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p53-Mediated Hematopoietic Stem and Progenitor Cell Competition
Open accessAbstract
Cell competition was originally described in Drosophila as a process for selection of the fittest cells. It is likely to play an important role in tissue homeostasis in all metazoans, but little is known about its role and regulation in mammals. By using genetic mosaic mouse models and bone marrow chimeras, we describe here a form of cell competition that selects for the least damaged cells. This competition is controlled by p53 but is distinct from the classical p53-mediated DNA damage response: it persists for months, is specific to the hematopoietic stem and progenitor cells, and depends on the relative rather than absolute level of p53 in competing cells. The competition appears to be mediated by a non-cell-autonomous induction of growth arrest and senescence-related gene expression in outcompeted cells with higher p53 activity. p53-mediated cell competition of this type could potentially contribute to the clonal expansion of incipient cancer cells.
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“Tp53 is also involved in cell competition regulation in both hematopoietic and non-hemopoietic tissues (Bondar & Medzhitov, 2010, Zhang, Xie et al., 2017).”
From Pu.1/Spi1 dosage controls the turnover and maintenance of microglia in zebrafish and mammals (2023) · cites this paper as Bondar & Medzhitov, 2010
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In the citing paper
“we further showed that the chronic elimination of pu.1 -deficent microglia in zebrafish is mediated by Tp53-dependent cell competition”
From Pu.1/Spi1 dosage controls the turnover and maintenance of microglia in zebrafish and mammals (2023) · cites this paper as Bondar & Medzhitov, 2010
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Tp53 is also involved in cell competition regulation in both hematopoietic and non-hemopoietic tissues (Bondar and Medzhitov, 2010; Zhang et al., 2017).”
From Pu.1/Spi1 dosage controls the turnover and maintenance of microglia in zebrafish and mammals (2025) · cites this paper as Bondar and Medzhitov, 2010
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In the citing paper
“which has been shown to depend on the relative level of Tp53 in competing cells (Bondar & Medzhitov, 2010, Zhang et al., 2017).”
From Pu.1/Spi1 dosage controls the turnover and maintenance of microglia in zebrafish and mammals (2023) · cites this paper as Bondar & Medzhitov, 2010
The cited source says what the claim attributes to it.
In the citing paper
“which has been shown to depend on the relative level of Tp53 in competing cells (Bondar and Medzhitov, 2010; Zhang et al., 2017).”
From Pu.1/Spi1 dosage controls the turnover and maintenance of microglia in zebrafish and mammals (2025) · cites this paper as Bondar and Medzhitov, 2010
In the citing paper
“and p53 upregulation in the haematopoietic system engenders myeloablation82,83”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [82]
In the citing paper
“HSCs from mice with mutations in both Tp53 42 and Ppm1d, a gene encoding a regulator of p53 and other members of the DNA damage response pathway, 43,44 are able to enter cell cycle despite the presence of DNA damage, leading to a stem cell advantage in the setting of cytotoxic drugs.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [42]
In the citing paper
“The desired cohort size was determined based on observations from previously reported experiments20”
From Role of TP53 mutations in the origin and evolution of therapy-related acute myeloid leukaemia (2015) · cites this paper as [20]
In the citing paper
“Importantly, a prior study similarly showed that Tp53+/− HSCs also have a competitive advantage following irradiation, which appeared to be due, at least in part, to reduced irradiation-induced senescence in Tp53+/− HSCs 20,21.”
From Role of TP53 mutations in the origin and evolution of therapy-related acute myeloid leukaemia (2015) · cites this paper as [20]
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Metadata
- Authors
- Bondar, T., & Medzhitov, R.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Medzhitov, Ruslan
- Venue
- Cell Stem Cell
- Publisher
- Elsevier BV
- Published
- 2010-04
- Volume
- 6
- Issue
- 4
- Pages
- 309-322
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- PMC
- PMC2872065
- OpenAlex
- W2163067447
- Cited by
- 342
- References
- 83
- Citations by year
- 2026: 15 · 2025: 17 · 2024: 14 · 2023: 23 · 2022: 22 · 2021: 25 · 2020: 29 · 2019: 22 · 2018: 18 · 2017: 21 · 2016: 24 · 2015: 25 · 2014: 23 · 2013: 20 · 2012: 12
- FWCI
- 10.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1203 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell stem cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institute of Allergy and Infectious Diseases (R01AI055502, R01AI046688)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK071754, P30DK072442)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Keywords
- cell competition, p53, hematopoietic stem cells, hematopoietic progenitor cells, clonal selection, DNA damage response, cellular senescence, growth arrest, bone marrow chimeras, genetic mosaicism, tissue homeostasis
- MeSH terms
- Animals, Cell Communication, Clone Cells, DNA Damage, Genes, Dominant, Hematopoietic Stem Cells, Models, Biological, Mutation, Phenotype, Radiation, Ionizing, Stress, Physiological, Tumor Suppressor Protein p53, Cellular Senescence, Apoptosis, Gene Expression Regulation, Developmental, Gene Expression Profiling, Cell Proliferation, Mice
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