acid (SA) levels and signaling, while galactinol enhances jasmonic acid (JA)-dependent induced systemic resistance to necrotrophic pathogens. To investigate the function of these compounds in biotrophic pathogen defense, we characterized the defense response of Populus alba × grandidentata overexpressing Arabidopsis GALACTINOL SYNTHASE3 (AtGolS) and Cucumber sativus RAFFINOSE SYNTHASE (CsRFS) challenged with Melampsora aecidiodes, a causative agent of poplar leaf rust disease. Relative to wild-type leaves, the overexpression of AtGolS3 and CsRFS increased accumulation of galactinol and raffinose and led to increased leaf rust infection. During the resistance response, inoculated wild-type leaves displayed reduced levels of galactinol and repressed transcript abundance of two endogenous GolS genes compared to un-inoculated wild-type leaves prior to the up-regulation of NON-EXPRESSOR OF PR1 and PATHOGENESIS-RELATED1. Transcriptome analysis and qRT-PCR validation also revealed the repression of genes participating in calcium influx, phosphatidic acid biosynthesis and signaling, and salicylic acid signaling in the transgenic lines. In contrast, enhanced tolerance to H2O2 and up-regulation of antioxidant biosynthesis genes were exhibited in the overexpression lines. Thus, we conclude that overexpression of AtGolS and CsRFS antagonizes the defense response to poplar leaf rust disease through repressing reactive oxygen species and attenuating calcium and phosphatidic acid signaling events that lead to SA defense.
DOI: 10.1093/treephys/tpx100
PubMed: 28981890
Links to Exploration step
pubmed:28981890Le document en format XML
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<affiliation><nlm:affiliation>United States Department of Agriculture, Wooster, OH 44691, USA.</nlm:affiliation>
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<author><name sortKey="Unda, Faride" sort="Unda, Faride" uniqKey="Unda F" first="Faride" last="Unda">Faride Unda</name>
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<author><name sortKey="Mansfield, Shawn D" sort="Mansfield, Shawn D" uniqKey="Mansfield S" first="Shawn D" last="Mansfield">Shawn D. Mansfield</name>
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<term>Basidiomycota (physiology)</term>
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<term>Disease Resistance (genetics)</term>
<term>Gene Expression Regulation, Plant (MeSH)</term>
<term>Plant Diseases (microbiology)</term>
<term>Plants, Genetically Modified (genetics)</term>
<term>Plants, Genetically Modified (immunology)</term>
<term>Plants, Genetically Modified (microbiology)</term>
<term>Populus (genetics)</term>
<term>Populus (immunology)</term>
<term>Populus (microbiology)</term>
<term>Reactive Oxygen Species (metabolism)</term>
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<term>Cucumis sativus</term>
<term>Disease Resistance</term>
<term>Plants, Genetically Modified</term>
<term>Populus</term>
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<term>Populus</term>
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<term>Plants, Genetically Modified</term>
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<front><div type="abstract" xml:lang="en">Plants respond to pathogens through an orchestration of signaling events that coordinate modifications to transcriptional profiles and physiological processes. Resistance to necrotrophic pathogens often requires jasmonic acid, which antagonizes the salicylic acid dependent biotrophic defense response. Recently, myo-inositol has been shown to negatively impact salicylic acid (SA) levels and signaling, while galactinol enhances jasmonic acid (JA)-dependent induced systemic resistance to necrotrophic pathogens. To investigate the function of these compounds in biotrophic pathogen defense, we characterized the defense response of Populus alba × grandidentata overexpressing Arabidopsis GALACTINOL SYNTHASE3 (AtGolS) and Cucumber sativus RAFFINOSE SYNTHASE (CsRFS) challenged with Melampsora aecidiodes, a causative agent of poplar leaf rust disease. Relative to wild-type leaves, the overexpression of AtGolS3 and CsRFS increased accumulation of galactinol and raffinose and led to increased leaf rust infection. During the resistance response, inoculated wild-type leaves displayed reduced levels of galactinol and repressed transcript abundance of two endogenous GolS genes compared to un-inoculated wild-type leaves prior to the up-regulation of NON-EXPRESSOR OF PR1 and PATHOGENESIS-RELATED1. Transcriptome analysis and qRT-PCR validation also revealed the repression of genes participating in calcium influx, phosphatidic acid biosynthesis and signaling, and salicylic acid signaling in the transgenic lines. In contrast, enhanced tolerance to H2O2 and up-regulation of antioxidant biosynthesis genes were exhibited in the overexpression lines. Thus, we conclude that overexpression of AtGolS and CsRFS antagonizes the defense response to poplar leaf rust disease through repressing reactive oxygen species and attenuating calcium and phosphatidic acid signaling events that lead to SA defense.</div>
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<Abstract><AbstractText>Plants respond to pathogens through an orchestration of signaling events that coordinate modifications to transcriptional profiles and physiological processes. Resistance to necrotrophic pathogens often requires jasmonic acid, which antagonizes the salicylic acid dependent biotrophic defense response. Recently, myo-inositol has been shown to negatively impact salicylic acid (SA) levels and signaling, while galactinol enhances jasmonic acid (JA)-dependent induced systemic resistance to necrotrophic pathogens. To investigate the function of these compounds in biotrophic pathogen defense, we characterized the defense response of Populus alba × grandidentata overexpressing Arabidopsis GALACTINOL SYNTHASE3 (AtGolS) and Cucumber sativus RAFFINOSE SYNTHASE (CsRFS) challenged with Melampsora aecidiodes, a causative agent of poplar leaf rust disease. Relative to wild-type leaves, the overexpression of AtGolS3 and CsRFS increased accumulation of galactinol and raffinose and led to increased leaf rust infection. During the resistance response, inoculated wild-type leaves displayed reduced levels of galactinol and repressed transcript abundance of two endogenous GolS genes compared to un-inoculated wild-type leaves prior to the up-regulation of NON-EXPRESSOR OF PR1 and PATHOGENESIS-RELATED1. Transcriptome analysis and qRT-PCR validation also revealed the repression of genes participating in calcium influx, phosphatidic acid biosynthesis and signaling, and salicylic acid signaling in the transgenic lines. In contrast, enhanced tolerance to H2O2 and up-regulation of antioxidant biosynthesis genes were exhibited in the overexpression lines. Thus, we conclude that overexpression of AtGolS and CsRFS antagonizes the defense response to poplar leaf rust disease through repressing reactive oxygen species and attenuating calcium and phosphatidic acid signaling events that lead to SA defense.</AbstractText>
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