Engineering Resistance to Fungal Pathogens

The strategy used to engineer resistance to fungal pathogens often depends on the nature of the host–pathogen interaction. As indicated in the previous section, for biotrophic fungal pathogens, a specific R-gene approach can be used since there is often a gene-for-gene interaction between pathogen and host and natural or modified R-genes may be transferred to other genotypes of the same species or to other species, which may confer resistance to the race of pathogen which they recognised in the host plant. However, for necrotrophic fungal pathogens, which kill tissues in advance of hyphal invasion, other approaches are required. These include induction of systemic acquired resistance, production of a range of antifungal proteins,41 or introduction of genes which can degrade fungal toxins. Examples include:
(i) genes for toxin inactivation (e.g. HM1);
(ii) genes encoding anti-fungal proteins (e.g. plant defensins such as radish anti-fungal protein, thionins such as macadamia nut antifungal protein);
(iii) genes encoding PR proteins (e.g. chitinases, b,3-glucanases);
(iv) genes that will activate the systemic acquired resistance response;
(v) artificially induced hypersensitive reaction.
In general, the approaches which involve transformation of plants with genes for anti-fungal proteins do not give complete resistance to fungal pathogens. As a result, it is envisaged that stacking of such resistance genes will be required to provide effective fungal resistance. This may be achieved by multiple transformations or by joining the coding sequences of different anti-fungal protein genes with linkers for peptides recognised by proteases, such that the anti-fungal proteins are translated as one polyprotein and subsequently cleaved to their separate active constituents by protease digestion.