The diverse cell types of the body exhibit distinct morphologies and functions, despite the fact that (with the exception of antigen receptor genes in lymphocytes) the genome sequence is essentially identical among all cell types in an individual. The molecular basis for this diversity is that among the approximately 22,000 genes encoded by the human genome, only a specific set is expressed in a given cell type. The differentiation of stem or progenitor cells to mature cells is a sequential process of activation, inactivation, or maintenance of the selected genes—i.e., transcriptional control—that ultimately determines cell fate. Numerous studies have shown that transcription factors and epigenetic regulators play essential roles in cell differentiation. Dysregulation of these processes can result in various diseases, including cancers, such as leukemias in the case of hematopoiesis. Myeloid cells, e.g., granulocytes, monocytes/macrophages, dendritic cells, and mast cells, are generated from hematopoietic stem cells in the bone marrow via multipotent progenitors, common myeloid progenitors, granulocyte–monocyte progenitors, and more committed progenitors. (Quoted from an Editorial by Tamura, Int J Hematol. 2015 Apr;101(4):317-8. doi: 10.1007/s12185-015-1770-8.)
In this “Myeloid Chromatin Atlas”, we provide the platform of grasping the changes in epigenetic landscape and key transcription factors binding during the development of myeloid cells, particularly mononuclear phagocytes such as monocytes and dendritic cells. Our high-quality data by chromatin immunoprecipitation-sequencing (ChIP-seq), microarray, RNA-seq, and more can be viewed and downloaded in this Altas.
Please do not forget to cite our paper (Kurotaki et al., Cell Reports
2018 Mar 6;22(10):2628-2641. ) whenever you publish a paper using our data