In the 1980s and 1990s, Pierre de Wit and his research group were responsible for a better understanding of the gene-for-gene model in phytopathology. Fungi have genes that produce proteins, called effectors, which cause disease in plants. Luckily, some plants also have immune genes that produce receptors to recognise the effectors and so defend themselves against the fungus. When they do, the fungus is unable to develop and reproduce. To transfer this immunity, de Wit’s research group cross-fertilised wild species containing these immune genes with crops such as tomato plants.
Spontaneous mutationFungi are spread through the air using billions of spores – the seeds of the fungus. Because there are so many, there is always the chance of a spontaneous mutation, resulting in the fungus suddenly producing a slightly different effector protein. This protein is no longer recognised by the immune receptor, so that the pathogen can enter the plant and develop. When this altered pathogen produces spores, these spores will all make the new protein and therefore also no longer be recognised by the plant as an invader. The result is that all the plants of the same species in a particular area become diseased.
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