Overview

Also Known As:p53 KO

Trp53 knockout mutant mice develop tumors at three to six months of age. They are suitable for use in applications related to the study of familial breast cancers such as Li-Fraumeni syndrome as well as research of lung, brain and bone tumors, lymphoma and leukemia, and other rare cancers.

Donating Investigator

IMR Colony, The Jackson Laboratory

Genetic overview

Genetic Background	Generation
000664 C57BL/6J	N5F6pF1+N2F2 (2021-07-22 00:00:00)

Trp53^tm1Tyj

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Trp53	transformation related protein 53

View Genetics

Research Applications

Apoptosis Research
Cancer Research
Immunology, Inflammation and Autoimmunity Research
Mouse/Human Gene Homologs
Research Tools

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Base Price

Starting at:

$236.78 Domestic price for female 4-week

473.55 Domestic price for breeder pair

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Details

Detailed Description

A neomycin cassette replaces exons 2-6 (including the start codon) of the transformation related protein 53 gene (Trp53). Mice homozygous for the mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at three to six months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.

For the C57BL/6-J congenic Trp53^tm1Tyj mouse line (Stock No. 002101), it is the experience of The Jackson Laboratory that homozygous males have expected Mendelian survival rates at wean age, but homozygous females have significantly reduced survival by wean age. Specifically, breeding heterozygous females to heterozygous males results in only ~3.5% homozygous females by wean age (expected Mendelian 12.5%). Additionally, breeding heterozygous females to homozygous males results in only ~6.8% homozygous females by wean age (expected Mendelian 25%).

Development

The Trp53^tm1Tyj mutant strain was developed in the laboratory of Dr. Tyler Jacks at the Center for Cancer Research at the Massachusetts Institute of Technology. The 129-derived D3 ES cell line was used. The C57BL/6J strain was produced by backcrossing the Trp53^tm1Tyj mutation at least five times to C57BL/6J inbred mice.

A 48 SNP (single nucleotide polymorphism) panel analysis, with 43 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. One of the 43 markers, on Chromosome 8, was segregating with 129.

Control Suggestions

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Jacks T; Remington L; Williams BO; Schmitt EM; Halachmi S; Bronson RT; Weinberg RA. 1994. Tumor spectrum analysis in p53-mutant mice. Curr Biol 4(1):1-7PubMed: 7922305 MGI: J:17728

View All References

Genetics

Trp53^tm1Tyj

Allele Symbol: Trp53^tm1Tyj

Allele Name	targeted mutation 1, Tyler Jacks
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	p53-; p53^delta; p53^null; p53KO; Trp53-; Trp53^KO
Gene Symbol and Name	Trp53, transformation related protein 53
Gene Synonym(s)
Site of Expression	Normal Trp53 expression is widespread.
Strain of Origin	129S2/SvPas
Chromosome	11
General Note	This mutant allele was produced by a targeted neo insertion into the Trp53 locus. Homozygotes show no visible phenotype but develop tumors at 3-6 months of age. Heterozygotes develop tumors at 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome (OMIM 151623), a form of familial breast cancer with mutations in TRP53 (J:16022)(J:16023) A specific human mutation found in hepatocellular carcinomas caused by hepatitis B infection or by aflatoxin exposure has been created in a mouse model, resulting in a similar gene product (J:27363).
Molecular Note	A neomycin cassette replaced 40% of the coding sequences beginning with exon 2 (upstream of the translation start site) and extending into exon 6.
Mutations Made By	Dr. Tyler Jacks, Massachusetts Institute of Technology

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Li-Fraumeni syndrome

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Trp53^tm1Tyj related

Apoptosis Research
- Endogenous Regulators
Cancer Research
- Toxicology
- Tumor Suppressor Genes
- Increased Tumor Incidence
  - Lymphomas
  - Other Tissues/Organs: osteosarcoma
  - Other Tissues/Organs
Immunology, Inflammation and Autoimmunity Research
- Intracellular Signaling Molecules
Mouse/Human Gene Homologs
- Li-Fraumeni syndrome
Research Tools
- Toxicology Research
  - drug/compound testing
  - B and T cell deficiency, xenograft transplant host

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129S2/SvPas

cellular phenotype

decreased thymocyte apoptosis
- in response to irradiation

increased fibroblast proliferation
- a larger fraction of MEFs are in S phase compared to wild-type mice

mortality/aging

premature death
- mean life span is 15.4 months

neoplasm

increased urinary system tumor incidence
- 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

increased tumor incidence
- 19% have multiple tumors compared to 44% of Trp53^tm3.1Tyj heterozygotes

increased carcinoma incidence
- 4 of 37 develop low grade carcinomas including 1 with a well differentiated lung carcinoma

increased incidence of tumors by chemical induction
- 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

renal/urinary system phenotype

increased urinary system tumor incidence
- 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

endocrine/exocrine gland phenotype

decreased thymocyte apoptosis
- in response to irradiation

hematopoietic system phenotype

abnormal hematopoietic system physiology
- hematopoietic stem and progenitor cells (HSPC) from irradiated mice transplanted into irradiated mice reconstitute the HSPC population exhibit a competitive advantage over HSPC from untreated mice compared with cells from similarly irradiated wild-type mice
- Normal - however, no competitive advantage is observed over similarly treated Cdkn2a^tm2.1Rdp cells in irradiation chimera experiments
- ce

decreased thymocyte apoptosis
- in response to irradiation

homeostasis/metabolism phenotype

increased incidence of tumors by chemical induction
- 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

immune system phenotype

decreased thymocyte apoptosis
- in response to irradiation

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129S2/SvPas * C57BL/6 * FVB/N

mortality/aging

premature death
- median survival is 64 weeks

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas * C57BL/6

endocrine/exocrine gland phenotype

increased T cell derived lymphoma incidence
- 75% of observed tumors are thymic lymphomas
- most lymphomas are thymic lymphomas

homeostasis/metabolism phenotype

abnormal protein level
- MEFs show reduced protein levels of FDXR and CDKN1A (aka p21)

abnormal iron homeostasis
- mouse embryonic fibroblasts (MEFs) show increased protein expression of IREB2 (iron responsive element binding protein 2; aka IRP2) and TFRC (transferrin receptor; aka TfR1) but reduced expression of ACO1 (aconitase 1; aka IRP1) and FTH1 (ferritin heavy polypeptide 1)

abnormal iron level
- MEFs show mitochondrial iron accumulation
- Pearl's Prussian blue staining revealed mild iron overload in E8.0 embryos

mortality/aging

premature death
- homozygous mutants die between ~50 to 250 days after birth
- 90% succumb to tumors and die by 7 months of age
- average life span 160 days

preweaning lethality, incomplete penetrance
- 16.6% rather than the expected 25% of mutants are observed at weaning, indicating partial lethality either during embryogenesis or after birth but before weaning

cellular phenotype

abnormal mitochondrial morphology
- MEFs show mitochondrial iron accumulation

abnormal apoptosis

decreased cell proliferation
- in mouse embryonic fibroblasts treated with UV irradiation

decreased cellular sensitivity to ultraviolet irradiation
- in mouse embryonic fibroblasts

aneuploidy

decreased cellular sensitivity to gamma-irradiation
- irradiated E13.5 heterozygous embryos showed no evidence of apoptosis in the hypothalamus compared to wildtype and heterozygotes that showed a high number of apoptotic cells

increased fibroblast proliferation
- MEFs initially did not show any significant differences in growth rate but by day 4, grew more rapidly than wildtype or heterozygous MEFs

muscle phenotype

increased rhabdomyosarcoma incidence

neoplasm

increased fibrosarcoma incidence
- 13% incidence

increased sarcoma incidence
- 50% incidence
- 40% of homozygous nulls developed sarcomas

increased squamous cell carcinoma incidence
- 3.3% incidence of stomach squamous cell carcinoma

increased T cell derived lymphoma incidence
- 75% of observed tumors are thymic lymphomas
- most lymphomas are thymic lymphomas

increased tumor incidence
- predominantly lymphomas with sarcomas and teratomas

increased hemangiosarcoma incidence
- 20% incidence

increased lymphoma incidence
- 56% of homozygous nulls developed lymphomas
- 70% incidence
- 71% of mice develop lymphoma, usually affecting the thymus

increased osteosarcoma incidence
- 13% incidence

increased teratoma incidence

increased carcinoma incidence
- 3.3% incidence

increased hemangioma incidence
- 3.3% incidence

increased rhabdomyosarcoma incidence

skeleton phenotype

increased osteosarcoma incidence
- 13% incidence

digestive/alimentary phenotype

gastric polyps
- 3.3% incidence of stomach polyps

colon polyps
- 6.7% incidence

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
129S6.129-Trp53 Rb1

digestive/alimentary phenotype

intestinal ulcer
- Normal - after 7 days of dextran sodium sulfate treatment, mice develop large ulcers in the colon

endocrine/exocrine gland phenotype

increased testicular teratoma incidence

growth/size/body region phenotype

weight loss
- with DSS treatment, double mutants have an average weight of 14% of body weight

mortality/aging

premature death
- mice become moribund from lymphoma involving various tissues within >30 weeks; mice with aggressive lymphoma have a mean survival time of 18 weeks

neoplasm

increased testicular teratoma incidence

increased lymphoma incidence
- mice develop lymphomas

increased teratoma incidence
- median survival time of mice with teratomas is 7 weeks
- no mice living beyond median survival age show extratesticular teratomas

reproductive system phenotype

increased testicular teratoma incidence

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas * C57BL/6 * CBA

cellular phenotype

decreased thymocyte apoptosis
- radiation-induced apoptosis in the thymus is decreased as compared to wild-type

endocrine/exocrine gland phenotype

decreased thymocyte apoptosis
- radiation-induced apoptosis in the thymus is decreased as compared to wild-type

hematopoietic system phenotype

decreased thymocyte apoptosis
- radiation-induced apoptosis in the thymus is decreased as compared to wild-type

immune system phenotype

decreased thymocyte apoptosis
- radiation-induced apoptosis in the thymus is decreased as compared to wild-type

mortality/aging

premature death
- average lifespan is 4.5 months

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129S2/SvPas * C57BL/6 * CBA

cellular phenotype

decreased thymocyte apoptosis
- radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type

endocrine/exocrine gland phenotype

decreased thymocyte apoptosis
- radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type

hematopoietic system phenotype

decreased thymocyte apoptosis
- radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type

immune system phenotype

decreased thymocyte apoptosis
- radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type

mortality/aging

premature death
- average lifespan is 14 months

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129S2/SvPas * C57BL/6

digestive/alimentary phenotype

gastric polyps
- 2.9% incidence of stomach polyps

intestine polyps
- 2.9% incidence of small intestinal polyps

muscle phenotype

increased rhabdomyosarcoma incidence

increased leiomyosarcoma incidence

neoplasm

increased carcinoma incidence
- 12% of heterozygous mutants developed carcinomas, which are rare in homozygotes
- 35% incidence of carcinomas
- 2.9% incidence of pancreatic adenocarcinomas

increased sarcoma incidence
- 2.9% incidence of undifferentiated sarcomas
- 56% incidence of sarcomas
- 56% of heterozygous mutants developed sarcomas
- 57% of mutants exhibit sarcomas

increased tumor incidence
- age of onset 9 months
- over 95% of mice have tumors by 2 years of age

increased adenocarcinoma incidence
- 18% incidence

increased leiomyosarcoma incidence

increased lymphoma incidence
- 25% of mutants exhibit lymphomas
- 32% incidence

increased mammary adenocarcinoma incidence
- 2.9% incidence

increased pancreas tumor incidence
- 2.9% incidence of pancreatic adenocarcinomas

increased adenoma incidence
- 5.9% incidence

increased osteosarcoma incidence
- 29% incidence

increased rhabdomyosarcoma incidence

increased squamous cell carcinoma incidence
- 18% incidence of ear squamous cell carcinoma

increased hemangiosarcoma incidence
- 8.8% incidence

increased histiocytic sarcoma incidence
- 15% incidence

increased leukemia incidence
- is observed in 2.6% of mice by 24 months of age

abnormal tumor morphology
- tumors show loss of heterozygosity for Trp53

increased fibrosarcoma incidence

increased lung adenocarcinoma incidence
- 12% incidence

endocrine/exocrine gland phenotype

increased mammary adenocarcinoma incidence
- 2.9% incidence

increased pancreas tumor incidence
- 2.9% incidence of pancreatic adenocarcinomas

respiratory system phenotype

increased lung adenocarcinoma incidence
- 12% incidence

skeleton phenotype

increased osteosarcoma incidence
- 29% incidence

homeostasis/metabolism phenotype

abnormal iron level
- Pearl's Prussian blue staining revealed mild iron overload in E8.0 embryos

integument phenotype

increased mammary adenocarcinoma incidence
- 2.9% incidence

mortality/aging

premature death
- 28% of mutants die by 17 months of age due to tumors
- less than 5% of mice live past two years due to cancerous tumors
- heterozygous mutants die between 150 to 750 days after birth

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas

cellular phenotype

decreased thymocyte apoptosis
- in irradiated thymocytes
- rare following exposure to ionizing radiation
- in response to irradiation

decreased cellular sensitivity to ultraviolet irradiation
- reduced sensitivity to UV-induced cell death in MEFs compared to wild-type cells

decreased splenocyte apoptosis
- in irradiated spleen cells

abnormal cell cycle checkpoint function
- gamma-irradiation fails to produce an increase in the relative number of cells in G1 compared to S phase
- mouse embryonic fibroblasts exposed to radiation fail to arrest at the G1/S transition unlike similarly treated wild-type cells

increased fibroblast proliferation
- in MEFs

polyploidy
- after irradiation with UVC light, MEFs from null mice show higher levels of polyploidy than Trp53^tm2Xu homozygotes

abnormal neuron differentiation
- GNPs from mutants show ~50% levels of proliferation compared to Cdkn2c, Trp53-double null cells after 3 days in culture and levels of cells incorporating BrdU are still less in single mutants in tests where cells are stimulated with Shh after culture

decreased T cell apoptosis
- thymocytes are essentially resistant to Trp53-mediated apoptosis

endocrine/exocrine gland phenotype

decreased thymocyte apoptosis
- in irradiated thymocytes
- rare following exposure to ionizing radiation
- in response to irradiation

increased T cell derived lymphoma incidence
- 66% of homozygotes display hematological malignancies, primarily T cell lymphomas
- mice start to develop T cell malignancies at 14-16 weeks
- mice present with thymic lymphoma at around 180 days of age
- 6 of 10 mice develop thymic lymphomas

growth/size/body region phenotype

cardiac hypertrophy
- increased hypertrophy as a result of transverse aortic restriction

hematopoietic system phenotype

decreased T cell apoptosis
- thymocytes are essentially resistant to Trp53-mediated apoptosis

decreased splenocyte apoptosis
- in irradiated spleen cells

decreased thymocyte apoptosis
- in response to irradiation
- in irradiated thymocytes
- rare following exposure to ionizing radiation

cardiovascular system phenotype

increased angiogenesis
- increased number of microvessels form 2 weeks after transverse aortic constriction

abnormal cardiovascular system physiology
- better systolic function than control

cardiac hypertrophy
- increased hypertrophy as a result of transverse aortic restriction

immune system phenotype

decreased T cell apoptosis
- thymocytes are essentially resistant to Trp53-mediated apoptosis

decreased thymocyte apoptosis
- rare following exposure to ionizing radiation
- in irradiated thymocytes
- in response to irradiation

decreased splenocyte apoptosis
- in irradiated spleen cells

mortality/aging

premature death
- animals die by about 26 weeks
- majority of mice (82%) die before 9 months of age, or are euthanized due to occurrence of obvious tumor mass
- mean life span is 4.4 months

prenatal lethality, incomplete penetrance
- a slight decrease is seen in the number of females born

neoplasm

increased medulloblastoma incidence
- 13/19 (68%) of animals receiving 4 Gy radiation at P5 or 6 develop cerebellar tumors

increased T cell derived lymphoma incidence
- 6 of 10 mice develop thymic lymphomas
- mice start to develop T cell malignancies at 14-16 weeks
- 66% of homozygotes display hematological malignancies, primarily T cell lymphomas
- mice present with thymic lymphoma at around 180 days of age

increased hemangiosarcoma incidence
- the incidence of hemangiosarcomas is 32% compared to 62% in Trp53^tm1Tyj/Trp53^tm2.1Tyj mice

increased lymphoma incidence
- 3 of 10 mice develop lymphomas involving the spleen and lymph nodes

increased tumor incidence
- 32% have multiple tumors

nervous system phenotype

increased medulloblastoma incidence
- 13/19 (68%) of animals receiving 4 Gy radiation at P5 or 6 develop cerebellar tumors

abnormal neuron differentiation
- GNPs from mutants show ~50% levels of proliferation compared to Cdkn2c, Trp53-double null cells after 3 days in culture and levels of cells incorporating BrdU are still less in single mutants in tests where cells are stimulated with Shh after culture

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
129-Trp53/J

cardiovascular system phenotype

abnormal retinal vasculature morphology
- Background Sensitivity - abnormally dilated peripheral retinal blood vessels, with some mice exhibiting thin blood vessels extending from the optic nerve head toward the lens, but few reach the lens surface

vision/eye phenotype

abnormal retinal vasculature morphology
- Background Sensitivity - abnormally dilated peripheral retinal blood vessels, with some mice exhibiting thin blood vessels extending from the optic nerve head toward the lens, but few reach the lens surface

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas * FVB/N

cellular phenotype

decreased cellular sensitivity to ionizing radiation
- following ionizing radiation treatment, arrested cell growth in the epidermis is partially abrogated compared to in similarly treated wild-type mice
- following ionizing radiation treatment, hair follicles do not exhibit apoptosis unlike in similarly treated wild-type mice

integument phenotype

decreased sensitivity to skin irradiation
- following ionizing radiation treatment, arrested cell growth in the epidermis is partially abrogated compared to in similarly treated wild-type mice

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas * C57BL/6 * FVB/N

homeostasis/metabolism phenotype

decreased mortality induced by ionizing radiation
- median survival following exposure to 8 gray of whole body gamma-irradiation is 34 days

mortality/aging

premature death
- longest lifespan is 34 weeks, median survival is 25 weeks

decreased mortality induced by ionizing radiation
- median survival following exposure to 8 gray of whole body gamma-irradiation is 34 days

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129S2/SvPas * BALB/cJ * C57BL/6

neoplasm

abnormal tumor incidence
- 42.8% of mice (6 of 14) develop thymic lymphomas after exposure to ionizing radiation

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6

mortality/aging

decreased survivor rate
- 50% survival at 63 weeks

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas * BALB/c

cellular phenotype

increased cellular sensitivity to ionizing radiation
- at P10, pattern and extent of oocyte loss in ovaries of mutants after exposure to 0.45 Gy radiation on P5 is similar to wild-type and much more sever than Trp63^tm2Fmc mutants

The following phenotype relates to a compound genotype created using this strain

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
B6.129S2-Trp53/J

cardiovascular system phenotype

abnormal retinal vasculature morphology
- Background Sensitivity - abnormal blood vessels are found to extend from the peripapillary inner retina through the posterior vitreous and into the retrolental membranes
- abnormally dilated peripheral retinal blood vessels

nervous system phenotype

optic nerve hypoplasia
- Background Sensitivity - bilateral or unilateral optic nerve hypoplasia is found on the C57BL/6J background, but not on the 129 or F1 background

optic nerve degeneration
- Background Sensitivity - degeneration is found to varying degrees on the C57BL/6J background, but not the 129 background

abnormal optic nerve morphology
- Background Sensitivity - the pial septae in many areas are disorganized on the C57BL/6J background but not the 129 or F1 backgrounds

vision/eye phenotype

abnormal ocular fundus morphology
- Background Sensitivity - pigmented or nonpigmented fibrous retrolental tissue is commonly found in homozygotes on the C57BL/6J background

abnormal retinal vasculature morphology
- Background Sensitivity - abnormal blood vessels are found to extend from the peripapillary inner retina through the posterior vitreous and into the retrolental membranes
- abnormally dilated peripheral retinal blood vessels

opacity of vitreous body
- Background Sensitivity - fine snowflake-like vitreal opacities can be found on the C57BL/6J background by 21 days of age and may result from the accumulation of fibrous and vascular debris in the vitreous

abnormal optic nerve morphology
- Background Sensitivity - the pial septae in many areas are disorganized on the C57BL/6J background but not the 129 or F1 backgrounds

optic nerve hypoplasia
- Background Sensitivity - bilateral or unilateral optic nerve hypoplasia is found on the C57BL/6J background, but not on the 129 or F1 background

abnormal retina morphology
- Background Sensitivity - retinal folds are found in some homozygotes on the C57BL/6J background

abnormal posterior eye segment morphology
- Background Sensitivity - on the C57BL/6J background aberrant ocular phenotypes are observed as early as 14 days of age

optic nerve degeneration
- Background Sensitivity - degeneration is found to varying degrees on the C57BL/6J background, but not the 129 background

References

Jacks T; Remington L; Williams BO; Schmitt EM; Halachmi S; Bronson RT; Weinberg RA. 1994. Tumor spectrum analysis in p53-mutant mice. Curr Biol 4(1):1-7PubMed: 7922305 MGI: J:17728

Additional References

Aleyasin H; Cregan SP; Iyirhiaro G; O'Hare MJ; Callaghan SM; Slack RS; Park DS. 2004. Nuclear factor-(kappa)B modulates the p53 response in neurons exposed to DNA damage. J Neurosci 24(12):2963-73PubMed: 15044535 MGI: J:90221
Botchkarev VA; Komarova EA; Siebenhaar F; Botchkareva NV; Komarov PG; Maurer M; Gilchrest BA; Gudkov AV. 2000. p53 is essential for chemotherapy-induced hair loss. Cancer Res 60(18):5002-6PubMed: 11016618 MGI: J:64779
Cunningham JJ; Levine EM; Zindy F; Goloubeva O; Roussel MF; Smeyne RJ. 2002. The Cyclin-Dependent Kinase Inhibitors p19(Ink4d) and p27(Kip1) Are Coexpressed in Select Retinal Cells and Act Cooperatively to Control Cell Cycle Exit. Mol Cell Neurosci 19(3):359-74PubMed: 11906209 MGI: J:75882
Fong LY; Ishii H; Nguyen VT; Vecchione A; Farber JL; Croce CM; Huebner K. 2003. p53 Deficiency Accelerates Induction and Progression of Esophageal and Forestomach Tumors in Zinc-deficient Mice. Cancer Res 63(1):186-95PubMed: 12517797 MGI: J:81055
Freie B; Li X; Ciccone SL; Nawa K; Cooper S; Vogelweid C; Schantz L; Haneline LS; Orazi A; Broxmeyer HE; Lee SH; Clapp DW. 2003. Fanconi anemia type C and p53 cooperate in apoptosis and tumorigenesis. Blood 102(12):4146-52PubMed: 12855557 MGI: J:84980
Ikeda S; Hawes NL; Chang B; Avery CS; Smith RS; Nishina PM. 1999. Severe ocular abnormalities in C57BL/6 but not in 129/Sv p53-deficient mice. Invest Ophthalmol Vis Sci 40(8):1874-8PubMed: 10393064 MGI: J:55873
Ito M; Okano HJ; Darnell RB; Roeder RG. 2002. The TRAP100 component of the TRAP/Mediator complex is essential in broad transcriptional events and development. EMBO J 21(13):3464-75PubMed: 12093747 MGI: J:77765
Komarova EA; Christov K; Faerman AI; Gudkov AV. 2000. Different impact of p53 and p21 on the radiation response of mouse tissues. Oncogene 19(33):3791-8PubMed: 10949934 MGI: J:63921
Komarova EA; Kondratov RV; Wang K; Christov K; Golovkina TV; Goldblum JR; Gudkov AV. 2004. Dual effect of p53 on radiation sensitivity in vivo: p53 promotes hematopoietic injury, but protects from gastro-intestinal syndrome in mice. Oncogene 23(19):3265-71PubMed: 15064735 MGI: J:89739
Lowe SW; Schmitt EM; Smith SW; Osborne BA; Jacks T. 1993. p53 is required for radiation-induced apoptosis in mouse thymocytes [see comments] Nature 362(6423):847-9PubMed: 8479522 MGI: J:16022
Lu YP; Lou YR; Peng QY; Xie JG; Conney AH. 2004. Stimulatory effect of topical application of caffeine on UVB-induced apoptosis in the epidermis of p53 and Bax knockout mice. Cancer Res 64(14):5020-7PubMed: 15256477 MGI: J:91506
McCarthy EE; Celebi JT; Baer R; Ludwig T. 2003. Loss of Bard1, the heterodimeric partner of the Brca1 tumor suppressor, results in early embryonic lethality and chromosomal instability. Mol Cell Biol 23(14):5056-63PubMed: 12832489 MGI: J:84329
McGlynn KA; Hunter K; LeVoyer T; Roush J; Wise P; Michielli RA; Shen FM; Evans AA; London WT; Buetow KH. 2003. Susceptibility to aflatoxin B1-related primary hepatocellular carcinoma in mice and humans. Cancer Res 63(15):4594-601PubMed: 12907637 MGI: J:85696
Opitz OG; Harada H; Suliman Y; Rhoades B; Sharpless NE; Kent R; Kopelovich L; Nakagawa H; Rustgi AK. 2002. A mouse model of human oral-esophageal cancer. J Clin Invest 110(6):761-9PubMed: 12235107 MGI: J:79110
Reilly KM; Loisel DA; Bronson RT; McLaughlin ME; Jacks T. 2000. Nf1;Trp53 mutant mice develop glioblastoma with evidence of strain-specific effects Nat Genet 26(1):109-13PubMed: 10973261 MGI: J:64364
Sah VP; Attardi LD; Mulligan GJ; Williams BO; Bronson RT; Jacks T. 1995. A subset of p53-deficient embryos exhibit exencephaly. Nat Genet 10(2):175-80PubMed: 7663512 MGI: J:23197
Sata M; Tanaka K; Ishizaka N; Hirata Y; Nagai R. 2003. Absence of p53 Leads to Accelerated Neointimal Hyperplasia After Vascular Injury. Arterioscler Thromb Vasc Biol 23(9):1548-52PubMed: 12893686 MGI: J:84981
Scoggins CR; Meszoely IM; Wada M; Means AL; Yang L; Leach SD. 2000. p53-dependent acinar cell apoptosis triggers epithelial proliferation in duct-ligated murine pancreas Am J Physiol Gastrointest Liver Physiol 279(5):G827-36PubMed: 11005771 MGI: J:65224
Takeda K; Smyth MJ; Cretney E; Hayakawa Y; Kayagaki N; Yagita H; Okumura K. 2002. Critical role for tumor necrosis factor-related apoptosis-inducing ligand in immune surveillance against tumor development. J Exp Med 195(2):161-9PubMed: 11805143 MGI: J:74411
Verschuren EW; Hodgson JG; Gray JW; Kogan S; Jones N; Evan GI. 2004. The role of p53 in suppression of KSHV cyclin-induced lymphomagenesis. Cancer Res 64(2):581-9PubMed: 14744772 MGI: J:88091
Weber GF; Bronson RT; Ilagan J; Cantor H; Schmits R; Mak TW. 2002. Absence of the CD44 gene prevents sarcoma metastasis. Cancer Res 62(8):2281-6PubMed: 11956084 MGI: J:76201
Wen R; Wang D; McKay C; Bunting KD; Marine JC; Vanin EF; Zambetti GP; Korsmeyer SJ; Ihle JN; Cleveland JL. 2001. Jak3 selectively regulates Bax and Bcl-2 expression to promote T-cell development. Mol Cell Biol 21(2):678-89PubMed: 11134353 MGI: J:67378
Yamanishi Y; Boyle DL; Pinkoski MJ; Mahboubi A; Lin T; Han Z; Zvaifler NJ; Green DR; Firestein GS. 2002. Regulation of Joint Destruction and Inflammation by p53 in Collagen-Induced Arthritis. Am J Pathol 160(1):123-30PubMed: 11786406 MGI: J:73730
Yang X; Klein R; Tian X; Cheng HT; Kopan R; Shen J. 2004. Notch activation induces apoptosis in neural progenitor cells through a p53-dependent pathway. Dev Biol 269(1):81-94PubMed: 15081359 MGI: J:90392

Additional - Trp53^tm1Tyj related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Trp53 Alternate2
- Probe:Trp53-Probe
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This strain is a challenging breeder.

This Trp53^tm1Tyj strain is maintained by mating heterozygous mice together or by mating heterozygous females with homozygous males.

For the C57BL/6-J congenic Trp53^tm1Tyj mouse line (Stock No. 002101), it is the experience of The Jackson Laboratory that homozygous males have expected Mendelian survival rates at wean age, but homozygous females have significantly reduced survival by wean age. Specifically, breeding heterozygous females to heterozygous males results in only ~3.5% homozygous females by wean age (expected Mendelian 12.5%). Additionally, breeding heterozygous females to homozygous males results in only ~6.8% homozygous females by wean age (expected Mendelian 25%).
- Additional Breeding and Husbandry Support
Mating System
- Heterozygote x Homozygote
Appearance
- black
  Related Genotype: a/a
Citation
When using the p53 KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #002101 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX10 (Standard)

Pricing & Availability

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Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Breeder Pair

Sex

Genotype

Price

Female
Male

Cryorecovery - Pricing

Service/Product	Description	Price
> >	Heterozygous or Wildtype for

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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General Terms and Conditions

Questions about Terms of Use

Additional Use Restrictions Apply

Use of MICE by companies or for-profit entities requires a license prior to shipping.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:p53 KO

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Trp53tm1Tyj

Allele Symbol: Trp53tm1Tyj

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Trp53tm1Tyj related

Mammalian Phenotype Terms by Genotype

Genotype: Trp53tm1Tyj/Trp53+involves: 129S2/SvPas

cellular phenotype

mortality/aging

neoplasm

renal/urinary system phenotype

endocrine/exocrine gland phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Trp53tm1Tyj/Trp53+involves: 129S2/SvPas * C57BL/6 * FVB/N

mortality/aging

Genotype: Trp53tm1Tyj/Trp53tm1Tyjinvolves: 129S2/SvPas * C57BL/6

endocrine/exocrine gland phenotype

homeostasis/metabolism phenotype

mortality/aging

cellular phenotype

muscle phenotype

neoplasm

skeleton phenotype

digestive/alimentary phenotype

Genotype: Trp53tm1Tyj/Trp53tm1Tyj129S6.129-Trp53 Rb1

digestive/alimentary phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

mortality/aging

neoplasm

reproductive system phenotype

Genotype: Trp53tm1Tyj/Trp53tm1Tyjinvolves: 129S2/SvPas * C57BL/6 * CBA

cellular phenotype

endocrine/exocrine gland phenotype

hematopoietic system phenotype

immune system phenotype

mortality/aging

Genotype: Trp53tm1Tyj/Trp53+involves: 129S2/SvPas * C57BL/6 * CBA

cellular phenotype

endocrine/exocrine gland phenotype

hematopoietic system phenotype

immune system phenotype

mortality/aging

Genotype: Trp53tm1Tyj/Trp53+involves: 129S2/SvPas * C57BL/6

digestive/alimentary phenotype

muscle phenotype

neoplasm

endocrine/exocrine gland phenotype

respiratory system phenotype

skeleton phenotype

homeostasis/metabolism phenotype

integument phenotype

mortality/aging

Genotype: Trp53tm1Tyj/Trp53tm1Tyjinvolves: 129S2/SvPas

cellular phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

hematopoietic system phenotype

cardiovascular system phenotype

immune system phenotype

mortality/aging

neoplasm

nervous system phenotype

Genotype: Trp53tm1Tyj/Trp53tm1Tyj129-Trp53/J

cardiovascular system phenotype

vision/eye phenotype

Trp53^tm1Tyj

Allele Symbol: Trp53^tm1Tyj

Genotype: Trp53^tm1Tyj related

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129S2/SvPas

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129S2/SvPas * C57BL/6 * FVB/N

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas * C57BL/6

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
129S6.129-Trp53 Rb1

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas * C57BL/6 * CBA

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129S2/SvPas * C57BL/6 * CBA

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129S2/SvPas * C57BL/6

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
129-Trp53/J

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas * FVB/N

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas * C57BL/6 * FVB/N

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129S2/SvPas * BALB/cJ * C57BL/6

Genotype: Trp53^tm1Tyj/Trp53⁺
involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
involves: 129S2/SvPas * BALB/c

Genotype: Trp53^tm1Tyj/Trp53^tm1Tyj
B6.129S2-Trp53/J

Additional - Trp53^tm1Tyj related