Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/34195
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dc.contributor.authorCollins, N.-
dc.contributor.authorThordal-Christensen, H.-
dc.contributor.authorLipka, V.-
dc.contributor.authorBau, S.-
dc.contributor.authorKombrink, E.-
dc.contributor.authorQiu, J.-
dc.contributor.authorHuckelhoven, R.-
dc.contributor.authorStein, M.-
dc.contributor.authorFreialdenhoven, A.-
dc.contributor.authorSomerville, S.-
dc.contributor.authorSchulze-Lefert, P.-
dc.date.issued2003-
dc.identifier.citationNature, 2003; 425(6961):973-977-
dc.identifier.issn0028-0836-
dc.identifier.issn1476-4687-
dc.identifier.urihttp://hdl.handle.net/2440/34195-
dc.description.abstractFailure of pathogenic fungi to breach the plant cell wall constitutes a major component of immunity of non-host plant species—species outside the pathogen host range—and accounts for a proportion of aborted infection attempts on 'susceptible' host plants (basal resistance).Neither form of penetration resistance is understood at the molecular level. We developed a screen for penetration (pen) mutants of Arabidopsis, which are disabled in non-host penetration resistance against barley powdery mildew, Blumeria graminis f. sp. hordei, and we isolated the PEN1 gene. We also isolated barley ROR2 , which is required for basal penetration resistance against B. g. hordei. The genes encode functionally homologous syntaxins, demonstrating a mechanistic link between non-host resistance and basal penetration resistance in monocotyledons and dicotyledons. We show that resistance in barley requires a SNAP-25 (synaptosome-associated protein, molecular mass 25 kDa) homologue capable of forming a binary SNAP receptor (SNARE) complex with ROR2. Genetic control of vesicle behaviour at penetration sites, and plasma membrane location of PEN1/ROR2, is consistent with a proposed involvement of SNARE-complex-mediated exocytosis and/or homotypic vesicle fusion events in resistance. Functions associated with SNARE-dependent penetration resistance are dispensable for immunity mediated by race-specific resistance (R) genes, highlighting fundamental differences between these two resistance forms.-
dc.description.statementofresponsibilityNicholas C. Collins, Hans Thordal-Christensen, Volker Lipka, Stephan Bau, Erich Kombrink, Jin-Long Qiu, Ralph Hückelhoven, Mónica Stein, Andreas Freialdenhoven, Shauna C. Somerville and Paul Schulze-Lefert-
dc.language.isoen-
dc.publisherNature Publishing Group-
dc.source.urihttp://dx.doi.org/10.1038/nature02076-
dc.subjectCell Wall-
dc.subjectFungi-
dc.subjectArabidopsis-
dc.subjectHordeum-
dc.subjectMembrane Proteins-
dc.subjectVesicular Transport Proteins-
dc.subjectNerve Tissue Proteins-
dc.subjectArabidopsis Proteins-
dc.subjectCloning, Molecular-
dc.subjectTwo-Hybrid System Techniques-
dc.subjectPlant Diseases-
dc.subjectProtein Binding-
dc.subjectMutation-
dc.subjectMolecular Sequence Data-
dc.subjectSNARE Proteins-
dc.subjectQa-SNARE Proteins-
dc.subjectSynaptosomal-Associated Protein 25-
dc.titleSNARE-protein-mediated disease resistance at the plant cell wall-
dc.typeJournal article-
dc.identifier.doi10.1038/nature02076-
pubs.publication-statusPublished-
dc.identifier.orcidCollins, N. [0000-0002-5447-6755]-
Appears in Collections:Aurora harvest
Australian Centre for Plant Functional Genomics publications

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