Plant disease-resistance proteins and the gene-for-gene concept.

working with flax and the flax rust fungus, defined plant–pathogen interactions genetically, producing the gene-for-gene hypothesis1. This classic concept is based on the observation that disease resistance in plants commonly requires two complementary genes: an avirulence (Avr) gene in the pathogen and a matching, resistance (R) gene in the host. The biochemical interpretation of this hypothesis is a receptor–ligand model in which plants activate defence mechanisms upon R-protein-mediated recognition of pathogen-derived Avr products. During pathogen infections of plants that lack corresponding R proteins, Avr products might function as virulence factors, subverting host cellular functions through interactions with plant-encoded pathogenicity targets2. In order to combat infection, plants produce R proteins that specifically detect the appearance of Avr products. For example, resistance against viruses involves recognition of the viral coat protein or the viral replicase1. R-protein-mediated recognition of Avr products causes activation of host defences, which commonly are associated with calcium fluxes, generation of superoxide and nitric oxide, and localized plant cell death3–5. Pathogens are able to evade recognition when the Avr proteins are lost or mutated1. Both pathogen and plant have therefore developed specialized strategies to secure their survival and propagation.