NATURAL RESISTANCE MECHANISMS IN PLANTS

To complete their life cycles, viruses undergo a multistep process that includes entry into plant cells, uncoating of nucleic acid, translation of viral proteins, replication of viral nucleic acid, assembly of progeny virions, cell-to-cell movement, systemic movement, and plant-to-plant movement. Plant viruses typically initiate infection by penetrating through the plant cell wall into a living cell through wounds caused by mechanical abrasion or by vectors such as insects and nematodes. Unlike animal viruses, there are no known specific mechanisms for entry of plant viruses into plant cells. When virus particles enter a susceptible plant cell, the genome is released from the capsid, typically in the plant cytoplasm. Although not yet comprehensively analyzed, current work suggests this uncoating process is not host-specific, e.g., TMV and Tobacco yellow mottle virus were uncoated in both host and non-host plants. Once the genome becomes available, it can be translated from mRNAs to give early viral products such as viral replicase and other virus-specific proteins. Hereafter the virus faces various constraints imposed by the host and also requires the involvement of many host proteins, typically diverted for function in the viral infection cycle. Successful infection of a plant by a virus therefore requires a series of compatible interactions between the host and a limited number of viral gene products. Absence of a necessary host factor or mutation to incompatibility has long been postulated to account for recessively inherited disease resistance in plants, termed “passive resistance” by R.S.S. Fraser.

                          

In contrast, dominant resistance (Figure Below) has been shown in a number of plant pathosystems to result from an active recognition event that occurs between host and viral factors, resulting in the induction of host defense responses. Despite the availability of well-characterized genetic systems and intensive investigation in this area, the biochemistry of this recognition event is still not  thoroughly  understood.  Genes  that  contribute to this response are likely to be dominant or

Figure: Possible virus resistance mechanisms showing dominant or recessive inheritance contrasted with a susceptible interaction

(Kang B-C et al. 2005. Annu Rev Phytopathol 43: 581-621)

incompletely dominant, unless the resistant response occurs as a result of derepression of a defense pathway. In theory, passive or active resistance can function at any stage of the virus life cycle, although most known viral resistance mechanisms appear to target virus replication or movement. It is still technically difficult to quantify levels of viral accumulation with precision in asynchronous infections of intact tissue (as opposed to protoplasts). Even with the use of fluorescent reporter genes, the extent to which viral accumulation reflects replication and translation versus variations in virus movement cannot be easily discerned. Several lines of evidence suggest that the level of viral accumulation may affect the ability of virus to move systemically. For example, the amount of the α and γ protein produced by RNA 3 of Barley stripe mosaic virus can determine systemic movement of the virus, and dose-dependence has been observed in a number of viral/host interactions. Caution may therefore be needed before concluding that the molecular defect resulting in resistance specifically affects the viral infection cycle stage at which the defect, i.e., resistance, is observed.