Curent Position :
CNRS Research Scientist (CR2)
Post-Doctoral Training :
2008 - 2010 INSERM Young Researcher, Institut Cochin, Maire Lab.
2005 - 2008 Post-doctoral Fellow, Ottawa Health Research Institute, Rudnicki Lab.
2004 - 2005 Temporary Teacher Position, Nantes University.
Education :
2001 - 2004 PhD for Sciences in Developmental Biology, University of Nantes, France. Thesis title : Embryonic cells : Tools for skeletal muscle reconstruction.
1999 – 2001 Master in Science, University of Nantes, France
Skeletal muscles are one of the two sorts of striated muscles of the vertebrate body (the other being the cardiac muscle). They are fixed to the bones by the tendons, and have the function to move the body in space, under the control of the central nervous system. A skeletal muscle is constituted of individual components known as muscle fibers (myofibers), cylindrical multinucleated cells containing contracting myofibrils.
Homeostasis of the adult skeletal muscle tissue relies on a pool of quiescent resident precursors located in a niche around the myofibers: the satellite cells. Satellite cells are committed muscle stem cells responsible for the postnatal growth and the regenerative capacity of the muscle tissue. During muscle regeneration, satellite cells leave quiescence to proliferate and then differentiate to form new myofibers, while a sub-population exit the cell cycle to self-renew and replenish the satellite niche in the new tissue. During this process signals from the local milieu and the microenvironment instruct cycling satellite cells and control myogenic fate choice.
Our previous report highlighted that numerous Wnt proteins are secreted during muscle regeneration. In the recent years, the canonical Wnt cascade has emerged as a critical regulator of stem cells in many adult tissues. However, conflicting reports established roles for the canonical Wnt/ß-Catenin pathway during adult skeletal muscle regeneration. Our goal is to comprehend the roles of Wnt/β-Catenin signals during adult muscle regeneration. We thus designed a research strategy based on the generation of mouse genetic models with satellite cell specific Wnt/ß-Catenin gain- and loss-of-function mutations.