Plants have their own networks of defense against plant pathogens that include a vast array of proteins and other organic molecules produced prior to infection or during pathogen attack. Not all pathogens can attack all plants and a single plant is not susceptible to the whole plethora of plant pathogenic fungi, viruses, bacteria or nematodes. Recombinant DNA technology allows the enhancement of inherent plant responses against a pathogen by either using single dominant resistance genes not normally present in the susceptible plant (Keen 1999) or by choosing plant genes that intensify or trigger the expressions of existing defense mechanisms (Bent and Yu 1999, Rommens and Kishore 2000). What is useful in one plant/pathogen system may be transferred to another, increasing the recipient plant’s ability to defend itself from a previously uncontrollable pathogen. Furthermore, biotechnology facilitates the discovery and elucidation of the molecular interactions between plants and pathogens. Understanding the molecular basis of plant-pathogen interactions increases our ability to deploy selected plant resistance genes from virtually any plant. A short description of the use of plant genes to fight against pathogens within the framework of genetic engineering and plant transgenic research is given below.

Plant intrinsic responses that can be engineered to attain a wider, more durable resistance include the Hypersensitive Response (HR) and Systemic Acquired Resistance (SAR) (http://ppathw3.cals.cornell.edu/Delaney/labres.html ) (Honèe 1999, Strittmatter et al. 1995). Although these phenomena are complex and our knowledge of them incomplete, this is an area of enormous promise in plant protection. Ideally a plant could be engineered to show an incompatible reaction with an invading pathogen that leads to localized cell death through HR by transforming it with an appropriate plant resistance gene or an elicitor molecule. Furthermore, the same plant could be engineered so that SAR is expressed even in the absence of a pathogen. For example, the over-expression of the transcriptional regulator Npr1 in transgenic Arabidopsis thaliana enhanced the plant’s resistance level against a diverse array of pathogens (Cao et al. 1998). Plants potentially could be engineered to change a previously compatible reaction with a pathogen (disease) to an incompatible reaction or HR (localized cell death, no disease). This approach would provide the transgenic plant with a first level of pathogen control. A second infection control point would be provided by a systemic acquired resistance state (SAR) that is already functioning before the physical presence of the pathogen. Although we have yet to apply this sophisticated approach to bolster plant resistance networks, individual components of such systems are being tried with different degrees of success.

Pathogenesis Related (PR) proteins, for example, are a group of diverse proteins whose accumulation is triggered by pathogen attack or abiotic stress (http://www.ars.usda.gov/is/AR/archive/may98/prot0598.htm). In a sense, PR proteins constitute a point where the various response networks intersect by reacting with different inducers such as salicylic acid, jasmonic acid, systemin, and ethylene. PR proteins have been classified into 12 major groups or families. Some of them show antifungal activity. The functions of most PR proteins remain a mystery but some of them are known to be b -1,3-glucanases (PR-2), chitinases (PR-3) or fungal membrane permeablizers (PR-5) (Honèe 1999). In theory, the constitutive expression of PR proteins, either singly or combined, might confer decreased susceptibility to a specific group of pathogens (Bent and Yu 1999, Broglie et al. 1991, Jongedick et al. 1995, Liu et al. 1994, Tabei et al. 1998).

Finally, pathosystem-specific plant resistance genes, e.g. Pto (Tang et al. 1999), Cf-9 (Hammond et al. 1998), N (Witham et al. 1996), etc, have been used as transgenes to confer resistance in different plants. Briefly, a gene that confers resistance to a certain pathogen in plant species A is identified, cloned and transformed into plant species B. Plant species B, the recipient genotype, by virtue of the new gene acquired by transformation, becomes resistant to the same pathogen plant species A inherently is resistant to. Unfortunately, in some cases the gene separated from its original genetic background is not able to confer resistance. In other words, the pathway that makes the resistance gene work properly in plant species A may not be complete or functional in plant species B. However, there is usually a way to engineer the downstream responses triggered by those genes (Rommens and Kishore 2000). Plant pathologists are using this ‘obstacle’ (i.e. absence of the complete regulatory pathway allowing a foreign gene to function in the transgenic plant) to fuel their efforts to obtain greater insights into how plant-pathogen interactions work at the molecular level. A more refined knowledge of plant-pathogen interactions is expected to lead to more consistent, accurate and successful resistance engineering strategies.