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PU.1 regulates both cytokine‐dependent proliferation and differentiation of granulocyte/macrophage progenitors
Open accessAbstract
PU.1 is a unique regulatory protein required for the generation of both the innate and the adaptive immune system. It functions exclusively in a cell-intrinsic manner to control the development of granulocytes, macrophages, and B and T lymphocytes. We demonstrate that mutation of the PU.1 gene causes a severe reduction in myeloid (granulocyte/macrophage) progenitors. PU.1 -/- myeloid progenitors can proliferate in vitro in response to the multilineage cytokines interleukin-3 (IL-3), IL-6 and stem cell factor but are unresponsive to the myeloid-specific cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF), G-CSF and M-CSF. The failure of PU.1 -/- progenitors to respond to G-CSF is bypassed by transient signaling with IL-3. In the presence of IL-3 and G-CSF, PU.1 -/- progenitors can differentiate into granulocytic precursors containing myeloperoxidase-positive granules. Thus PU.1 is not essential for specification of granulocytic precursors, but is required for their further differentiation. The failure of PU.1 -/- progenitors to respond to M-CSF is due to lack of c-fms gene transcription. Transduction of c-fms into PU.1 -/- myeloid progenitors bypasses the block to M-CSF-dependent proliferation but does not induce detectable macrophage differentiation. Therefore, PU. 1 appears to be essential for specification of monocytic precursors. Importantly, retroviral transduction of PU.1 into mutant progenitors restores responsiveness to myeloid-specific cytokines and development of mature granulocytes and macrophages. Thus PU.1 controls myelopoiesis by regulating both proliferation and differentiation pathways.
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“These findings are consistent with prior work indicating PU.1 can constrain myelopoietic activity (DeKoter et al., 1998; Dakic et al., 2005)”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as DeKoter et al., 1998
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“We and others have previously shown that the myeloid ‘master regulator’ transcription factor PU.1 (DeKoter et al., 1998; Singh et al., 1999) is upregulated at the transcriptional and protein levels in HSC by chronic inflammatory signals such as the pro-inflammatory cytokine IL-1β (Algeciras-Schimnich et al., 2003; Pietras et al., 2016; Hernandez et al., 2020; Rabe et al., 2020; Chavez et al., 2021”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as DeKoter et al., 1998
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“Consistent with this, PU.1 is expressed at low levels in hematopoietic stem cells and is relatively more abundant during monocyte versus neutrophil differentiation (43).”
From PU.1, Interferon Regulatory Factor (IRF) 2, and the Interferon Consensus Sequence-binding Protein (ICSBP/IRF8) Cooperate to Activate NF1 Transcription in Differentiating Myeloid Cells (2007) · cites this paper as [43]
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Imperatore, F. (2013) · theses.fr (ABES) · doi:10.70675/c50451dcz5c35z4befzba7dze6365925fc5f
Balancing inflammatory signaling in hematopoiesis: roles of MIRC11 and miR-146a
Boucher, A. C., Payne, T. J., Pulakanti, K., Rao, S., & Dahl, R. E. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1828453
“Hematopoietic colony assays were performed as described previously with minor modi fi cations (42, 43).”
Ramani, M., Nguyen, N., Solis, J., Tenen, D. G., & Trinh, B. Q. (2026) · Biology · doi:10.3390/biology15181657
“Through these dynamic partnerships, PU.1 integrates developmental signals, cytokine responses, and chromatin state to govern lineage commitment, immune activation, and cellular plasticity [80,103].”
The molecular mechanism of the aberrant expression of the B-cell specific PAX5 gene in t(8;21) AML
Ray, D. (2013) · University of Birmingham Institutional Research Archive (University of Birmingham)
Metadata
- Authors
- DeKoter, R. P., Walsh, J. C., & Singh, H.
- Affiliations
- Howard Hughes Medical Institute (US)
- University of Chicago (US)
- Corresponding author
- Singh, Harinder
- Venue
- The EMBO Journal
- Published
- 1998-08-03
- Volume
- 17
- Issue
- 15
- Pages
- 4456-4468
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC1170777
- OpenAlex
- W2081654176
- Cited by
- 296
- References
- 77
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 4 · 2023: 6 · 2022: 1 · 2021: 3 · 2020: 5 · 2019: 9 · 2018: 4 · 2017: 6 · 2016: 12 · 2015: 11 · 2014: 10 · 2013: 13 · 2012: 6
- FWCI
- 7.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- University of Toronto
- National Institutes of Health
- National Heart, Lung, and Blood Institute (T32HL007237)
- National Institute of General Medical Sciences (T32GM007151)
- Topics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- PU.1, ETS transcription factors, myeloid progenitor cells, granulocytic differentiation, macrophage differentiation, myelopoiesis, cytokine responsiveness, interleukin-3, granulocyte colony-stimulating factor, macrophage colony-stimulating factor, c-fms, granulocytic precursors, retroviral transduction
- MeSH terms
- Proto-Oncogene Protein Spi-1, Animals, Cell Differentiation, Cell Division, Colony-Forming Units Assay, Female, Gene Expression Regulation, Granulocytes, Hematopoietic Stem Cells, Interleukin-3, Macrophages, Male, Mutation, Proto-Oncogene Proteins, Retroviridae, Transduction, Genetic, Trans-Activators, Interleukin-6, Macrophage Colony-Stimulating Factor, Granulocyte-Macrophage Colony-Stimulating Factor, Granulocyte Colony-Stimulating Factor, Cytokines, Genes, fms, Mice, Knockout, Stem Cell Factor, Mice
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