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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PU.1 can constrain myelopoietic activity.
“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
The Discussion reports that PU.1-deficient progenitors are reduced in number and that restoring PU.1 restores their ability to form macrophage and neutrophil colonies. In the conditions studied, the paper presents PU.1 as supporting myeloid proliferation and differentiation, not constraining myelopoietic activity. (LLM, conf=0.87)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredPU.1 is upregulated at the transcriptional and protein levels in HSC by chronic inflammatory signals such as IL-1β.
“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
PU.1 is expressed at low levels in hematopoietic stem cells and is relatively more abundant during monocyte versus neutrophil differentiation.
“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]
The Introduction (page unavailable) says PU.1 is expressed in various hematopoietic lineages, but does not give its level in hematopoietic stem cells. The discussion of monocytic and granulocytic development addresses PU.1’s functional roles, not whether its expression is higher during monocyte than neutrophil differentiation. Searches for stem-cell expression levels and a monocyte–neutrophil expression comparison found no passage establishing either claim. (LLM, conf=0.74)
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- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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