| Abstract: | The major method of control of virus diseases in crop plants is breeding for resistance. The genetics of resistance, and of matching virulence (the ability of a virus strain to overcome a specific host resistance gene) have been studied less for viruses than for fungal and bacterial pathogens. This paper draws on a survey of the genetics of resistance to a large number of viruses in cultivated crops, and makes some generalisations and predictions about mechanisms. Most resistance to viruses in crops is monogenic. Dominant alleles are associated with virus-localisation mechanisms, which are induced after infection. The nature of the ‘recognition event’ between plant- and virus-coded functions, which triggers resistance plus a cascade of secondary responses, is not yet known. Gene dosage-dependent alleles tend to be associated with non-localising resistance, which allows some virus spread, but inhibits multiplication. Recessive alleles may involve a negative type of resistance mechanism, whereby the resistant plant lacks some function normally required by the virus for pathogenesis. Such resistance tends to be expressed as complete immunity. Many resistance genes have been overcome by virulent isolates of viruses; only 10 % of the sample of resistance genes have proved exceptionally durable. Virulence may involve different viral functions. The production of infectious cDNA clones, and construction of chimaeric recombinants between clones of virulent and avirulent isolates, is now allowing detailed mapping of virulence determinants. Transformation of plants with ‘novel’ genes for virus resistance, based on coat proteins and viral satellites, may allow construction of more robust resistance systems. |
