SNARE-protein-mediated disease resistance at the plant cell wall

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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.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.identifier.citationNature, 2003; 425(6961):973-977
dc.identifier.doi10.1038/nature02076
dc.identifier.issn0028-0836
dc.identifier.issn1476-4687
dc.identifier.orcidCollins, N. [0000-0002-5447-6755]
dc.identifier.urihttp://hdl.handle.net/2440/34195
dc.language.isoen
dc.publisherNature Publishing Group
dc.source.urihttps://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
pubs.publication-statusPublished

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