Dissecting Phytophthora blight; making sense out of signalling, effectors and host targets

The plant pathogen Phytophthora infestans causes late blight, the disease that was responsible for the Irish potato famine in the mid-nineteenth century. This oomycete has a hemibiotrophic life style, a narrow host range and a large genome of ~ 240 Mb. Comparative genomics revealed features illuminating its success as a pathogen, such as rapid turnover and massive expansion of families encoding secreted proteins, and peculiar gene innovations resulting in proteins with oomycete-specific domain combinations. An example of a novel protein family is the GPCR-PIPK family. Its twelve members all have a N-terminal 7-transmembrane domain typical for G-protein coupled receptors (GPCRs) combined with a phosphatidylinositol phosphate kinase (PIPK) domain at the C-terminus. This domain structure suggests that GPCR-PIPKs use GPCRs to directly feed extracellular signals into phospholipid signalling pathways. Their differential expression and localization point to distinct roles in various cellular processes. For one GPCR-PIPK we could demonstrate a role in asexual development, including spore germination, hyphal elongation and sporangia cleavage, whereas inactivation of another GPCR-PIPK disturbs sexual development. For successful infection Phytophthora secretes a variety of proteins including a large number of effectors that share the host-cell targeting motif RXLR. Inside host cells these RXLR effectors promote virulence by manipulating the cell machinery via interaction with host targets thereby suppressing host defence. However, in plants carrying matching resistance genes RXLR effectors trigger defence and thus act as avirulence factors. Here I will focus on an RXLR effector that interacts with an exocyst component and show how the interplay between this effector and its host target influences the host-pathogen interaction.