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Program Book - 27th Fungal Genetics Conference

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PLENARY SESSION ABSTRACTSDissecting Phytophthora blight; making sense out of signalling, effectors and host targets. Francine Govers. Lab. of Phytopathology, WageningenUniversity, Wageningen, Netherlands.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 illuminatingits success as a pathogen, such as rapid turnover and massive expansion of families encoding secreted proteins, and peculiar gene innovations resulting inproteins 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) domainat 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 asexualdevelopment, including spore germination, hyphal elongation and sporangia cleavage, whereas inactivation of another GPCR-PIPK disturbs sexualdevelopment. For successful infection Phytophthora secretes a variety of proteins including a large number of effectors that share the host-cell targetingmotif RXLR. Inside host cells these RXLR effectors promote virulence by manipulating the cell machinery via interaction with host targets therebysuppressing host defence. However, in plants carrying matching resistance genes RXLR effectors trigger defence and thus act as avirulence factors. Here Iwill focus on an RXLR effector that interacts with an exocyst component and show how the interplay between this effector and its host target influencesthe host-pathogen interaction.Understanding directional growth in fungi. Alexandra C. Brand. Aberdeen <strong>Fungal</strong> Group, Univ Aberdeen, Scotland, United Kingdom.<strong>Fungal</strong> hyphae are programmed to explore their surroundings in search of nutrients and, for pathogens, success can depend on locating and identifyingsuitable host penetration sites. Fungi have therefore evolved mechanisms that link the sensing of environmental cues with an appropriate growthresponse. The intracellular components involved in polarised growth in fungi are generally well-conserved and have been studied in model organisms suchas Saccharomyces cerevisiae, Neurospora crassa and Aspergillus spp. However, how environmental signals interact with the molecular machinery of hyphaltip growth is less well-understood. Candida albicans is an opportunistic pathogen that exhibits pre-programmed, or tropic, growth responses to specificstimuli. This makes it a useful model for dissection of the regulatory pathways that control hyphal tip behaviour. A variety of external stimuli, includingelectric fields, surface modification and nanofabrication techniques, have been used to examine the physical properties of apical growth, such asdirectional memory, asymmetric tip organisation and hyphal tip force. In addition, these methods have been coupled with reverse genetics, fluorescenceprotein-tagging and live-cell imaging to identify cell-polarity components that can enhance, or even reverse, the direction of hyphal growth. The evidenceto date suggests that the direction of hyphal growth reflects the net output from overlapping positional determinants. In addition, there is a strongassociation between proper hyphal tip regulation and the ability of a fungus to invade and damage host tissue.24

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