• DOI:10.1038/nature02076
• Corpus ID: 4408024

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

@article{Collins2003SNAREproteinmediatedDR,
  title={SNARE-protein-mediated disease resistance at the plant cell wall},
  author={Nicholas C. Collins and Hans Thordal-Christensen and Volker Lipka and Stephan Bau and Erich Kombrink and Jin‐Long Qiu and Ralph H{\"u}ckelhoven and Monica Stein and Andreas Freialdenhoven and Shauna C Somerville and Paul Schulze-Lefert},
  journal={Nature},
  year={2003},
  volume={425},
  pages={973-977}
}

• N. Collins, H. Thordal-Christensen, +8 authors P. Schulze-Lefert
• Published 30 October 2003
• Biology
• Nature

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). 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.