As our knowledge of the cellular and genetic mechanisms of plant disease resistance increase, so does the potential for modifying these processes to achieve broad-spectrum durable disease resistance. A number of approaches have been taken by researchers to identify and understand the complex chain of events that is set in motion when a plant is challenged by a pathogen (Table 18.1) (reviewed by Broekaert et al., 2000; Cornelissen and Schram, 2000; Punja, 2001). Most effort has been applied to studying the constitutive production in transgenic plants of antifungal compounds. These include production of naturally occurring pathogenesisrelated (PR) proteins that may inhibit or prevent pathogen growth in the plant, such as hydrolytic enzymes, antifungal proteins, antimicrobial peptides, ribosome inactivating proteins, and phytoalexins. Others involve the expression of gene products that are either antagonistic to pathogen virulence products, such as polygalacturonase, oxalic acid and lipase, or which enhance the structural defenses within the plant, such as peroxidases and lignins. There has also been research into modifying pathways such as those regulated by salicylic acid, jasmonic acid, ethylene, and hydrogen peroxide that are important in plant defenses. Such resistance mechanisms occur naturally in the plant and the objective is to manipulate the system so that gene products are expressed at levels that defend the plant against pathogen attack, or render the pathogen incapable of attack. Alternative approaches concern the interactions between R genes in plants and the corresponding dominant Avr genes in the pathogen that culminate in the hypersensitive response (HR) in incompatible reactions, and the molecular genotyping of plant lines using DNA-based techniques to facilitate the "pyramiding" of desirable disease resistance traits into elite germplasm.

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Gilbert, J. (J.), Jordan, M. (M.), Somers, D.J. (D. J.), Xing, T, & Punja, Z.K. (Z. K.). (2006). Engineering plants for durable disease resistance. In Multigenic and Induced Systemic Resistance in Plants (pp. 415–455). doi:10.1007/0-387-23266-4_18