Plants have evolved an innate immunity that relies on the recognition of pathogenic determinants. A major consequence of recognition is a rapid and massive transcriptional reprogramming of defense genes that involves changes in chromatin composition and remodeling. Nevertheless, we are far from understanding the chromatin remodeling events that are associated either with the development of disease or with the activation of plant immunity. Moreover, from a pathogen’s perspective, epigenome reprogramming by bacterial pathogens represents a potent virulence strategy to take the control of host gene expression, although the underlying mechanisms remain poorly characterized. Another unexplored question is how chromatin changes occurring at a distance from the infection site may contribute to biotic stress memory. This highly innovative and ambitious project is aimed at investigating for the first time and in a cell-specific manner the chromatin remodeling events that are associated either with the development of plant disease or the activation of plant immunity in response to a bacterial bioagressor. Bacterial wilt caused by Ralstonia solancearum is one of the most destructive bacterial plant diseases because of its extreme aggressiveness, worldwide geographic distribution and broad host range (more than 200 plant species including Solanacea, among which tomato). The Ralstonia PopP2 acetyltransferase effector was previously shown to targets several WKRY defensive transcription factors (TFs) to block their trans-regulating functions needed for defense gene expression, inhibiting basal resistance. PopP2 also targets various epigenetic readers and dissociates them from chromatin. Therefore, it does represent a powerful tool to study effector interference on host epigenome. By using cutting edge technologies and experimental approaches (GFP strand, INTACT, RNA-seq, ChIP-seq, Hi-ChIP), we will try to answer the following questions : (1) How does PopP2 effector affect the host epigenome? For this, we will investigate how the transcriptome responses can be linked with chromatin dynamics impacted by PopP2 that inhibits basal resistance or activate strong immune responses in susceptible and resistant Arabidopsis plants, respectively. (2) What are the chromatin changes induced by Ralstonia solanacearum in infected cells of Arabidopsis and tomato? This analysis will be performed in purified infected cells to provide the necessary resolution. In addition, we would like to investigate how meristematic cells respond to the infection by Ralstonia and whether particular chromatin features shape the plant resistance response to subsequent pathogen attacks (priming). (3) Can disease resistance be improved by manipulating epigenetic processes? To assess the role of particular chromatin modifications in Arabidopsis and tomato response to Rs, we will use reverse genetics (T-DNA insertions, VIGS or CRISPR genome editing) and overexpression approaches. Overall, this project is expected to provide key insights into microbial pathogenesis and reveal important regulatory epigenetic mechanisms of plant immunity. The obtained knowledge will be exploited to determine how epigenetic-related mechanisms can be manipulated to modulate plant response to microbial infection. The long-term goal of this research proposal is to improve current disease management strategies.