The scab fungus, Venturia inaequalis, is one of the most devastating pathogens of apple worldwide. Regular epidemics result in the need for frequent fungicide applications throughout the growing season. The appearance of fungicide resistance has heightened the need for additional control options, and resistant hosts are a potential alternative. Apple has a long breeding cycle, and resistance is often found in species with relatively poor quality traits. The difficulty of selecting cultivars with scab resistance has frequently led to the production of apple cultivars incorporating single major resistance genes. This type of resistance is usually vulnerable to breakdown, due to selection of virulence in the sexually reproducing pathogen population. Multiple types of resistance stacked in a cultivar is likely to be more durable, however breeding cultivars harbouring multiple scab resistance genes is challenging. This breeding challenge is facilitated by the identification of specific pathogen races or, even better, pathogen proteins (effectors) that trigger specific, differential resistance responses. Whilst races of V. inaequalis have been identified, no specific effector proteins have been characterised to date. We are taking a systems biology approach to identify specific effector proteins that trigger resistance in apple to the scab fungus.
We have sequenced the genomes of several races of V. inaequalis and are using comparative transcriptomics and genomics to narrow down the search for specific effectors in the apple scab fungus. Genetic crosses between pathogen races are also being used in this hunt. We have identified genes encoding proteins that are secreted by the fungus, and we are characterising specific pathogen proteins that trigger the resistance responses. We are also identifying conserved V. inaequalis proteins that are essential for the pathogen to infect apple and hope to identify resistance proteins that can recognise these factors, reducing the ability of the pathogen to mutate to virulence.