Mechanism of the Hypersensitivity Reaction of Plants

Summary

Active defence of plants (hypersensitive resistance) is induced by the pathogen itself. This is illustrated using the example of two almost isogenic lines of Nicotiana tabacum micro-inoculated with the U1 strain of tobacco mosaic virus. Necrotic stress, accompanied by metabolic alterations which are responsible for the antiviral resistance, is triggered after 33–36 hours of interaction between the plant resistance gene product and the corresponding viral avirulence gene product. The same set of metabolic changes is found in most examples of active defence during various interactions of the incompatible type. These changes are specific to the host but not to the triggering parasite. The alterations include cell wall thickening resulting from production of macromolecules, and the production of defence enzymes and proteins. Defence enzymes fall into two classes: enzymes that catalyse the production of various metabolites participating in resistance (ethylene, phytoalexins, aromatic compounds, oxidized metabolites); and direct defence enzymes (hydrolases such as chitinases and glucanases). The defence proteins include inhibitors of proteases and of polygalacturonases and pathogenesis-related (PR) proteins. Several tobacco PR proteins are in fact hydrolases. A general mechanism for the elicitation of active defence (including antiviral defence) is proposed and discussed in relation to strategies that can be used to engineer plants and confer resistance to a wide range of microorganisms.