Abstract EN:

Classical melanocytes of the skin synthesize the melanin which protects the organism against the deleterious effects of UV rays. It is generally thought that melanocytes derive from neural crest cell (NCC) migrating along the dorso-lateral pathway. However, it seems that a substantial number c melanocytes may come from Schwann cell precursors (SCPs), cells derived from the NCC migrating ventrally. Non-classical melanocytes are present in the heart, where their function remains poorly understood. These mélanocytes derive from a sub-population of NCC called cardiac neural crest but the molecular mechanisms regulating their development are still unknown. During embryonic development, beta-catenin plays a crucial role in the spécification of NCC to become melanocytes that migrate dorso-laterally. Therefore, we were interested in the role of this protein in the specification of cardiac melanocytes on the one hand, and of melanocytes derived from SCPs 01 the other hand. To do so, we chose to constitutively activate beta-catenin in vivo in cells derive from the neural crest using the Tyr::Cre transgene. We found that beta-catenin regulates the specification of a bipotent precursor coming from the cardiac neural crest, which has the ability to form smooth muscle cells (SMCs) and melanocytes in the Ductus Arteriosus, an embryonic artery Connecting the aorta to the pulmonary artery. Beta-catenin favors the melanocytic fate at the expense of the SMC fate, leading to a congenital cardiac pathology called Patent Ductus Arteriosus Preliminary results show that beta-catenin also controls the cell fate of SCPs, favorising the melanocytic fate at the expense of the glial fate.