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.
Plant disease resistance (R) genes trigger innate immune responses upon pathogen attack. RAR1 is an early convergence point in a signaling pathway engaged by multiple R genes. Here, we show that RAR1 interacts with plant orthologs of the yeast protein SGT1, an essential regulator in the cell cycle. Silencing the barley gene Sgt1 reveals its role in R gene-triggered, Rar1-dependent disease resistance. SGT1 associates with SKP1 and CUL1, subunits of the SCF (Skp1-Cullin-F-box) ubiquitin ligase complex. Furthermore, the RAR1-SGT1 complex also interacts with two COP9 signalosome components. The interactions among RAR1, SGT1, SCF, and signalosome subunits indicate a link between disease resistance and ubiquitination.
Race-specific resistance in barley to the powdery mildew fungus (Erysiphe graminis f sp hordei) is associated with a cell death reaction (hypersensitive response [HR]). Genetically, it is dependent on dominant resistance genes (Mlx), and in most cases, it is also dependent on Rar1 and Rar2. Non-race-specific resistance to the fungus, which is due to the lack of the Mlo wild-type allele, is dependent on Ror1 and Ror2 and is not associated with an HR in the region of pathogen attack. However, the absence of the Mlo wild-type allele stimulates a spontaneous cell death response in foliar tissue. This response is also controlled by Ror1 and Ror2, as indicated by trypan blue staining patterns. Lack of Mlo enhances transcript accumulation of pathogenesis-related genes upon fungal challenge, and this response is diminished by mutations in Ror genes. Using DNA marker-assisted selection of genotypes, we provide evidence, via gene interaction studies, that Ror1 and Ror2 are not essential components of race-specific resistance and do not compromise hypersensitive cell death. Reciprocal experiments show that neither is Rar1 a component of mlo-controlled resistance nor does it affect spontaneous cell death. We show that mlo- and Ror-dependent resistance is active when challenged with E. g. f sp tritici, a nonhost pathogen of barley. Our observations suggest separate genetic pathways operating in race-specific and non-race-specific resistance; they indicate also a separate genetic control of hypersensitive and spontaneous cell death in foliar tissue.
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