Barley MLA3 recognizes the host-specificity effector Pwl2 from Magnaporthe oryzae.

Plant nucleotide-binding leucine-rich repeat (NLRs) immune receptors directly or indirectly recognize pathogen-secreted effector molecules to initiate plant defense. Recognition of multiple pathogens by a single NLR is rare and usually occurs via monitoring for changes to host proteins; few characterized NLRs have been shown to recognize multiple effectors. The barley (Hordeum vulgare) NLR gene Mildew locus a (Mla) has undergone functional diversification, and the proteins encoded by different Mla alleles recognize host-adapted isolates of barley powdery mildew (Blumeria graminis f. sp. hordei [Bgh]). Here, we show that Mla3 also confers resistance to the rice blast fungus Magnaporthe oryzae in a dosage-dependent manner. Using a forward genetic screen, we discovered that the recognized effector from M. oryzae is Pathogenicity toward Weeping Lovegrass 2 (Pwl2), a host range determinant factor that prevents M. oryzae from infecting weeping lovegrass (Eragrostis curvula). Mla3 has therefore convergently evolved the capacity to recognize effectors from diverse pathogens.

Necrotrophic Exploitation and Subversion of Plant Defense: A Lifestyle or Just a Phase, and Implications in Breeding Resistance.

Breeding disease-resistant plants is a critical, environmentally friendly component of any strategy to sustainably feed and clothe the 9.8 billion people expected to live on Earth by 2050. Here, I review current literature detailing plant defense responses as they relate to diverse biological outcomes; disease resistance, susceptibility, and establishment of mutualistic plant-microbial relationships. Of particular interest is the degree to which these outcomes are a function of plant-associated microorganisms' lifestyles; biotrophic, hemibiotrophic, necrotrophic, or mutualistic. For the sake of brevity, necrotrophic pathogens and the necrotrophic phase of pathogenicity are emphasized in this review, with special attention given to the host-specific pathogens that exploit defense. Defense responses related to generalist necrotrophs and mutualists are discussed in the context of excellent reviews by others. In addition, host evolutionary trade-offs of disease resistance with other desirable traits are considered in the context of breeding for durable disease resistance.

Characterization of natural and induced variation in the LOV1 gene, a CC-NB-LRR gene conferring victorin sensitivity and disease susceptibility in Arabidopsis.

The fungus Cochliobolus victoriae, the causal agent of Victoria blight, produces a compound called victorin that is required for pathogenicity of the fungus. Victorin alone reproduces disease symptoms on sensitive plants. Victorin sensitivity and susceptibility to C. victoriae were originally described on oats but have since been identified on Arabidopsis thaliana. Victorin sensitivity and disease susceptibility in Arabidopsis are conferred by LOV1, a coiled-coil-nucleotide-binding-leucine-rich repeat (CC-NB-LRR) protein. We sequenced the LOV1 gene from 59 victorin-insensitive mutants and found that the spectrum of mutations causing LOV1 loss of function was similar to that found to cause loss of function of RPM1, a CC-NB-LRR resistance protein. Also, many of the mutated residues in LOV1 are in conserved motifs required for resistance protein function. These data indicate that LOV1 may have a mechanism of action similar to resistance proteins. Victorin sensitivity was found to be the prevalent phenotype in a survey of 30 Arabidopsis ecotypes, and we found very little genetic variation among LOV1 alleles. As selection would not be expected to preserve a functional LOV1 gene to confer victorin sensitivity and disease susceptibility, we propose that LOV1 may function as a resistance gene to a naturally-occurring pathogen of Arabidopsis.

Identification and characterization of victorin sensitivity in Arabidopsis thaliana.

Cochliobolus victoriae is a necrotrophic fungus that produces a host-selective toxin called victorin. Victorin is considered to be host selective because it has been known to affect only certain allohexaploid oat cultivars containing the dominant Vb gene. Oat cultivars containing Vb are also the only genotypes susceptible to C. victoriae. Assays were developed to screen the "nonhost" plant of C. victoriae, Arabidopsis thaliana, for victorin sensitivity. Sensitivity to victorin was identified in six of 433 bulk populations of Arabidopsis. In crosses of Col-4 (victorin-insensitive) x victorin-sensitive Arabidopsis ecotypes, victorin sensitivity segregated as a single dominant locus, as it does in oats. This Arabidopsis locus was designated LOV, for locus orchestrating victorin effects. Allelism tests indicate that LOV loci are allelic or closely linked in all six victorin-sensitive ecotypes identified. LOV was localized to the north arm of Arabidopsis thaliana chromosome I. The victorin-sensitive Arabidopsis line LOV1 but not the victorin-insensitive line Col-4 was susceptible to C. victoriae infection. Consequently, the LOV gene appears to be a genetically dominant, disease susceptibility gene.

Plant disease susceptibility conferred by a "resistance" gene.

The molecular nature of many plant disease resistance (R) genes is known; the largest class encodes nucleotide-binding site-leucine-rich repeat (NBS-LRR) proteins that are structurally related to proteins involved in innate immunity in animals. Few genes conferring disease susceptibility, on the other hand, have been identified. Recent identification of susceptibility to the fungus Cochliobolus victoriae in Arabidopsis thaliana has enabled our cloning of LOV1, a disease susceptibility gene that, paradoxically, is a member of the NBS-LRR resistance gene family. We found LOV1 mediates responses associated with defense, but mutations in known defense response pathways do not prevent susceptibility to C. victoriae. These findings demonstrate that NBS-LRR genes can condition disease susceptibility and resistance and may have implications for R gene deployment.