Plants and pathogenic microorganisms are in constant conflict with each other. Understanding the molecular networks that trigger resistance, along with the molecular networks that pathogens might co-opt to infect susceptible plants, is important for developing the integrated, holistic perspective that is necessary for innovative development of engineered resistance to current and emerging pathogens. The first objective of the dissertation was to increase the understanding of mechanisms by which plants recognize pathogen attack and mount an appropriate defense response. These experiments focused on resistance triggered by the Arabidopsis thaliana R gene, RPP7, which encodes a coiled-coil nucleotide binding-leucine-rich repeat (CC-NB-LRR) protein that activates race-specific resistance to the downy mildew pathogen, Hyaloperonospora parasitica (Hpa). Previously-published genetic epistasis tests have established that RPP7 activates defense responses through a signaling mechanism that does not require accumulation of salicylic acid (SA), or components of the ethylene and jasmonate response pathways. Furthermore, RPP7 is not strongly compromised by mutations in genes associated with defense signal transduction (PAD4, NDR1, NPR1, RAR1). Double mutant combinations of these signal transduction components were analyzed to detect additive or functionally-redundant contributions to RPP7-dependent resistance. Most of the double mutants support an enhanced level of asexual sporulation compared to the single mutant parental lines. Time-course experiments with histochemical stains revealed that these double mutants delay, but do not suppress, the oxidative burst and the hypersensitive response. These results suggest that RPP7 activates multiple signaling pathways, each of which makes incremental contributions to the timing of defense activation. The second objective of the dissertation was to investigate the role that auxin plays in enabling virulent H. parasitica to colonize Arabidopsis. Transcript profiling revealed induction of auxin-associated genes in response to infection of Arabidopsis thaliana by virulent strains of the oömycete pathogen, H. parasitica. Experiments with the DR5 / Ph. D.

La vigne (Vitis vinifera) est sensible à de nombreuses maladies, nécessitant l'utilisation massive de produits phytosanitaires. Des méthodes alternatives doivent être développées. Chez la plante modèle Arabidopsis thaliana, les gènes AtNPR1, AtNDR1 et AtEDS1 interviennent dans la voie de signalisation contrôlée par l'acide salicylique (SA) en réponse aux agents pathogènes biotrophes. Nous avons identifié par une approche gène candidat chez V. vinifera, de potentiels orthologues de ces trois gènes (VvNPR1.1, VvNPR1.2, VvNHL1 et VvEDS1).Nos travaux ont montré que les protéines VvNPR1 fusionnées à la GFP sont localisées dans le noyau. De plus, la surexpression transitoire des VvNPR1 stimule l'expression de gènes de défense en système hétérologue et homologue. La surexpression de VvNPR1.1 chez le mutant npr1 restaure les différents phénotypes du mutant, contrairement à la surexpression de VvNPR1.2. VvNPR1.1 est semble être l'orthologue d'AtNPR1. La surexpression de VvNHL 1 chez le mutant ndr1 ne rétablit pas la résistance à Pseudomonas syringae. Cependant, ces plantes sont plus sensibles à Botrytis cinerea, probablement par l'accentuation d'un processus de mort cellulaire. L'expression de VvNHL 1 est réprimée en réponse à B. cinerea, constituant un mécanisme de défense contre les nécrotrophes. VvNHL1 semble donc promouvoir la mort cellulaire. L'expression de VvEDS1 est stimulée en réponse à des agents pathogènes et à un traitement par le SA. L'étude de sa fonction est en cours par surexpression chez des mutants eds1. La compréhension des voies de signalisation des réponses de défense chez la vigne devrait permettre l'obtention de vignes plus résistantes aux agents pathogènes. / Vitis vinifera is susceptible to many pathogens, thus requiring a massive use of phytochemicals. Alternative methods have to be developed. In the madel plant Arabidopsis thaliana, the AtNPR1, AtNDR1 and AtEDS1 genes are components of the salicylic acid (SA) signalling pathway involved in resistance to biotrophic pathogens. Using a candidate gene approach, we have identified putative orthologs of these genes in the grapevine genome (VvNPR1.1, VvNPR1.2, VvNHL 1 and VvEDS1).Our work shows thal VvNPR1-GFP fusion proteins are localized in the nucleus. Moreover, transient overexpression of VvNPR1 genes induces defence gene expression, in bath heterologous and homologous systems. Overexpression of VvNPR1.1 in npr1 mutants restores the different phenotypes of the mutants, while VvNPR1.2 overexpression does not. These results strongly suggest that VvNPR1.1 is the AtNPR1 ortholog. Overexpression of VvNHL 1 in ndr1 mutants does not restore resistance to Pseudomonas syringae. However, resistance to Botrytis cinerea in these plants is weakened, probably because of stimulation of cell death. Furthermore, VvNHL1 repression following B. cinerea infection in V. vinifera could be considered as a defence mechanism against necrotrophic pathogens and suggests thal VvNHL1 is involved in promotion of cell death. VvEDS1 expression is induced by pathogens infection and SA treatment. VvEDS1 functional characterization is in progress using eds1 Arabidopsis mutants overexpressing VvEDS1. Knowledge of defence signalling pathways in V. vinifera will contribute to obtain pathogen resistant grapevines.