Cadherins are intercellular adhesion receptors allowing to make a link between the adjacent cell and the cytoskeleton. During cell contact formation, cadherins association to the actin cytoskeleton, through the recruitment of alpha- and beta-catenins, has been extensively studied. Yet, the contribution of microtubules (MTs) in this context begins only to be unraveled. My thesis work focused on a better understanding of the relationship between N-cadherin (Ncad) and MTs in two particular processes: cell adhesion and migration. Using Ncad recombinant substrates, I first showed that, in a context of cell adhesion (myogenic cell line), (i) Ncad engagement was inhibiting MT recruitment and dynamics through actin regulation and (ii) MT stabilization led to Ncad accumulation at cell contacts. Thus Ncad and MTs establish a negative regulation loop in this cellular context. Next I showed that, during cell migration (model of rat hippocampal neurons), Ncad stimulates MT dynamics. In conclusion, these results reveal a functional link between Ncad and MTs dependent of actin, which nature is different depending on the cellular context. My work highlights a novel molecular mechanism involved in contact formation and cellular migration. I have also participated to the study of the role of Ncad during survival, work published in PlOS ONE. We showed that Ncad promotes neuronal survival by stimulating a signaling pathway activating the Mek1/2 kinases, leading to the degradation of the pro-apoptotic protein Bim
