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Microbial pathogens have evolved sophisticated strategies to infect their hosts, often resulting in disease. The host, in turn, can produce proteins (ie receptors) that specifically recognize pathogen molecules to trigger immune responses. In plants, effector-triggered immunity (ETI) is mediated by intracellular nucleotide-binding–leucine-rich repeat receptors (NLRs) that resemble mammalian NLRs. To date, the mechanisms by which NLRs activate immunity pathways are still poorly understood. In this context, we are trying to investigate receptor signaling dynamics at the chromatin during transcriptional reprogramming in ETI controlled by the RRS1-R/RPS4 NLR pair from Arabidopsis. The acetyltransferase PopP2 effector from Ralstonia solanacearum is recognized by this NLR pair. Indeed, PopP2 acetylates a key lysine within the integrated WRKY domain of RRS1-R receptor leading to the disruption of RRS1-R-DNA association and the activation of RPS4-dependent immune response. The nature of NLR dynamics at the DNA and its relation to gene expression changes are not known. We specifically aim to elucidate at which chromatin sites pre-activated RPS4/RRS1-R bind and if the effector–activated immune complex relocates on the DNA. For this, we use of a DNA adenine methylation IDentification (DamID) approach that will be presented. We are also exploring how PopP2 function might involve the targeting of specific chromatin sites through the acetylation of epigenetic readers.