Case Studies

Summary

Tobacco mosaic virus (TMV) was first studied scientifically as a plant pathogen 100 years ago. A form of hypersensitive resistance transferred from the wild species Nicotiana glutinosa to cultivated tobacco was shown 60 years ago to be due to a single dominant gene, named N. This causes the virus to be localised to necrotic lesions which form around each site of infection: the hypersensitive response (HR). N-gene resistance has proved extremely durable: only one virulent (resistance-breaking) TMV isolate has been reported to date. Another resistance gene, N’, thought to be allelomorphic with N, causes a hypersensitive reaction to avirulent isolates of TMV, but numerous virulent isolates are also known. These do not induce necrosis but spread systemically and cause normal mosaic symptoms. The single known example of virulence against N has been mapped on TMV RNA to the replicase gene, whereas virulence against N’ in different TMV isolates has been mapped to a number of locations, all within the coat protein gene. The N gene has been isolated and sequenced: it shows structural and possibly functional features in common with certain other genes for resistance to bacterial and fungal pathogens, and to other genes with known functions in control of development or response to hormones in animals. These similarities give some clues about how the N-gene product might be involved in TMV recognition and in signalling the cascade of resistance and other responses which follows. The actual mechanism which inhibits TMV spread or multiplication after resistance is induced is not yet fully clear, but may involve an inhibition of multiplication or blocking of cell-to-cell spread of the infection front.