Plants are attacked by a multitude of pathogens and pests, some of which cause epidemics that threaten food security. Yet a fundamental concept in plant pathology is that most plants are actively resistant to most pathogens and pests. Plants fend off their innumerable biotic foes primarily through innate immune receptors that detect the invading pathogens and trigger a robust immune response. The conceptual basis of such interactions was elegantly articulated by Harold H. Flor, who, in 1942, proposed the hypothesis that single genes in plants and pathogens define the outcome of their interactions; that is, a plant harboring a specific gene displays resistance against a pathogen that carries an interacting virulence gene ( 1 ). This gene-for-gene model was hugely insightful and influential—it has helped to guide applied and basic research on disease resistance. However, recent findings are taking the field beyond this simplified binary view of plant-pathogen interactions. Plants carry extremely diverse and dynamic repertoires of immune receptors that are interconnected in complex ways. Conversely, plant pathogens secrete a diversity of virulence proteins and metabolites called effectors, and pathogen genomics has revealed hundreds of effector genes in many species. These effectors have evidently evolved to favor pathogen infection and spread, but a subset of them inadvertently activate plant immune receptors. The emerging paradigm is that dynamic webs of genetic and biochemical networks underpin the early stages of plant-pathogen interactions.
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