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Nature 425, 973-977 (30 October 2003) | doi:10.1038/nature02076; Received 16 June 2003; Accepted 15 September 2003

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

Nicholas C. Collins1,6, Hans Thordal-Christensen2,6, Volker Lipka3, Stephan Bau3, Erich Kombrink3, Jin-Long Qiu2, Ralph Hückelhoven4, Mónica Stein5, Andreas Freialdenhoven3, Shauna C. Somerville5 & Paul Schulze-Lefert3

  1. Sainsbury Laboratory John Innes Centre, Norwich, Norfolk NR4 7UH, UK
  2. Plant Research Department, Risø National Laboratory, DK-4000 Roskilde, Denmark
  3. Department of Plant Microbe Interactions, Max Planck Institute for Plant Breeding Research, Cologne D-50829, Germany
  4. Institute of Phytopathology and Applied Zoology Justus-Liebig-University, Giessen D-35392, Germany
  5. Department of Plant Biology, Carnegie Institute of Washington, Stanford, California 94305, USA
  6. These authors contributed equally to this work

Correspondence to: Paul Schulze-Lefert3 Email: schlef@mpiz-koeln.mpg.de
Sequences are deposited in GenBank under accession numbers AY246893 to AY246907 and AY247208 to AY247214.

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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.