ABSTRACT
Plants are able to successfully defend themselves against most potential pathogens in their environment, because they are not an appropriate host plant for the majority of pathogens they encounter (species, non-host, or basic resistance). Only relatively few true hostpathogen pairs exist in which a particular pathogen has evolved the capability to resist or prevent a specific plant’s defense response (species, host, or basic compatibility). Distinct cultivars of such host plant species have developed specific resistances against single pathogen races (cultivar resistance). In these plant-pathogen combinations resistance relies on the presence of corresponding plant resistance and pathogen avirulence genes according to the gene-for-gene hypothesis (Flor, 1955, 1971; Alfano and Collmer, 1996; Bent, 1996). In both, species and cultivar resistance, plants appear to recognize pathogens through receptors located intracellularly or on the plasma membrane (Alfano and Collmer, 1996; Knogge, 1996). Signal molecules either released from the plant surface during pathogen attack (endogenous elicitors) or originating directly from the pathogen (exogenous elicitors) appear to function as ligands for these receptors in non-host recognition and thereby initiate the plant’s defense response (Figure 1) (Ebel and Scheel, 1992; Knogge, 1996). In host-incompatible interactions race-cultivar-specific elicitors are encoded by avirulence genes of the pathogen (De Wit, 1992; Alfano and Collmer, 1996; Bent, 1996; Knogge, 1996). The corresponding plant receptors are believed to be products of the matching plant resistance genes (Alfano and Collmer, 1996; Bent, 1996). Although several plant resistance genes have now been isolated, their receptor function remains to be demonstrated (Bent, 1996).
