Silencing of acidic pathogenesis-related PR-1 genes increases extracellular beta-(1->3)-glucanase activity at the onset of tobacco defence reactions.
Identifieur interne : 001C22 ( Main/Exploration ); précédent : 001C21; suivant : 001C23Silencing of acidic pathogenesis-related PR-1 genes increases extracellular beta-(1->3)-glucanase activity at the onset of tobacco defence reactions.
Auteurs : Marie-Pierre Rivière [France] ; Antoine Marais ; Michel Ponchet ; William Willats ; Eric GalianaSource :
- Journal of experimental botany [ 1460-2431 ] ; 2008.
Descripteurs français
- KwdFr :
- Acide salicylique (pharmacologie), Données de séquences moléculaires (MeSH), Extinction de l'expression des gènes (effets des médicaments et des substances chimiques), Glucan 1,3-beta-glucosidase (analyse), Glucan 1,3-beta-glucosidase (antagonistes et inhibiteurs), Glucan 1,3-beta-glucosidase (métabolisme), Glucanes (métabolisme), Immunité innée (MeSH), Interférence par ARN (effets des médicaments et des substances chimiques), Isoformes de protéines (génétique), Isoformes de protéines (métabolisme), Maladies des plantes (génétique), Phytophthora (MeSH), Protéines d'algue (pharmacologie), Protéines fongiques (MeSH), Protéines recombinantes (analyse), Protéines recombinantes (génétique), Protéines recombinantes (métabolisme), Protéines végétales (analyse), Protéines végétales (génétique), Protéines végétales (métabolisme), Régulation de l'expression des gènes végétaux (effets des médicaments et des substances chimiques), Régulation positive (effets des médicaments et des substances chimiques), Tabac (enzymologie), Tabac (génétique), Tabac (immunologie), Tabac (parasitologie), Test de complémentation (MeSH), Végétaux génétiquement modifiés (MeSH).
- MESH :
- analyse : Glucan 1,3-beta-glucosidase, Protéines recombinantes, Protéines végétales.
- antagonistes et inhibiteurs : Glucan 1,3-beta-glucosidase.
- effets des médicaments et des substances chimiques : Extinction de l'expression des gènes, Interférence par ARN, Régulation de l'expression des gènes végétaux, Régulation positive.
- enzymologie : Tabac.
- génétique : Isoformes de protéines, Maladies des plantes, Protéines recombinantes, Protéines végétales, Tabac.
- immunologie : Tabac.
- métabolisme : Glucan 1,3-beta-glucosidase, Glucanes, Isoformes de protéines, Protéines recombinantes, Protéines végétales.
- parasitologie : Tabac.
- pharmacologie : Acide salicylique, Protéines d'algue.
- Données de séquences moléculaires, Immunité innée, Phytophthora, Protéines fongiques, Test de complémentation, Végétaux génétiquement modifiés.
English descriptors
- KwdEn :
- Algal Proteins (pharmacology), Fungal Proteins (MeSH), Gene Expression Regulation, Plant (drug effects), Gene Silencing (drug effects), Genetic Complementation Test (MeSH), Glucan 1,3-beta-Glucosidase (analysis), Glucan 1,3-beta-Glucosidase (antagonists & inhibitors), Glucan 1,3-beta-Glucosidase (metabolism), Glucans (metabolism), Immunity, Innate (MeSH), Molecular Sequence Data (MeSH), Phytophthora (MeSH), Plant Diseases (genetics), Plant Proteins (analysis), Plant Proteins (genetics), Plant Proteins (metabolism), Plants, Genetically Modified (MeSH), Protein Isoforms (genetics), Protein Isoforms (metabolism), RNA Interference (drug effects), Recombinant Proteins (analysis), Recombinant Proteins (genetics), Recombinant Proteins (metabolism), Salicylic Acid (pharmacology), Tobacco (enzymology), Tobacco (genetics), Tobacco (immunology), Tobacco (parasitology), Up-Regulation (drug effects).
- MESH :
- chemical , analysis : Glucan 1,3-beta-Glucosidase, Plant Proteins, Recombinant Proteins.
- chemical , antagonists & inhibitors : Glucan 1,3-beta-Glucosidase.
- chemical , genetics : Plant Proteins, Protein Isoforms, Recombinant Proteins.
- chemical , metabolism : Glucan 1,3-beta-Glucosidase, Glucans, Plant Proteins, Protein Isoforms, Recombinant Proteins.
- chemical , pharmacology : Algal Proteins, Salicylic Acid.
- chemical : Fungal Proteins.
- drug effects : Gene Expression Regulation, Plant, Gene Silencing, RNA Interference, Up-Regulation.
- enzymology : Tobacco.
- genetics : Plant Diseases, Tobacco.
- immunology : Tobacco.
- parasitology : Tobacco.
- Genetic Complementation Test, Immunity, Innate, Molecular Sequence Data, Phytophthora, Plants, Genetically Modified.
Abstract
The class 1 pathogenesis-related (PR) proteins are thought to be involved in plant defence responses, but their molecular functions are unknown. The function of PR-1 was investigated in tobacco by generating stable PR-1a-silenced lines in which other acidic PR-1 genes (PR-1b and PR-1c) were silenced. Plants lacking extracellular PR-1s were more susceptible than wild-type plants to the oomycete Phytophthora parasitica but displayed unaffected systemic acquired resistance and developmental resistance to this pathogen. Treatment with salicylic acid up-regulates the PR-1g gene, encoding a basic protein of the PR-1 family, in PR-1-deficient tobacco, indicating that PR-1 expression may repress that of PR-1g. This shows that acidic PR-1s are dispensable for expression of salicylic acid-dependent acquired resistances against P. parasitica and may reveal a functional overlap in tobacco defence or a functional redundancy in the PR-1 gene family. The data also show that there is a specific increase in apoplastic beta-(1-->3)-glucanase activity and a decrease in beta-(1-->3)-glucan deposition in PR-1-silenced lines following activation of defence reactions. Complementation of the silencing by apoplastic treatment with a recombinant PR-1a protein largely restores the wild-type beta-(1-->3)-glucanase activity and callose phenotype. Taken together with the immunolocalization of PR-1a to sites of beta-(1-->3)-glucan deposition in wild-type plants, these results are indicative of a function for PR-1a in regulation of enzymatic activity of extracellular beta-(1-->3)-glucanases.
DOI: 10.1093/jxb/ern044
PubMed: 18390849
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Algal Proteins (pharmacology)</term>
<term>Fungal Proteins (MeSH)</term>
<term>Gene Expression Regulation, Plant (drug effects)</term>
<term>Gene Silencing (drug effects)</term>
<term>Genetic Complementation Test (MeSH)</term>
<term>Glucan 1,3-beta-Glucosidase (analysis)</term>
<term>Glucan 1,3-beta-Glucosidase (antagonists & inhibitors)</term>
<term>Glucan 1,3-beta-Glucosidase (metabolism)</term>
<term>Glucans (metabolism)</term>
<term>Immunity, Innate (MeSH)</term>
<term>Molecular Sequence Data (MeSH)</term>
<term>Phytophthora (MeSH)</term>
<term>Plant Diseases (genetics)</term>
<term>Plant Proteins (analysis)</term>
<term>Plant Proteins (genetics)</term>
<term>Plant Proteins (metabolism)</term>
<term>Plants, Genetically Modified (MeSH)</term>
<term>Protein Isoforms (genetics)</term>
<term>Protein Isoforms (metabolism)</term>
<term>RNA Interference (drug effects)</term>
<term>Recombinant Proteins (analysis)</term>
<term>Recombinant Proteins (genetics)</term>
<term>Recombinant Proteins (metabolism)</term>
<term>Salicylic Acid (pharmacology)</term>
<term>Tobacco (enzymology)</term>
<term>Tobacco (genetics)</term>
<term>Tobacco (immunology)</term>
<term>Tobacco (parasitology)</term>
<term>Up-Regulation (drug effects)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Acide salicylique (pharmacologie)</term>
<term>Données de séquences moléculaires (MeSH)</term>
<term>Extinction de l'expression des gènes (effets des médicaments et des substances chimiques)</term>
<term>Glucan 1,3-beta-glucosidase (analyse)</term>
<term>Glucan 1,3-beta-glucosidase (antagonistes et inhibiteurs)</term>
<term>Glucan 1,3-beta-glucosidase (métabolisme)</term>
<term>Glucanes (métabolisme)</term>
<term>Immunité innée (MeSH)</term>
<term>Interférence par ARN (effets des médicaments et des substances chimiques)</term>
<term>Isoformes de protéines (génétique)</term>
<term>Isoformes de protéines (métabolisme)</term>
<term>Maladies des plantes (génétique)</term>
<term>Phytophthora (MeSH)</term>
<term>Protéines d'algue (pharmacologie)</term>
<term>Protéines fongiques (MeSH)</term>
<term>Protéines recombinantes (analyse)</term>
<term>Protéines recombinantes (génétique)</term>
<term>Protéines recombinantes (métabolisme)</term>
<term>Protéines végétales (analyse)</term>
<term>Protéines végétales (génétique)</term>
<term>Protéines végétales (métabolisme)</term>
<term>Régulation de l'expression des gènes végétaux (effets des médicaments et des substances chimiques)</term>
<term>Régulation positive (effets des médicaments et des substances chimiques)</term>
<term>Tabac (enzymologie)</term>
<term>Tabac (génétique)</term>
<term>Tabac (immunologie)</term>
<term>Tabac (parasitologie)</term>
<term>Test de complémentation (MeSH)</term>
<term>Végétaux génétiquement modifiés (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Glucan 1,3-beta-Glucosidase</term>
<term>Plant Proteins</term>
<term>Recombinant Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Glucan 1,3-beta-Glucosidase</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Plant Proteins</term>
<term>Protein Isoforms</term>
<term>Recombinant Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glucan 1,3-beta-Glucosidase</term>
<term>Glucans</term>
<term>Plant Proteins</term>
<term>Protein Isoforms</term>
<term>Recombinant Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Algal Proteins</term>
<term>Salicylic Acid</term>
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<term>Protéines recombinantes</term>
<term>Protéines végétales</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Glucan 1,3-beta-glucosidase</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation, Plant</term>
<term>Gene Silencing</term>
<term>RNA Interference</term>
<term>Up-Regulation</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Extinction de l'expression des gènes</term>
<term>Interférence par ARN</term>
<term>Régulation de l'expression des gènes végétaux</term>
<term>Régulation positive</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Tabac</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Plant Diseases</term>
<term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Isoformes de protéines</term>
<term>Maladies des plantes</term>
<term>Protéines recombinantes</term>
<term>Protéines végétales</term>
<term>Tabac</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Tabac</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Tobacco</term>
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<term>Glucanes</term>
<term>Isoformes de protéines</term>
<term>Protéines recombinantes</term>
<term>Protéines végétales</term>
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<keywords scheme="MESH" qualifier="parasitologie" xml:lang="fr"><term>Tabac</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acide salicylique</term>
<term>Protéines d'algue</term>
</keywords>
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<term>Immunity, Innate</term>
<term>Molecular Sequence Data</term>
<term>Phytophthora</term>
<term>Plants, Genetically Modified</term>
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<term>Immunité innée</term>
<term>Phytophthora</term>
<term>Protéines fongiques</term>
<term>Test de complémentation</term>
<term>Végétaux génétiquement modifiés</term>
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<front><div type="abstract" xml:lang="en">The class 1 pathogenesis-related (PR) proteins are thought to be involved in plant defence responses, but their molecular functions are unknown. The function of PR-1 was investigated in tobacco by generating stable PR-1a-silenced lines in which other acidic PR-1 genes (PR-1b and PR-1c) were silenced. Plants lacking extracellular PR-1s were more susceptible than wild-type plants to the oomycete Phytophthora parasitica but displayed unaffected systemic acquired resistance and developmental resistance to this pathogen. Treatment with salicylic acid up-regulates the PR-1g gene, encoding a basic protein of the PR-1 family, in PR-1-deficient tobacco, indicating that PR-1 expression may repress that of PR-1g. This shows that acidic PR-1s are dispensable for expression of salicylic acid-dependent acquired resistances against P. parasitica and may reveal a functional overlap in tobacco defence or a functional redundancy in the PR-1 gene family. The data also show that there is a specific increase in apoplastic beta-(1-->3)-glucanase activity and a decrease in beta-(1-->3)-glucan deposition in PR-1-silenced lines following activation of defence reactions. Complementation of the silencing by apoplastic treatment with a recombinant PR-1a protein largely restores the wild-type beta-(1-->3)-glucanase activity and callose phenotype. Taken together with the immunolocalization of PR-1a to sites of beta-(1-->3)-glucan deposition in wild-type plants, these results are indicative of a function for PR-1a in regulation of enzymatic activity of extracellular beta-(1-->3)-glucanases.</div>
</front>
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<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18390849</PMID>
<DateCompleted><Year>2008</Year>
<Month>06</Month>
<Day>24</Day>
</DateCompleted>
<DateRevised><Year>2013</Year>
<Month>11</Month>
<Day>21</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2431</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>59</Volume>
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<PubDate><Year>2008</Year>
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<Title>Journal of experimental botany</Title>
<ISOAbbreviation>J Exp Bot</ISOAbbreviation>
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<ArticleTitle>Silencing of acidic pathogenesis-related PR-1 genes increases extracellular beta-(1->3)-glucanase activity at the onset of tobacco defence reactions.</ArticleTitle>
<Pagination><MedlinePgn>1225-39</MedlinePgn>
</Pagination>
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<Abstract><AbstractText>The class 1 pathogenesis-related (PR) proteins are thought to be involved in plant defence responses, but their molecular functions are unknown. The function of PR-1 was investigated in tobacco by generating stable PR-1a-silenced lines in which other acidic PR-1 genes (PR-1b and PR-1c) were silenced. Plants lacking extracellular PR-1s were more susceptible than wild-type plants to the oomycete Phytophthora parasitica but displayed unaffected systemic acquired resistance and developmental resistance to this pathogen. Treatment with salicylic acid up-regulates the PR-1g gene, encoding a basic protein of the PR-1 family, in PR-1-deficient tobacco, indicating that PR-1 expression may repress that of PR-1g. This shows that acidic PR-1s are dispensable for expression of salicylic acid-dependent acquired resistances against P. parasitica and may reveal a functional overlap in tobacco defence or a functional redundancy in the PR-1 gene family. The data also show that there is a specific increase in apoplastic beta-(1-->3)-glucanase activity and a decrease in beta-(1-->3)-glucan deposition in PR-1-silenced lines following activation of defence reactions. Complementation of the silencing by apoplastic treatment with a recombinant PR-1a protein largely restores the wild-type beta-(1-->3)-glucanase activity and callose phenotype. Taken together with the immunolocalization of PR-1a to sites of beta-(1-->3)-glucan deposition in wild-type plants, these results are indicative of a function for PR-1a in regulation of enzymatic activity of extracellular beta-(1-->3)-glucanases.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rivière</LastName>
<ForeName>Marie-Pierre</ForeName>
<Initials>MP</Initials>
<AffiliationInfo><Affiliation>UMR 1301 Interactions Biotiques et Santé Végétale, INRA-Université Nice-SophiaAntipolis-CNRS, F-06903 Sophia Antipolis Cedex, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Marais</LastName>
<ForeName>Antoine</ForeName>
<Initials>A</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ponchet</LastName>
<ForeName>Michel</ForeName>
<Initials>M</Initials>
</Author>
<Author ValidYN="Y"><LastName>Willats</LastName>
<ForeName>William</ForeName>
<Initials>W</Initials>
</Author>
<Author ValidYN="Y"><LastName>Galiana</LastName>
<ForeName>Eric</ForeName>
<Initials>E</Initials>
</Author>
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<Month>04</Month>
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<MedlineTA>J Exp Bot</MedlineTA>
<NlmUniqueID>9882906</NlmUniqueID>
<ISSNLinking>0022-0957</ISSNLinking>
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<MeshHeading><DescriptorName UI="D011994" MajorTopicYN="N">Recombinant Proteins</DescriptorName>
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<MeshHeading><DescriptorName UI="D014026" MajorTopicYN="N">Tobacco</DescriptorName>
<QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName>
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<tree><noCountry><name sortKey="Galiana, Eric" sort="Galiana, Eric" uniqKey="Galiana E" first="Eric" last="Galiana">Eric Galiana</name>
<name sortKey="Marais, Antoine" sort="Marais, Antoine" uniqKey="Marais A" first="Antoine" last="Marais">Antoine Marais</name>
<name sortKey="Ponchet, Michel" sort="Ponchet, Michel" uniqKey="Ponchet M" first="Michel" last="Ponchet">Michel Ponchet</name>
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<country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Riviere, Marie Pierre" sort="Riviere, Marie Pierre" uniqKey="Riviere M" first="Marie-Pierre" last="Rivière">Marie-Pierre Rivière</name>
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