crystalline proteins. Commercial transgenic varieties of corn, cotton, and potato that express Bt protein have been successful in reducing the incidence of pest damage and in reducing use of chemical pesticides in many cases (Robinson 1998; USDA 1999d; Gianessi 1999; Mullins and Mills 1999). These varieties may also be less susceptible to opportunistic pathogens that invade through wounds. The incidence of Fusarium ear rot and stalk rots in corn caused by several fungi may be significantly lower in Bt plants (Munkvold 1998). This would have the added benefit of lowering the exposure of humans and animals to fungal mycotoxins.
Pathogen-derived resistance involves the use of genes from a known pathogen in ways that result in protection from that pathogen (Beachy 1997; Sanford and Johnston 1985). The resistance can occur through a number of mechanisms. Expression of a normal or altered form of a pathogen protein in transgenic plants can disrupt the pathogen 's normal pattern or timing of expression of that protein, or interfere with the interaction between a host and the pathogen. Coat protein-mediated resistance to viruses (Baulcombe 1996; Lomonossoff 1995) is the best-known example of pathogen-derived resistance and has been developed commercially in a number of crops. Expression of viral coat protein in plants interferes with uncoating of the viral genome and thereby prevents or delays the establishment of infection. Expression of multiple coat-protein genes confers resistance to multiple viruses (Tricoli et al. 1995). Expression of other types of viral genes that code for replicases and other proteins required for virus replication or movement in plants, has also been demonstrated to confer resistance in many cases (Baulcombe 1996; Lomonossoff 1995).
Pathogen-derived resistance can also trigger mechanisms that initiate or intensify natural plant-protection processes. For example, introduction of functional or nonfunctional viral transgenes into a plant often results in activation PTGS that suppresses expression of the transgene (Baulcombe 1996). The PTGS mechanism involves sequence-specific recognition and degradation of RNA in the cytoplasm (Grant 1999). Plants that activate PTGS to suppress a transgene invariably are highly resistant or immune to infection by the virus in which the transgene originated. In fact, PTGS of transgenes closely resembles the natural silencing response of plants to viruses, which can result in a recovery from the initial symptoms of infection (Al-Kaff et al. 1998; Ratcliff et al. 1997).
The isolation of natural plant R and defensive genes provides the resources to transfer resistance from one plant species to another. Many