PU.1 Functions in a Cell-Autonomous Manner to Control the Differentiation of Multipotential Lymphoid–Myeloid Progenitors
Copyright policy )PU.1 Functions in a Cell-Autonomous Manner to Control the Differentiation of Multipotential Lymphoid–Myeloid Progenitors
Transcription factor PU.1 is required for the development of lymphoid and myeloid progenitors during fetal hematopoiesis. By generating chimeric animals using PU.1-/- ES cells or PU.1(-/-) hematopoietic progenitors, we demonstrate that PU.1 functions in an exclusively cell-autonomous manner to regulate the development of the lymphoid-myeloid system. Multipotential lymphoid-myeloid progenitors (AA4.1+, Lin-) are significantly reduced in PU.1(-/-) embryos and fail to differentiate into B lymphoid or myeloid cells in vitro. These results suggest that the lymphoid and myeloid lineages develop in the fetal liver from a common hematopoietic progenitor not shared with erythrocytes and megakaryocytes. Finally, the Ikaros gene is expressed in PU.1 mutant embryos, suggesting that PU.1 and Ikaros are independently required for specification of embryonic lymphoid cell fates.
- University of Pennsylvania United States
- University of Chicago United States
- Howard Hughes Medical Institute United States
- UNIVERSITY OF CHICAGO
Male, Lymphoid Tissue, Immunology, Bone Marrow Cells, Cell Count, Cell Line, Ikaros Transcription Factor, Mice, Proto-Oncogene Proteins, Immunology and Allergy, Animals, Erythropoiesis, Chimera, Cell Differentiation, Embryo, Mammalian, Hematopoietic Stem Cells, Mice, Mutant Strains, DNA-Binding Proteins, Mice, Inbred C57BL, Infectious Diseases, Gene Expression Regulation, Female, Erythrocyte Transfusion
Male, Lymphoid Tissue, Immunology, Bone Marrow Cells, Cell Count, Cell Line, Ikaros Transcription Factor, Mice, Proto-Oncogene Proteins, Immunology and Allergy, Animals, Erythropoiesis, Chimera, Cell Differentiation, Embryo, Mammalian, Hematopoietic Stem Cells, Mice, Mutant Strains, DNA-Binding Proteins, Mice, Inbred C57BL, Infectious Diseases, Gene Expression Regulation, Female, Erythrocyte Transfusion
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