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 involved in cell competition regulation in both hematopoietic and non-hemopoietic tissues.
“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
The Discussion says p53 mediates stress-induced cell competition in the mammalian hematopoietic system, specifically in hematopoietic stem and progenitor cells (page not provided). It does not establish p53-mediated cell competition in non-hematopoietic tissues, so Bondar and Medzhitov support only the hematopoietic part of the sentence. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe chronic elimination of pu.1-deficient microglia in zebrafish is mediated by Tp53-dependent cell competition.
“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
The Results section, “DNA damage triggers p53-dependent cell competition in HSCs,” reports p53-dependent competition and replacement of hematopoietic stem and progenitor cells in mice. It does not establish that chronic elimination of pu.1-deficient microglia in zebrafish is mediated by Tp53-dependent competition; searches for those terms found no such passage. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTp53 is involved in cell competition regulation in both hematopoietic and non-hemopoietic tissues.
“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
The Discussion (page not provided) says that p53 mediates cell competition in the mammalian hematopoietic system, specifically in hematopoietic stem and progenitor cells. It does not establish p53-mediated cell competition in non-hematopoietic tissues, so Bondar and Medzhitov support only the hematopoietic part of the sentence. (LLM, conf=0.87)
Experimental — accuracy not yet measuredTp53-dependent cell competition depends on the relative level of Tp53 in competing cells.
“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
Tp53-dependent cell competition depends on the relative level of Tp53 in competing cells.
“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
p53 upregulation in the haematopoietic system engenders myeloablation.
“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]
HSCs from mice with mutations in both Tp53 and Ppm1d are able to enter cell cycle despite the presence of DNA damage, leading to a stem cell advantage in the setting of cytotoxic drugs.
“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]
The desired cohort size was determined based on observations from previously reported experiments.
“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]
A prior study 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.
“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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“HSCs from mice with mutations in either Tp53 (43) or Ppm1d, a gene encoding a regulator of p53 and other members of the DNA damage response pathway (44, 45), can enter the cell cycle despite the presence of DNA damage, leading to a stem cell advantage in the setting of cytotoxic drugs.”
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- 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
- Health Sciences › Medicine › Physiology › 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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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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