Fucose-Dependent Differentiation and Gene Expression of Common Myeloid Progenitor Cells Through Notch Signaling Pathways

The Notch pathway is an extensively utilized, evolutionarily maintained regulatory system which mediates a wide range of fate decisions among multipotent precursor cells by inhibiting differentiation along one pathway while promoting self-renewal or differentiation along an alternative pathway. Notch signaling has been shown to affect haematopoietic stem cell (HSC) self-renewal and differentiation, T cell versus B cell fate specification, and myeloid cell differentiation. The diverse functions of Notch in vertebrates are facilitated by complex in-teractions between four Notch receptors and five Notch ligands, all of which are expressed by hematopoietic cells and stromal cells. More-over, Notch signaling is modulated by genes such as fringe as well as two unusual types of O-linked glycosylation; the addition of O-linked glucose (O-glucose) and O-linked fucose (O-fucose). Our goal is to determine whether in vitro myeloid differentiation is regulated by Notch activation, and whether this is a fucose-dependent process. Specifically, we focused our research on common myeloid progenitor (CMP) cell differentiation and the dynamic change of Notch-targeted genes during Notch regulated myeloid differentiation that is modified by fucosylation.