Investigating the biology of plant tissue invasion by the rice blast fungus Magnaporthe oryzae
Nicholas Talbot: University of Exeter
<div>During plant infection, the rice blast fungus <em>Magnaporthe oryzae</em> (syn. <em>Pyricularia </em>oryzae) is able to gain entry to rice leaves using a special infection structure called an appressorium. The infection cell generates enormous turgor, which is focused as mechanical force to breach the rice cuticle. We are studying how appressoria form on the rice leaf surface and how these infection cells function. Appressorium morphogenesis is tightly linked to cell cycle regulation and a specific S-phase checkpoint governs development, while a second S-phase checkpoint is necessary for appressorium function. Penetration peg formation involves re-organisation of the actin cytoskeleton mediated by septin GTPases, controlled by NADPH oxidase activity and a regulated burst of reactive oxygen species in the appressorium. The process is governed by a turgor-sensing mechanism that induces re-polarisation to occur. This involves a novel turgor-sensing kinase that is able to modulate melanisation and solute accumulation, and positively regulate septin-dependent cytoskeletal re-modellnig and re-polarisation of the appressorium. Following entry into the rice epidermis, <em>M. oryzae</em> is able to locate pit fields and use these site to facilitate its movement between rice cells. We have have found evidence that the Pmk1 MAP kinase cascade is involved in cell-to-cell movement by the rice blast fungus. Using a chemical genetic approach, we selectively inhibited the Pmk1 protein kinase, which prevented <em>M. oryzae</em> from moving between rice cells. We have investigated how the MAP kinase is able to exert this effect and how it regulates both the suppression of plasmodesmatal-mediated immune responses and septin-dependent hyphal constriction to allow traversal of the rice cell wall during tissue invasion.</div>
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