4771 Foxglove Crescent, Richmond, BC, Canada V7C 2K4

Management of virus disease in plants involves deployment of resistance genes, phytosanitary practices and cross-protection. A natural extension of cross-protection was the development in the mid-1980s of genetically engineered resistance in susceptible plants using viral genes (transgenes) or selected nucleotide sequences to express proteins which acted to protect plants against infection by related strains. This process, designated 'pathogen-derived resistance' (PDR) is being used to minimize the effects of infection by a range of viruses, e.g. single-stranded (ss) RNA viruses (tobamo-, cucumo-, potex-, carla- and tospo-virus genera), and several ss DNA viruses (geminiviruses). Three general classes of PDR have been designated.
(i) Protein-mediated resistance. Genes encoding viral coat proteins and movement proteins are most commonly used. Coat protein-mediated resistance (CPMR) is most effective against the homologous strain, less so with other strains, and generally ineffective against unrelated viruses. Resistance in transgenic plants to infection by tobacco mosaic virus (TMV) is associated with high levels of transgenic coat protein, but resistance can be overcome by RNA inoculum, suggesting that CPMR is effected by coat protein interfering with disassembly of incoming virions in inoculated primary cells. On the other hand, tobacco expressing the coat protein of potato virus X (PVX) is resistant to both virion and RNA inocula. Transgenic plants expressing dysfunctional movement proteins of TMV or PVX are resistant to the homologous viruses and several unrelated ones. Such resistance may be due to competition between the mutant proteins and those of the infecting virus for binding sites in plasmodesmata.
(ii) Nucleic acid-mediated resistance. Resistance in this class may be effected by transgenic viral RNA or DNA, defective interfering RNA or DNA, or RNA transcripts of transgenes. It is possible that the transgenic nucleic acid acts as a decoy, thus competing with the incoming viral genome and interfering with pathogenesis.
(iii) Resistance effected by post-transcriptional homology-related gene silencing (co-suppression). In this example, accumulation of RNA derived from a transgene and of related endogenous or viral genes is lost (silenced) in transgenic plants. This type of PDR operates at the RNA level, and thus would reduce accumulation of viral RNA which shares sequence identity with the silenced transgene. The presumed mechanism of suppression involves an antisense RNA, produced on the transgene template by a host-encoded RNA-dependent RNA polymerase, which hybridizes with viral and transgene RNAs. The resulting dsRNA is probably degraded by host-encoded ribonucleases specific for dsRNA.

Use of PDR may involve elements of risk. In laboratory experiments, viral transgenes have been shown to recombine with infecting viruses, leading in some instances to recombinants with altered host range or increased virulence. Transgenic potato expressing the 5' proximal regions of two potyviruses, when inoculated with PVX, expressed symptoms characteristic of the synergistic interaction between PVX and potato virus Y. The latter results suggest that severe disease may result when transgenic crops are infected by certain non-target viruses. Additional concerns about deployment of PDR strategies include possible spread of transgenes to related wild plants, and the intense, ongoing public debate about labelling and marketing of genetically engineered food products destined for domestic and international trade. Coincident with the development of PDR strategies, there is increasing interest in transforming plants with other agents for disease management, e.g. cloned ribozymes to provide resistance to potato spindle tuber viroid in potato, expression of the cloned rice gene Xa21 in transgenic rice for control of a broad range of isolates of the bacterial blight pathogen, and expression of a chimaeric fusion protein containing the secretory sequence from barley alpha-amylase and a modified cecropin-coding sequence to provide resistance to the tobacco wildfire bacterium. Continued research and development will undoubtedly improve current PDR strategies, and provide new and novel ones for more effective disease management.