Isolation of the Tobacco Mosaic Virus Resistance Gene N

Abstract

Plants resist microbial diseases by elaborating local resistance responses that halt pathogen growth and spread. The hypersensitive response (HR) is the most commonly activated resistance response and is characterized by the formation of necrotic lesions at the site of pathogen ingress. Activation of HR is specific and induced upon interaction of plants and pathogens genetically endowed with the capacity for mutual recognition [1]. Recognition is postulated to result from the interaction of the product of a plant resistance gene with a corresponding pathogen avirulence gene product [1]. Flor first proposed this “gene-for-gene” model of plant and pathogen interaction based on his studies of the fungal rust pathogen of flax, Melampsora lini [2]. The model accurately accounts for the outcome of numerous plant-pathogen interactions. Resistance genes, which are often dominant traits, have been hypothesized to encode products that function as receptors for recognition of specific pathogen avirulence gene products and initiation signal transduction pathways leading to expression of the resistance responses [3]. If either the plant or pathogen partner lacks a functional allele of the corresponding gene pair then resistance is not triggered and the plant becomes diseased.