PU.1 determines the self-renewal capacity of erythroid progenitor cells
Open accessAbstract
PU.1 is a hematopoietic-specific transcriptional activator that is absolutely required for the differentiation of B lymphocytes and myeloid-lineage cells. Although PU.1 is also expressed by early erythroid progenitor cells, its role in erythropoiesis, if any, is unknown. To investigate the relevance of PU.1 in erythropoiesis, we produced a line of PU.1-deficient mice carrying a green fluorescent protein reporter at this locus. We report here that PU.1 is tightly regulated during differentiation—it is expressed at low levels in erythroid progenitor cells and down-regulated upon terminal differentiation. Strikingly, PU.1-deficient fetal erythroid progenitors lose their self-renewal capacity and undergo proliferation arrest, premature differentiation, and apoptosis. In adult mice lacking one PU.1 allele, similar defects are detected following stress-induced erythropoiesis. These studies identify PU.1 as a novel and critical regulator of erythropoiesis and highlight the versatility of this transcription factor in promoting or preventing differentiation depending on the hematopoietic lineage.
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Spi-1 is expressed at low level in erythroid progenitors and downregulated upon terminal differentiation.
“Spi-1 is expressed at low level in erythroid progenitors and downregulated upon terminal differentiation (15,16).”
From Spi-1/PU.1 activates transcription through clustered DNA occupancy in erythroleukemia (2012) · cites this paper as [15]
TNF-a induces activation of caspases in erythroid precursor cells; subsequent cleavage and depletion of GATA-1 boosts PU.1-mediated skewing.
“In concert, another prominent inflammatory cytokine, TNF-a, induces activation of caspases in erythroid precursor cells.The subsequent cleavage and depletion of GATA-1 as vital transcription factor for the erythroid lineage boosts the PU.1-mediated skewing.29,30”
From Inflammatory bone marrow microenvironment (2019) · cites this paper as [29]
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- Authors
- Back, J., Dierich, A., Bronn, C., Kastner, P., & Chan, S.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- From the Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS-INSERM-ULP, ILLKIRCH CEDEX, France.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2004-05-15
- Volume
- 103
- Issue
- 10
- Pages
- 3615-3623
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2011346553
- Cited by
- 123
- References
- 50
- Citations by year
- 2025: 4 · 2024: 2 · 2023: 4 · 2022: 6 · 2021: 4 · 2020: 2 · 2019: 8 · 2018: 2 · 2017: 6 · 2016: 2 · 2015: 6 · 2014: 6 · 2013: 5 · 2012: 8
- FWCI
- 6.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Association pour la Recherche sur le Cancer
- Topics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Kruppel-like factors research
- Keywords
- PU.1, erythropoiesis, erythroid progenitor cells, self-renewal, transcription factors, terminal differentiation, apoptosis, proliferation arrest, hematopoietic lineage
- MeSH terms
- Proto-Oncogene Protein Spi-1, Animals, Cell Differentiation, Cell Division, Cells, Cultured, Erythroblasts, Erythropoiesis, Fetus, Gene Expression Regulation, Luminescent Proteins, Mice, Transgenic, Proto-Oncogene Proteins, Trans-Activators, Erythroid Precursor Cells, Apoptosis, Mice, Knockout, Green Fluorescent Proteins, Mice
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