Appressorium-mediated plant infection is a common strategy used by many plant pathogenic fungi. Understanding the underlying genetic network that controls cellular differentiation of appressorium is therefore pivotal to design durable resistance strategies for these devastating pathogens. This thesis describes four published studies, which investigate the role of septin GTPases in infection and the role of secretion during plant tissue invasion by the rice blast pathogen Magnaporthe oryzae. Appressorium development involves a series of morphogenetic changes that are tightly regulated by cell cycle checkpoints. Entry into mitosis allows differentiation of an appressorium, while penetration peg emergence appears to require progression through subsequent cell cycle checkpoints and cytokinesis. The studies presented here show that symmetry-breaking events that occur during appressorium differentiation are mediated by scaffold proteins, named septins. Septin GTPases recruit actomyosin ring components during septation and define the site of cytokinesis. They also recruit a toroidal cortical F-actin network to the appressorium pore that provides cortical rigidity to facilitate plant infection. Septins act as diffusion barriers for proteins that mediate membrane curvature necessary for penetration peg formation. Repolarization of the F-actin cytoskeleton at the appressorium pore is essential for plant penetration and is controlled by cell polarity regulators, such as Cdc42 and Chm1. Septin-mediated plant infection is regulated by NADPH oxidase (Nox) dependent generation of reactive oxygen species (ROS). The Nox2/NoxR complex is essential for septin organization at the appressorium pore. Septins are therefore key determinants of appressorium repolarization. I also report an investigation of fungal secretory processes during tissue invasion and present evidence that distinct pathways are involved in effector secretion by Magnaporthe oryzae. A BrefeldinA-sensitive pathway is necessary for secretion of apoplastic effectors, such as Bas4 and Slp1, while a BrefeldinA-insensitive pathway is necessary for secretion of effectors destined for delivery to rice cells.

La pyriculariose, maladie causée par le champignon phytopathogène Magnaporthe oryzae, affecte gravement le riz qui constitue l'aliment de base de plus de la moitié de la population mondiale. La connaissance des mécanismes de résistance est nécessaire pour guider la sélection variétale. Au cours de ce travail, une synthèse de la littérature a permis de recenser plus de 60 gènes régulateurs du riz impliqués dans la résistance du riz à différents agents pathogènes. Nous avons complété ces données en étudiant le rôle in planta de huit de ces régulateurs. Un rôle central du facteur de transcription OsWRKY28 a pu être établi et le rôle du récepteur CEBiP a été démontré. Ce travail a aussi exploré l'éventuelle implication d'une nouvelle famille de récepteurs, les Wall-Associated Kinases (WAK) dans la résistance chez le riz. Ce travail montre l'implication des WAK dans la résistance à M. oryzae. Alors que la transcription de la plupart de ces gènes est induite au cours de l'infection, celle du gène WAK112d est réprimée. La régulation transcriptionnelle précoce observée pour certains gènes WAK est déclenchée par la chitine et sous contrôle partiel du récepteur CEBiP et d'OsWRKY28. L'étude de mutants d'insertion et de lignées de surexpression a permis de montrer le rôle positif de trois gènes WAK et le rôle négatif du gène WAK112d dans la résistance. Des approches biochimiques seront nécessaires pour comprendre le mode de fonctionnement de ces récepteurs et pour les relier aux autres systèmes de défense connus. / Rice blast disease, caused by the fungus Magnaporthe oryzae, is one of the most serious diseases on rice which is the staple food of more than the half of the world population. Improving our knowledge of resistance mechanisms is necessary to guide breeding programs. In this study, we reviewed over 60 rice gene regulators involved in resistance against various pathogens. We completed these data by analyzing the role of eight of these regulators. A pivotal role for the transcription factor OsWRKY28 has been established and the role of the CEBiP receptor in planta has been demonstrated. This work also shows the implication of some WAKs in rice blast resistance. Whereas the transcription of most of these genes is induced, transcription of the OsWAK112d gene is repressed upon infection. The early transcriptional regulation observed for some OsWAK genes is triggered by chitin and partially under CEBiP and OsWRKY28 regulation. Analysis of insertion mu tants and over-expressor lines revealed a positive role for three OsWAK genes and a negative role for OsWAK112d gene in rice blast resistance. Biochemical studies will be essential to understand how these receptors work and to connect them to other known defense systems.