The blast fungus *Magnaporthe oryzae* builds a pressurised infection cell called an appressorium to punch through the tough outer layer of a rice plant, then switches to a second structure, the transpressorium, to move from one rice cell to the next. This project aims to understand how proteins called septins control the fungus's ability to build and operate both of these infection structures. Septins are known to be necessary for infection, but exactly how they are recruited, organised, and function inside the cell is not understood. The researchers will map the full set of proteins that interact with septins in both appressoria and transpressoria, identify the signalling pathways that trigger septin assembly, and test whether septin complexes act as organising hubs that direct virulence factors to the right place at the right time. This is fundamental science. If successful, it will reveal the molecular wiring that allows a devastating crop pathogen to invade its host, which could eventually inform new strategies for protecting rice from blast disease.
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The major aim of this research project is to understand how morphogenetic proteins called septins condition the ability of a pathogenic fungus to cause disease within a plant. Plant pathogenic fungi have evolved specialised infection structures to enter their hosts. The devastating blast fungus Magnaporthe oryzae infects rice plants using a pressurised infection cell called an appressorium to breach the tough outer layer of plants. Once inside plant tissue, the fungus then develops a second type of infection structure, called a transpressorium, which it uses to move from one rice cell to the next. Recent evidence has shown that heteromeric septin complexes are necessary for the function of both appressoria and transpressoria. This ambitious research project will define the molecular basis of septin recruitment, organisation and function within these infection structures. I propose to evaluate the membrane curvature dependency of septin aggregation and then identify upstream components that regulate septin recruitment. A comprehensive septin interactome will be defined for both cell types using proteomic analysis and proximity labelling methods, during a time series of appressorium and transpressorium development. In this way, novel septin interactors will be identified and functionally characterised. In parallel, phosphoproteomic analysis will be used to investigate the specific phosphorylation events necessary for septin assembly and to identify the corresponding signalling pathways. Using a combination of forward genetic screens, targeted gene editing, proteomic analysis and live cell imaging, the project will test the hypothesis that septin complexes act as major organising centres within fungal invasive cells, required for the focused deployment of polarity and virulence determinants to enable invasive growth by fungal infection cells.
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