During development, extensive cell movements change the shape the embryo from a sphere with a radial symmetry to an elongated, multilayered and asymmetric organism. The first morphogenetic movement occurs at gastrulation, when the mesoderm (that gives rise to the muscles, heart and blood vessels) and the endoderm (that gives rise to the gut, liver, pancreas etc…) are internalized. During neurulation, the neural tissue “rolls up” into a tube and the somitic mesoderm (future muscles) undergoes segmentation and rotation. After neurulation is complete, the dorsal most cells called neural crest cells undergo extensive migrations in the embryos and give rise to the melanocytes, and ganglia in the trunk and to most of the facial structures in the head. The Cranial Neural Crest (CNC) originate from the dorsal tube of the brain and migrate along define pathways (mandibular, hoid and branchial) and will coordinate the entire development of the face. They will eventually differentiate into many structures including the majority of the craniofacial bones, cranial nerves, glial cells and teeth. The CNC is one of the most plastic cell populations in the animal kingdom, capable of differentiating into structures of variable shape depending on the species, allowing them to adapt themselves to their feeding habits. For example, the jaw and nasal region of birds forms the beak capable of breaking hardest seeds (Toucan and parrots) or capable of reaching down the long nectar tubes of flowers (humming birds), while in elephants, it forms an elongated and flexible trunk. The plasticity of the CNC is also evident in the variety of birth defects associated with it, which result from improper migration, survival or differentiation of the CNC (Cleft palate, Treacher Collins syndrome, CHARGE syndrome etc…). What drives this plasticity? Can we manipulate it so prevent or correct craniofacial defects?
Two projects are currently developed. The first one concerns the role and the evolution of ADAM9, 12 13 and 19 during CNC migration and craniofacial development. The type extracellular metalloproteases are critical for CNC migration in the frog Xenopus laevis. We have showed that ADAM13 metalloprotease domain cleaves extracellular proteins important for cell migration like cadherin-11 while its cytoplasmic domain modulate the transcription of various genes by a mechanism similar to the described for Notch. Interestingly, a mutation event has deleted the cytoplasmic region in placental mammals, which raise the following questions: Are ADAM expressed in the CNC of other species? Are involved in their craniofacial development? Do they perform the same functions as the frog ADAM13? We are currently investigating these questions in zebrafish, chicken, grey tail opossum and mouse with Drs. Thisse, Taneyhill, Sears and Tremblay. The second project investigates the role of the protein LBH during CNC migration and craniofacial development in the frog embryo. This project is developed in collaboration with Dr Albertson, who works on the microevolution in cichlids and has found that lbh could be one of the genes involved in the rapid evolution of their jaw.
Learn more at www.vasci.umass.edu/research-faculty/helene-cousin
- PhD Université Paris VI, France (2000)
- Postdoctoral training: University of Virginia, Charlottesville; University of Massachusetts, Amherst