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

Nicholas 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 ()
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Nicholas C. Collins: Sainsbury Laboratory John Innes Centre
Hans Thordal-Christensen: Risø National Laboratory
Volker Lipka: Max Planck Institute for Plant Breeding Research
Stephan Bau: Max Planck Institute for Plant Breeding Research
Erich Kombrink: Max Planck Institute for Plant Breeding Research
Jin-Long Qiu: Risø National Laboratory
Ralph Hückelhoven: Institute of Phytopathology and Applied Zoology Justus-Liebig-University
Mónica Stein: Carnegie Institute of Washington
Andreas Freialdenhoven: Max Planck Institute for Plant Breeding Research
Shauna C. Somerville: Carnegie Institute of Washington
Paul Schulze-Lefert: Max Planck Institute for Plant Breeding Research

Nature, 2003, vol. 425, issue 6961, 973-977

Abstract: Abstract Failure 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)1,2,3,4. 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 (ref. 2), 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.

Date: 2003
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DOI: 10.1038/nature02076

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