Tooth enamel is the strongest, most densely mineralized tissue in the human body. Genetic defects in the development of tooth enamel can lead to the condition amelogenesis imperfecta – a genetic disorder that causes tooth enamel to be under mineralized and prone to rapid wear and breakage. While many genes have been implicated in the development of amelogenesis imperfecta, nearly 50 percent of all cases have an unknown cause. This highlights a critical need to identify new genes and proteins that are important for enamel development.

Of interest to us is the protein mediator of cell motility 1 (MEMO1). MEMO1 is a multifaceted protein with functions ranging from cell migration to production of redox species. Here we focus on the role of MEMO1 during tooth enamel development by using knockout mouse models. We found that loss of MEMO1 from the ameloblast causes less tooth enamel to form and for it to be less mineralized – a phenotype reminiscent of amelogenesis imperfecta. Furthermore, examination of cellular RNA from a knockout cell line and mouse ameloblasts point to a role for MEMO1 is regulating the cytoskeleton of the cell. These data suggest that MEMO1 has a critical function in the ameloblast and furthers our understanding of process of enamel formation.