DSSS - Investigating the Cell Biology of Rice Infection by the Blast Fungus Magnaporthe oryzae

Understanding the biology of plant infection by Magnaporthe oryzae, the causal agent of rice blast, is critical to address its sustainable control. During plant infection, M. oryzae forms a specialised infection structure called an appressorium. This cell forms in response to the hydrophobic leaf surface and requires a specific MAP kinase phosphorelay signalling pathway, coupled to cell cycle control and autophagic cell death of the fungal spore, and these signals collectively lead to appressorium morphogenesis. The appressorium generates enormous turgor, applied as mechanical force to breach the rice cuticle. We are studying the mechanisms that control appressorium function. Re-polarisation of the appressorium requires a turgor-dependent sensor kinase, Sln1, and leads to septin-dependent re-polarisation and plant infection. We have developed mechanosensory methods to directly measure turgor generated during plant infection and investigate its genetic regulation. We are investigating how the Pmk1 MAP kinase pathway regulates morphogenesis using a phosphoproteomic approach that has identified key regulators of plant infection by the fungus. Invasive growth of the fungus in plant tissue then requires differential expression and secretion of a large repertoire of effector proteins that are delivered into plant cells using a specific secretory pathway. The blast fungus develops a transpressorium, a specific invasion structure used by the fungus to move from cell-to-cell using pit field sites, containing plasmodesmata, to facilitate its spread in plant tissue. I will discuss recent progress into understanding the mechanisms of rice infection by this fungal pathogen and the live cell imaging, phosphoproteomic and mechanobiology procedures we have developed to understand its infection biology.