My research group belong to Laurent Boyer lab where we focus on microbial virulence and inflammatory signaling in diseases. We use various experimental models ranging from invertebrate to mammalian systems to understand the molecular bases of innate immune response during infection. My group focuses on the importance of ubiquitination, a post-translational modification altering protein stability, location or activity, in innate immune system. Indeed, ubiquitination is a reaction positively and negatively regulated by hundreds of enzymes and involved in virtually all physiological processes. Its implication in innate immunity has been particularly well described for the regulation of the NFkB pathway (Iwai, Biochim Biophys Acta 2014). However, less is known about the role that ubiquitination play in regulating other innate immune pathways. C. elegans has evolved an NFkB-independent innate immune system. We have previously identified the HLH-30 transcription factor as a key conserved immune regulator providing host defense against the human pathogen S. aureus (Visvikis et al. Immunity 2014). Our research aims at identifying and characterizing Ubiquitin-modifying enzymes regulating the HLH-30/TFEB-dependent immune response. Using RNAi-Seq analysis and fluorescent-reporter based cherry pick RNAi screen, we are identifying upstream regulating and downstream effector ubiquitin-modifying enzymes that modulate innate immune responses and host defense in C. elegans. Making use of mammalian experimental systems, we aim at identifying the conserved immune regulatory factors also providing host defense against infection in vertebrate model.