Notch-dependent control of myelopoiesis is regulated by fucosylation

摘要: Cell-cell contact–dependent mechanisms that modulate proliferation and/or differentiation in the context of hematopoiesis include characteristic interactions between members Notch family signal transduction molecules and their ligands. Whereas ligands clearly T lymphopoietic decisions, evidence for participation modulating myelopoiesis is much less clear, roles posttranslational control Notch-dependent are unexplored. We report here a myeloproliferative phenotype FX−/− mice, which conditionally deficient cellular fucosylation, consequent to loss on myeloid progenitor cells. In wild-type fucosylation phenotype, we find suppress cells enhance expression target genes. By contrast, fucosylation-deficient progenitors insensitive suppressive effects myelopoiesis, do not transcribe Notch1 genes when cocultured with ligands, have lost ligand-binding phenotype. Considered together, these observations indicate signaling controls vivo vitro identifies requirement ligand binding activity efficiency progenitors.