Serveur d'exploration sur les maladies des plantes grimpantes

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Defence responses in Rpv3-dependent resistance to grapevine downy mildew.

Identifieur interne : 000694 ( Main/Exploration ); précédent : 000693; suivant : 000695

Defence responses in Rpv3-dependent resistance to grapevine downy mildew.

Auteurs : Karen Casagrande [Italie] ; Luigi Falginella ; Simone Diego Castellarin ; Raffaele Testolin ; Gabriele Di Gaspero

Source :

RBID : pubmed:21735199

Descripteurs français

English descriptors

Abstract

The Rpv3 locus determines the ability to operate an isolate-specific hypersensitive response (HR) against Plasmopara viticola in grapevines that carry a resistant Rpv3 (+) haplotype. Artificial infection was performed on leaf discs of Rpv3 (+) and Rpv3 (-) grapevines with two distinct isolates of the pathogen (avrRpv3 (+) and avrRpv3 (-)). The plant response, including the establishment of HR and changes in expression of 33 genes, was compared to the development of the pathogen. HR was induced exclusively in the Rpv3 (+) host upon inoculation with the avrRpv3 (+) isolate of the pathogen, which is assumed to use avrRpv3 (+) effectors that are recognised by/through the plant Rpv3 (+) gene product. The limitation imposed on pathogen growth was the result of inducible responses elicited by the Rpv3 (+)-avrRpv3 (+) interaction. This host reaction relied on transcriptional induction of the HR-associated gene HSR1 and salicylic acid-induced pathogenesis-related (PR) genes PR-1 and PR-2 during the initial 24-48 h post-inoculation. These events had no parallel in the Rpv3 (-) host or upon infection with the avrRpv3 (-) isolate. The emerging model for Rpv3-mediated defence, which is dependent upon race-specific recognition, associated with up-regulation of PR-1 and PR-2 genes, and enforced by localised HR-type necrosis, is compatible with the cascade of events initiated by the products of NB-LRR and LRR-kinase receptor-like genes, such as those residing in the Rpv3 locus.

DOI: 10.1007/s00425-011-1461-5
PubMed: 21735199


Affiliations:


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Le document en format XML

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<term>Haplotypes (MeSH)</term>
<term>Host-Pathogen Interactions (MeSH)</term>
<term>Oomycetes (growth & development)</term>
<term>Oomycetes (immunology)</term>
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<term>Time Factors (MeSH)</term>
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<term>Feuilles de plante (génétique)</term>
<term>Feuilles de plante (immunologie)</term>
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<term>Oomycetes (pathogénicité)</term>
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<term>Résistance à la maladie (génétique)</term>
<term>Spécificité d'espèce (MeSH)</term>
<term>Transduction du signal (génétique)</term>
<term>Transduction du signal (immunologie)</term>
<term>Virulence (MeSH)</term>
<term>Vitis (génétique)</term>
<term>Vitis (immunologie)</term>
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<div type="abstract" xml:lang="en">The Rpv3 locus determines the ability to operate an isolate-specific hypersensitive response (HR) against Plasmopara viticola in grapevines that carry a resistant Rpv3 (+) haplotype. Artificial infection was performed on leaf discs of Rpv3 (+) and Rpv3 (-) grapevines with two distinct isolates of the pathogen (avrRpv3 (+) and avrRpv3 (-)). The plant response, including the establishment of HR and changes in expression of 33 genes, was compared to the development of the pathogen. HR was induced exclusively in the Rpv3 (+) host upon inoculation with the avrRpv3 (+) isolate of the pathogen, which is assumed to use avrRpv3 (+) effectors that are recognised by/through the plant Rpv3 (+) gene product. The limitation imposed on pathogen growth was the result of inducible responses elicited by the Rpv3 (+)-avrRpv3 (+) interaction. This host reaction relied on transcriptional induction of the HR-associated gene HSR1 and salicylic acid-induced pathogenesis-related (PR) genes PR-1 and PR-2 during the initial 24-48 h post-inoculation. These events had no parallel in the Rpv3 (-) host or upon infection with the avrRpv3 (-) isolate. The emerging model for Rpv3-mediated defence, which is dependent upon race-specific recognition, associated with up-regulation of PR-1 and PR-2 genes, and enforced by localised HR-type necrosis, is compatible with the cascade of events initiated by the products of NB-LRR and LRR-kinase receptor-like genes, such as those residing in the Rpv3 locus.</div>
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