Plant Defences Against Microbial Pathogens and Viruses

The interaction between a plant and a pathogen can have two principal outcomes. When no disease is caused, the interaction is incompatible. The pathogen is not able to differentiate and reproduce on the plant, because preformed and inducible defences prevent this. The plant is resistant. Successful colonisation, on the other hand, is referred to as compatible interaction. Pathogen propagation occurs at the expense of the host plant. Plant growth is slowed, tissues are damaged and a disease arises. The plant is susceptible, the pathogen virulent.

Three different scenarios for an incompatible interaction are distinguished (Fig. 8.5):
1. A pathogen cannot develop on a plant, because of efficient preformed defences.

Fig. 8.5. Types of plant immunity

2. None of the races (genotypes) of a pathogen is able to propagate on a particular plant species, because inducible defences restrict the invasion by the pathogen. This is called non-host resistance. The pathogens are non-adapted. Most pathogens are non-adapted to most plants. P. infestans can devastate potatoes, and barley powdery mildew can colonise barley leaves. Both are harmless to Arabidopsis thaliana or most other species, however, because they lack the specific means to overcome the defences of these plants.

3. The resistance is not species wide; it is restricted to certain genotypes (or cultivars in the agricultural context) of a plant species. Some genotypes (races) of a pathogen can propagate on a particular host genotype because they possess effectors that help overcome the plant’s defences. Resistance to other races of a pathogen is based on the recognition of effectors and the induction of the hypersensitive reaction.

The pathogen is avirulent because its effectors trigger rapid plant immune responses. The third scenario has long been recognised and described by the gene-for-gene hypothesis (Flor 1971). Genes encoding effectors (traditionally termed avirulence genes because their presence can induce defence in some host genotypes) interact with plant resistance genes (R genes). These encode proteins that recognise effector presence and activate cell death.