Understanding host plant susceptibility and resistance by indexing and deploying obligate pathogen effectors.

Diseases cause significant yield losses in crop plants. The downy mildews and their close relations represent a major group of pathogens, one of which is potato blight, the causal agent of the Irish Potato Famine. We aim to understand how these pathogens attack their host plants and the mechanisms used by plants to defend themselves. A downy mildew, Hyaloperonospora parasitica, is a natural pathogen of the molecular model plant Arabidopsis. We have recently identified a group of pathogen proteins, called effectors, that trigger host resistance and also play a role in suppressing host resistance. We are now able to recognise potential effector genes amongst all the genes of the downy mildew. So in this project we will isolate a large number of the effector genes and use them to understand how they alter their host plant to allow growth of the pathogen. In this way we identify host proteins that are important in resistance. By understanding this complex balance between disease and resistance we will reveal key components of the interactin between host and pathogen we will, in the future, design genetic or chemical approaches that protect crop plants in the field.

Arabidopsis is a natural host for the oomycete downy mildew pathogen Hyaloperonospora parasitica and, hence, can be used as a model system for infection of other oomycete pathogens such as Phytophthora infestans (potato blight). We have recently cloned two pathogenicity effector proteins from H. parasitica that trigger host resistance genes and have been able to define protein sequence motifs, a signal peptide plus a conserved amino acid sequence of RXLR, that allow easy recognition of this class of effectors. We are also part of the team sequencing the H. parasitica genome for which preliminary genome sequences are available. In this project we will bioinformtically identify the RXLR protein complement of the pathogen. For up to 100 of these genes we will assess allele diversity to determine which are under selective pressure driven by host resistance mechanisms. The role of these effector proteins in triggering host resistance genes and in enhancing pathogenicity will be determined in a range of Arabdiopsis accessions. Using these data we will select a range of effector proteins that play a role in pathogenicity and use them in yeast two hybrid and tandem affinity purification experiments to identify their host targets. As these effectors are likely to play a role in suppression of host immune repsonses their interacting partners will be key components of the host immune system. In this way we will decipher the host immune sytem at both a cellular and population level.