Centrosomal protein CEP55 is a critical regulator of cytokinesis, and its deregulation has been linked to tumorigenesis. Loss of function mutations in Cep55 have also been shown to perturb embryogenesis, particularly affecting neural development. Cep55 expression in cells must be tightly regulated, as both overexpression and reduced levels of expression can cause cytokinetic abscission defects leading to genomic instability. CEP55 also promotes PI3K/AKT signaling which confers a survival advantage to cancer cells. However, despite more than a decade of research into characterizing this protein, the molecular function of CEP55 during tumorigenesis and embryonic development in mammals is not well defined. In this thesis, we have generated a Cep55 knockout (Cep55-/-) mouse model, which is the first in vivo knockout model for this gene to our knowledge. Cep55-/- mice exhibited late embryonic lethality associated with a wide range of neural defects. We showed that Cep55-/- embryos at E14.5 exhibit depleted neural stem cells in the ventricular zone. This was caused by a significant decrease in proliferation with a concomitant increase in apoptosis of radial glial (RGCs : PAX6+), intermediate progenitor cells (IPC: TBR2+) and postmitotic neurons (PMN: TBR1+). As a consequence, we observed reduced numbers of neurons in the cortical plate at later stages of embryonic development. [...]