Cancer predisposition and hematopoietic failure in Rad50 S/S mice
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Mre11, Rad50, and Nbs1 function in a protein complex that is central to the metabolism of chromosome breaks. Null mutants of each are inviable. We demonstrate here that hypomorphic Rad50 mutant mice ( Rad50 S/S mice) exhibited growth defects and cancer predisposition. Rad50 S/S mice died with complete bone marrow depletion as a result of progressive hematopoietic stem cell failure. Similar attrition occurred in spermatogenic cells. In both contexts, attrition was substantially mitigated by p53 deficiency, whereas the tumor latency of p53 −/− and p53 +/− animals was reduced by Rad50 S/S . Indices of genotoxic stress and chromosomal rearrangements were evident in Rad50 S/S cultured cells, as well as in Rad50 S/S and p53 −/− Rad50 S/S lymphomas, suggesting that the Rad50 S/S phenotype was attributable to chromosomal instability. These outcomes were not associated with overt defects in the Mre11 complex's previously established double strand break repair and cell cycle checkpoint regulation functions. The data indicate that even subtle perturbation of Mre11 complex functions results in severe genotoxic stress, and that the complex is critically important for homeostasis of proliferative tissues.
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Genomic instability is detectable in cells derived from Rad50s/s mice.
“Genomic instability is detectable in cells derived from this animal.”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Bender et al., 2002
The attrition of the hematopoietic and male germ cell lineages in Rad50s/s mice occurs in large measure due to p53-mediated signaling triggered by genomic instability.
“The attrition of the hematopoietic and male germ cell lineages occurs in large measure due to p53-mediated signaling triggered by genomic instability (Bender et al., 2002”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Bender et al., 2002
Homozygosity for a Rad50 hypomorphic allele (Rad50s/s) permits viability; Rad50s/s mice show a shortened life span, cancer predisposition, and hematopoietic stem cell and spermatogenic failure.
“homozygosity for a Rad50 hypomorphic allele (Rad50s/s) permits viability; Rad50s/s mice show a shortened life span, cancer predisposition, and hematopoietic stem cell and spermatogenic failure (Bender et al., 2002”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Bender et al., 2002
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“Progressive bone marrow failure syndromes were also observed in mice lacking Atm [78] and in mice homozygous for a hypomorphic allele of Rad50 (Rad50s) [76, 79].”
BackgroundTwo roles for Rad50 in telomere maintenance
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Genetic variation in the NBS1, MRE11, RAD50 and BLM genes and susceptibility to non-Hodgkin lymphoma
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- Authors
- Bender, C. F., Sikes, M. L., Sullivan, R., Huye, L. E., Le Beau, M. M., Roth, D. B., Mirzoeva, O. K., Oltz, E. M., & Petrini, J. H. J.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2002-09-01
- Volume
- 16
- Issue
- 17
- Pages
- 2237-2251
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC186667
- OpenAlex
- W2091413140
- Cited by
- 213
- References
- 77
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 2 · 2023: 4 · 2022: 3 · 2021: 12 · 2020: 4 · 2019: 1 · 2018: 5 · 2017: 5 · 2016: 5 · 2015: 3 · 2014: 9 · 2013: 6 · 2012: 4
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation
- National Institutes of Health (5k02ai001412-04)
- National Cancer Institute (U01CA084221, UO1 CA84221)
- National Institute of General Medical Sciences (GM 56888, R01GM056888)
- National Institute of Allergy and Infectious Diseases (AI36944, AI01412, T32 AI07495, T32AI007495, AI 36420, R01AI036420)
- National Center for Research Resources (RR00144-01A1, K01RR000144)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- RAD50, Mre11 complex, NBS1, cancer susceptibility, hematopoietic failure, bone marrow depletion, hematopoietic stem cells, spermatogenesis, p53 deficiency, chromosomal instability, genotoxic stress, lymphoma, tissue homeostasis
- MeSH terms
- MRE11 Homologue Protein, Alleles, Animals, Base Sequence, DNA Damage, DNA Repair, DNA-Binding Proteins, Female, Hematopoiesis, Male, Mice, Inbred C57BL, Mice, Mutant Strains, Mutation, Neoplasms, Experimental, Phenotype, Recombination, Genetic, Spermatogenesis, Genes, p53, DNA, Complementary, Mice, Knockout, DNA Repair Enzymes, Mice
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