Overview

Also Known As:ATM^-

Mice homozygous for Atm^tm1Awb display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma between 2 and 4 months of age.

Donating Investigator

Dr. Anthony Wynshaw-Boris, Case Western Reserve University, School of Medicine

Genetic overview

Genetic Background	Generation

Atm^tm1Awb

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout, Humanized sequence)	Atm	ataxia telangiectasia mutated

View Genetics

Research Applications

Cancer Research
Mouse/Human Gene Homologs
Immunology, Inflammation and Autoimmunity Research
Neurobiology Research
Reproductive Biology Research

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

View Price List

Details

Detailed Description

Mice homozygous for the Atm^tm1Awb targeted mutation display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma between 2 and 4 months of age. Heterozygous mice display no abnormalities through eight months of age and are more sensitive to ionizing radiation than wildtype mice.

Development

This strain was developed in the laboratory of Dr. Anthony Wynshaw-Boris at the National Institutes of Health. The Atm gene was disrupted by using an insertion vector containing the neo resistance gene to produce a truncation mutation at approximately the site corresponding to that commonly mutated in ATM in many human beings with ataxia telangiectasia (AT).

Control Suggestions

Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

Barlow C; Hirotsune S; Paylor R; Liyanage M; Eckhaus M; Collins F; Shiloh Y; Crawley JN; Ried T; Tagle D; Wynshaw-Boris A. 1996. Atm-deficient mice: a paradigm of ataxia telangiectasia. Cell 86(1):159-71PubMed: 8689683 MGI: J:34193

View All References

Genetics

Atm^tm1Awb

Allele Symbol: Atm^tm1Awb

Allele Name	targeted mutation 1, Anthony Wynshaw Boris
Allele Type	Targeted (Null/Knockout, Humanized sequence)
Allele Synonym(s)	Atm-; ATM^-; Atm^ins5790neo; Atm^tm1Awbl
Gene Symbol and Name	Atm, ataxia telangiectasia mutated
Gene Synonym(s)
Strain of Origin	129S6/SvEvTac
Chromosome	9
Molecular Note	A PGK-neomycin cassette was inserted into position 5979 of the Atm gene. This mutation results in a truncated protein, and the position of the mutation corresponds to the location of truncation mutations known to exist in humans.
Mutations Made By	Dr. Anthony Wynshaw-Boris, Case Western Reserve University, School of Medicine

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).

ataxia telangiectasia

Research Areas By Phenotype

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

Genotype: Atm^tm1Awb related

Cancer Research
- Increased Tumor Incidence
  - Lymphomas: thymic
  - Lymphomas
- Tumor Suppressor Genes
Mouse/Human Gene Homologs
- ataxia telangiectasia
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency Associated with Other Defects
Neurobiology Research
- Ataxia (Movement) Defects
- Neurodevelopmental Defects
Reproductive Biology Research
- Fertility Defects

Mammalian Phenotype Terms by Genotype

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

Genotype: Atm^tm1Awb/Atm^tm1Awb
either: (129S6/SvEvTac-Atm x A.129S6-Atm)F1 or (A.129S6-Atm x 129S6/SvEvTac-Atm)F1

endocrine/exocrine gland phenotype

increased T cell derived lymphoma incidence
- almost all mice die of thymic lymphomas
- Background Sensitivity - mice have a higher thymic lymphoma incidence than do homozygous Atm^tm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds

growth/size/body region phenotype

decreased body weight
- pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points

mammalian phenotype

mortality/aging
- Background Sensitivity - the number of homozygous pups produced from heterozygote matings on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio; fewer homozygous pups are produced on the C57BL/6 and A/J backgrounds

mortality/aging

premature death
- 4 mice out of 39 survive to 18 months of age
- median survival time is 139 days
- Background Sensitivity - survival time (least to most) on the following strain backgrounds is ranked as BALB/c < 129S6/SvEvTac < 129S6AF1 < 129S6B6F1 < C57BL/6 < A/J < B6AF1

neoplasm

increased T cell derived lymphoma incidence
- almost all mice die of thymic lymphomas
- Background Sensitivity - mice have a higher thymic lymphoma incidence than do homozygous Atm^tm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds

Genotype: Atm^tm1Awb/Atm^tm1Awb
A.129S6-Atm

growth/size/body region phenotype

decreased body weight
- pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points

neoplasm

increased hepatocellular carcinoma incidence
- 4 out of 40 mice develop hepatocellular carcinomas as compared to 0 in wild type controls
- tumors were only found in male mice

abnormal tumor susceptibility
- 3 out of 40 mice develop thymic lymphomas by 18 months of age
- Background Sensitivity - mice are resistant to thymic lymphomas as compared to mice on the BALB/c, 129S6/SvEvTac, C57BL/6, B6AF1, 129S6B6F1, 129S6AF1 backgrounds

liver/biliary system phenotype

increased hepatocellular carcinoma incidence
- tumors were only found in male mice
- 4 out of 40 mice develop hepatocellular carcinomas as compared to 0 in wild type controls

mortality/aging

lethality, incomplete penetrance
- heterozygote x heterozygote matings produced fewer homozygotes than the expected Mendelian ratio
- Background Sensitivity - the number of homozygous pups produced from heterozygotes on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio

premature death
- median survival time is 385 days
- Background Sensitivity - survival time (least to most) on the following strain backgrounds is ranked as BALB/c < 129S6/SvEvTac < 129S6AF1 < 129S6B6F1 < C57BL/6 < A/J < B6AF1
- 4 mice out of 40 survive to 18 months of age

Genotype: Atm^tm1Awb/Atm^tm1Awb
either: (A.129S6-Atm x B6.129S6-Atm)F1 or (B6.129S6-Atm x A.129S6-Atm)F1

growth/size/body region phenotype

decreased body weight
- pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points

mammalian phenotype

mortality/aging
- Background Sensitivity - the number of homozygous pups produced from heterozygote matings on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio; fewer homozygous pups are produced on the C57BL/6 and A/J backgrounds

mortality/aging

premature death
- Background Sensitivity - survival time is longest on this background as compared to A/J, BALB/c, 129S6/SvEvTac, C57BL/6, 129S6B6F1 and 129S6AF1 backgrounds
- 6 mice out of 39 survive to 18 months of age
- median survival time is 451 days

neoplasm

abnormal tumor incidence
- 5 out of 20 males and 13 out of 20 mice die of thymic lymphomas
- Background Sensitivity - mice are less susceptible to thymic lymphomas than on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 backgrounds

Genotype: Atm^tm1Awb/Atm^tm1Awb
either: 129S6/SvEvTac-Atm or (involves: 129S6/SvEvTac * NIH Black Swiss)

behavior/neurological phenotype

decreased vertical activity
- mutant mice reared less often than controls

short stride length
- in addition, the maximum difference in stride lengths was greater in mutant mice, suggestive of ataxia

impaired coordination
- impaired performance was not due to decreased strength since mice were able to suspend from a wire lid as long as controls
- mutant mice were not able to stay on a rota-rod as long as controls

hypoactivity
- reduced horizontal activity was shown by reduced movement around an open field

cellular phenotype

oxidative stress
- oxidative damage to proteins and lipids as indicated by elevated nitrotyrosine levels in the brain (but not the liver) and elevated F2-isoprostanes in the testes (indicative of lipid damage)
- activity of the isozyme, heme oxygenase, is increased 600% in the cerebellum (but not in the cortex)
- tissues from mutants are under oxidative stress and suffer oxidative damage, especially in the brain

abnormal lysosome morphology
- significant increase in the number of lysosomes in cerebellar Purkinje cells and in pyramidal cells of the hippocampus in the absence of any neuronal degeneration at 4-12 weeks of age, before the onset of T cell lymphoma

azoospermia
- absence of mature sperm

absent oocytes
- complete absence of mature gametes

increased cellular sensitivity to gamma-irradiation
- mutant fibroblasts show increased radioresistant DNA synthesis (RDS) after 5 to 15 Gy of gamma-irradiation compared to controls, indicating that cell cycle checkpoints are abnormal

abnormal cell cycle

decreased fibroblast proliferation
- mutant fibroblasts grew more slowly in culture than control cells

endocrine/exocrine gland phenotype

increased T cell derived lymphoma incidence
- thymic lymphomas are highly metastatic and consist of immature T cells

small ovary

abnormal seminiferous tubule morphology
- degeneration of cells evident
- some barren of all cells except Sertoli cells
- reduced number of cells

small testis

absent ovarian follicles
- absence of primordial and mature ovarian follicles

growth/size/body region phenotype

decreased body weight
- female and male homozygotes weigh less that control littermates from P8 to 3 months of age

decreased body size
- homozygotes appear smaller at birth

hematopoietic system phenotype

increased double-positive T cell number
- increased number of immature double positive cells

decreased double-positive T cell number
- reduction in Cd5, Cd4, and Cd8 positive T lymphocytes
- 59% reduction in Cd3/Cd4 double positive T lymphocytes
- 67% reduction in Cd3/Cd8 double positive T lymphocytes

decreased activated T cell number
- using Cd69 as a marker of activation, the number of Cd3/Cd69 or Cd8/Cd69 positive cells is reduced, but still present

decreased T cell number
- reduced number of mature single-positive Cd4+ and Cd8+ T lymphocytes

homeostasis/metabolism phenotype

increased mortality induced by gamma-irradiation
- mutant mice die from radiation induced toxicity to the gastrointestinal tract at doses that do not kill control mice

immune system phenotype

decreased activated T cell number
- using Cd69 as a marker of activation, the number of Cd3/Cd69 or Cd8/Cd69 positive cells is reduced, but still present

decreased T cell number
- reduced number of mature single-positive Cd4+ and Cd8+ T lymphocytes

decreased double-positive T cell number
- reduction in Cd5, Cd4, and Cd8 positive T lymphocytes
- 59% reduction in Cd3/Cd4 double positive T lymphocytes
- 67% reduction in Cd3/Cd8 double positive T lymphocytes

increased double-positive T cell number
- increased number of immature double positive cells

mammalian phenotype

nervous system phenotype
- Normal - no evidence of neurodegeneration
- Normal - no defects in brain architecture

immune system phenotype
- Normal - no abnormalities in B lymphocytes, granulocytes or myeloid cells observed

mortality/aging

premature death
- many mice die from thymic lymphoma; none survived greater than 4.5 months of age without a thymic lymphoma

increased mortality induced by gamma-irradiation
- mutant mice die from radiation induced toxicity to the gastrointestinal tract at doses that do not kill control mice

neoplasm

increased T cell derived lymphoma incidence
- thymic lymphomas are highly metastatic and consist of immature T cells

nervous system phenotype

abnormal Purkinje cell morphology
- heme oxygenase 1 is increase in Purkinje cells, indicating oxidative damage particularly in these cells

reproductive system phenotype

abnormal gametogenesis

small ovary

abnormal male reproductive system morphology

absent estrus
- females never enter estrous

arrest of spermatogenesis

male infertility
- normal mating behavior evident by the presence of copulation plugs in control females; however, pregnancy never results

absent estrous cycle

abnormal seminiferous tubule morphology
- degeneration of cells evident
- some barren of all cells except Sertoli cells
- reduced number of cells

abnormal uterus morphology
- no proliferation or degeneration in as part of the estrous cycle

female infertility
- females never exhibit copulation plugs

absent oocytes
- complete absence of mature gametes

small testis

abnormal female reproductive system morphology

abnormal reproductive system physiology

absent ovarian follicles
- absence of primordial and mature ovarian follicles

azoospermia
- absence of mature sperm

Genotype: Atm^tm1Awb/Atm^tm1Awb
A.129S6-Atm/J

homeostasis/metabolism phenotype

increased mortality induced by gamma-irradiation
- following exposure to 5 Gy of whole-body gamma radiation, 2 of 2 mice (>12 weeks of age) die within 5 days post-treatment

mortality/aging

increased mortality induced by gamma-irradiation
- following exposure to 5 Gy of whole-body gamma radiation, 2 of 2 mice (>12 weeks of age) die within 5 days post-treatment

Genotype: Atm^tm1Awb/Atm^tm1Awb
B6.129S6-Atm

growth/size/body region phenotype

decreased body weight
- pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points

mortality/aging

lethality, incomplete penetrance
- heterozygote x heterozygote matings produced fewer homozygotes than the expected Mendelian ratio
- Background Sensitivity - the number of homozygous pups produced from heterozygotes on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio

premature death
- median survival time is 353 days
- Background Sensitivity - survival time (least to most) on the following strain backgrounds is ranked as BALB/c < 129S6/SvEvTac < 129S6AF1 < 129S6B6F1 < C57BL/6 < A/J < B6AF1
- 8 mice out of 40 survive to 18 months of age

neoplasm

abnormal tumor incidence
- 21 out of 40 mice die of thymic lymphomas
- Background Sensitivity - mice are less susceptible to thymic lymphomas than on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 backgrounds

Genotype: Atm^tm1Awb/Atm^tm1Awb
either: (129S6/SvEvTac-Atm x B6.129S6-Atm)F1 or (B6.129S6-Atm x 129S6/SvEvTac-Atm)F1

endocrine/exocrine gland phenotype

increased T cell derived lymphoma incidence
- almost all mice die of thymic lymphomas
- Background Sensitivity - mice have a higher thymic lymphoma incidence than do homozygous Atm^tm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds

growth/size/body region phenotype

decreased body weight
- pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points

mammalian phenotype

mortality/aging
- Background Sensitivity - the number of homozygous pups produced from heterozygote matings on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio; fewer homozygous pups are produced on the C57BL/6 and A/J backgrounds

mortality/aging

premature death
- 5 mice out of 39 survive to 18 months of age
- median survival time is 200 days
- Background Sensitivity - survival time (least to most) on the following strain backgrounds is ranked as BALB/c < 129S6/SvEvTac < 129S6AF1 < 129S6B6F1 < C57BL/6 < A/J < B6AF1

neoplasm

increased T cell derived lymphoma incidence
- almost all mice die of thymic lymphomas
- Background Sensitivity - mice have a higher thymic lymphoma incidence than do homozygous Atm^tm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds

Genotype: Atm^tm1Awb/Atm^tm1Awb
CByJ.129S6-Atm

endocrine/exocrine gland phenotype

increased T cell derived lymphoma incidence
- almost all mice die of thymic lymphomas
- Background Sensitivity - mice have a higher thymic lymphoma incidence than do homozygous Atm^tm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds

growth/size/body region phenotype

decreased body weight
- pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points

mammalian phenotype

mortality/aging
- Background Sensitivity - the number of homozygous pups produced from heterozygote matings on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio; fewer homozygous pups are produced on the C57BL/6 and A/J backgrounds

mortality/aging

premature death
- Background Sensitivity - survival time is shortest on this background as compared to the A/J, C57BL/6, 129S6B6F1, B6AF1 and 129S6AF1 backgrounds
- median survival time is 74 days, no mice survive beyond 109 days

neoplasm

increased T cell derived lymphoma incidence
- almost all mice die of thymic lymphomas
- Background Sensitivity - mice have a higher thymic lymphoma incidence than do homozygous Atm^tm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds

Genotype: Atm^tm1Awb/Atm^tm1Awb
involves: 129S6/SvEvTac * C57BL/6

cellular phenotype

abnormal cell cycle checkpoint function
- MEFs exhibit defects in G1/S, intra-S-phase, and G2/M checkpoints after ionizing radiation induced DNA damage

chromosome breakage

endocrine/exocrine gland phenotype

increased T cell derived lymphoma incidence
- majority die with thymic lymphomas

mortality/aging

premature death
- majority die with thymic lymphomas by 5 months of age, 2.9% live up to 10 months, and none live beyond 15 months

neoplasm

increased T cell derived lymphoma incidence
- majority die with thymic lymphomas

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

Genotype: Atm^tm1Awb/Atm^tm1Awb
129S6/SvEvTac-Atm

endocrine/exocrine gland phenotype

increased T cell derived lymphoma incidence
- almost all mice die of thymic lymphomas
- Background Sensitivity - mice have a higher thymic lymphoma incidence than do homozygous Atm^tm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds

growth/size/body region phenotype

decreased body weight
- pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points

mammalian phenotype

mortality/aging
- Background Sensitivity - the number of homozygous pups produced from heterozygote matings on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio; fewer homozygous pups are produced on the C57BL/6 and A/J backgrounds

mortality/aging

premature death
- one mouse out of 40 survives to 18 months of age
- median survival time is 113 days
- Background Sensitivity - survival time (least to most) on the following strain backgrounds is ranked as BALB/c < 129S6/SvEvTac < 129S6AF1 < 129S6B6F1 < C57BL/6 < A/J < B6AF1

neoplasm

increased T cell derived lymphoma incidence
- Background Sensitivity - mice have a higher thymic lymphoma incidence than do homozygous Atm^tm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds
- almost all mice die of thymic lymphomas

Genotype: Atm^tm1Awb/Atm^tm1Awb
involves: 129S6/SvEvTac

cellular phenotype

abnormal cell cycle checkpoint function
- mouse embryonic fibroblasts exposed to radiation fail to arrest at the G1/S transition unlike similarly treated wild-type cells

abnormal chromosome morphology
- DNA losses in distal Chromosome 12 near the Igh locus
- lymphoma cells show Chromosome 14 translocations at the TCR alpha/delta locus

spontaneous chromosome breakage
- 10%-20% of B cells harbored IgH-specific breaks, 0.5%-3.5% carried IgH translocations, and 20%-30% had non-IgH associated instability
- incubation with DNA-PKcs kinase inhibitors dramatically increases genomic instability and almost doubles the frequency of myc/IgH translocations

homeostasis/metabolism phenotype

increased mortality induced by gamma-irradiation

immune system phenotype

abnormal class switch recombination
- there is small increase in switch junctions showing three or more nucleotide insertions
- B cells have about a 5-fold reduction in class switch recombination to IgG1

decreased CD4-positive, alpha beta T cell number
- in thymus and spleen

decreased CD8-positive, alpha-beta T cell number
- in thymus and spleen

mammalian phenotype

cellular phenotype
- Normal - mouse embryonic fibroblast cells arrest and undergo apoptosis following exposure to ionizing radiation

immune system phenotype
- Normal - thymic apoptosis following exposure to radiation is normal

mortality/aging

increased mortality induced by gamma-irradiation

premature death
- median survival is 16 weeks

neoplasm

increased T cell derived lymphoma incidence

endocrine/exocrine gland phenotype

increased T cell derived lymphoma incidence

growth/size/body region phenotype

decreased body weight
- 25%

hematopoietic system phenotype

abnormal class switch recombination
- B cells have about a 5-fold reduction in class switch recombination to IgG1
- there is small increase in switch junctions showing three or more nucleotide insertions

decreased CD8-positive, alpha-beta T cell number
- in thymus and spleen

decreased CD4-positive, alpha beta T cell number
- in thymus and spleen

Genotype: Atm^tm1Awb/Atm^tm1Awb
129S6/SvEvTac-Atm/J

endocrine/exocrine gland phenotype

increased T cell derived lymphoma incidence

neoplasm

increased T cell derived lymphoma incidence

hematopoietic system phenotype

decreased T cell number
- reduction in the percentage of T-cell subsets within the circulating lymphocyte population at 2 months of age

decreased single-positive T cell number
- thymocytes exhibit a decrease in the levels of more mature CD4 and CD8 single positive cells

increased B cell number
- increase in the percentage of B cells within the circulating lymphocyte populations at 2 months of age

increased double-positive T cell number
- thymocytes exhibit an increase in the levels of immature CD4/CD8 double positive T-cells

immune system phenotype

decreased single-positive T cell number
- thymocytes exhibit a decrease in the levels of more mature CD4 and CD8 single positive cells

decreased T cell number
- reduction in the percentage of T-cell subsets within the circulating lymphocyte population at 2 months of age

increased double-positive T cell number
- thymocytes exhibit an increase in the levels of immature CD4/CD8 double positive T-cells

increased B cell number
- increase in the percentage of B cells within the circulating lymphocyte populations at 2 months of age

References

Barlow C; Hirotsune S; Paylor R; Liyanage M; Eckhaus M; Collins F; Shiloh Y; Crawley JN; Ried T; Tagle D; Wynshaw-Boris A. 1996. Atm-deficient mice: a paradigm of ataxia telangiectasia. Cell 86(1):159-71PubMed: 8689683 MGI: J:34193

Additional References

Macleod MR; Ramage L; McGregor A; Seckl JR. 2003. Reduced NMDA-induced apoptosis in neurons lacking ataxia telangiectasia mutated protein. Neuroreport 14(2):215-7PubMed: 12598732 MGI: J:89866
Shackelford RE; Manuszak RP; Johnson CD; Hellrung DJ; Link CJ; Wang S. 2004. Iron chelators increase the resistance of Ataxia telangeictasia cells to oxidative stress. DNA Repair (Amst) 3(10):1263-72PubMed: 15336622 MGI: J:92530
Smilenov LB; Brenner DJ; Hall EJ. 2001. Modest increased sensitivity to radiation oncogenesis in ATM heterozygous versus wild-type mammalian cells. Cancer Res 61(15):5710-3PubMed: 11479203 MGI: J:70725
Weil MM; Kittrell FS; Yu Y; McCarthy M; Zabriskie RC; Ullrich RL. 2001. Radiation induces genomic instability and mammary ductal dysplasia in Atm heterozygous mice. Oncogene 20(32):4409-11PubMed: 11466622 MGI: J:70611
Yan M; Kuang X; Qiang W; Shen J; Claypool K; Lynn WS; Wong PK. 2002. Prevention of thymic lymphoma development in atm-/- mice by dexamethasone. Cancer Res 62(18):5153-7PubMed: 12234978 MGI: J:79018

Additional - Atm^tm1Awb related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Atm Alternate1
- Genotyping resources and troubleshooting
Appearance
- white-bellied agouti, ataxic
  Related Genotype: A^w/A^w Atm^tm1Awb/Atm^tm1Awb
Citation
When using the ATM^- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002753 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or Wild-type for Atm<tm1Awb>

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

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.

Terms Of Use

General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:ATM-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Atmtm1Awb

Allele Symbol: Atmtm1Awb

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: Atmtm1Awb related

Mammalian Phenotype Terms by Genotype

Genotype: Atmtm1Awb/Atmtm1Awbeither: (129S6/SvEvTac-Atm x A.129S6-Atm)F1 or (A.129S6-Atm x 129S6/SvEvTac-Atm)F1

endocrine/exocrine gland phenotype

growth/size/body region phenotype

mammalian phenotype

mortality/aging

neoplasm

Genotype: Atmtm1Awb/Atmtm1AwbA.129S6-Atm

growth/size/body region phenotype

neoplasm

liver/biliary system phenotype

mortality/aging

Genotype: Atmtm1Awb/Atmtm1Awbeither: (A.129S6-Atm x B6.129S6-Atm)F1 or (B6.129S6-Atm x A.129S6-Atm)F1

growth/size/body region phenotype

mammalian phenotype

mortality/aging

neoplasm

Genotype: Atmtm1Awb/Atmtm1Awbeither: 129S6/SvEvTac-Atm or (involves: 129S6/SvEvTac * NIH Black Swiss)

behavior/neurological phenotype

cellular phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

mammalian phenotype

mortality/aging

neoplasm

nervous system phenotype

reproductive system phenotype

Genotype: Atmtm1Awb/Atmtm1AwbA.129S6-Atm/J

homeostasis/metabolism phenotype

mortality/aging

Genotype: Atmtm1Awb/Atmtm1AwbB6.129S6-Atm

growth/size/body region phenotype

mortality/aging

neoplasm

Genotype: Atmtm1Awb/Atmtm1Awbeither: (129S6/SvEvTac-Atm x B6.129S6-Atm)F1 or (B6.129S6-Atm x 129S6/SvEvTac-Atm)F1

endocrine/exocrine gland phenotype

growth/size/body region phenotype

mammalian phenotype

mortality/aging

neoplasm

Genotype: Atmtm1Awb/Atmtm1AwbCByJ.129S6-Atm

endocrine/exocrine gland phenotype

growth/size/body region phenotype

mammalian phenotype

mortality/aging

neoplasm

Genotype: Atmtm1Awb/Atmtm1Awbinvolves: 129S6/SvEvTac * C57BL/6

cellular phenotype

endocrine/exocrine gland phenotype

mortality/aging

neoplasm

Genotype: Atmtm1Awb/Atmtm1Awb129S6/SvEvTac-Atm

endocrine/exocrine gland phenotype

growth/size/body region phenotype

mammalian phenotype

mortality/aging

neoplasm

Genotype: Atmtm1Awb/Atmtm1Awbinvolves: 129S6/SvEvTac

cellular phenotype

homeostasis/metabolism phenotype

Also Known As:ATM^-

Atm^tm1Awb

Allele Symbol: Atm^tm1Awb

Genotype: Atm^tm1Awb related

Genotype: Atm^tm1Awb/Atm^tm1Awb
either: (129S6/SvEvTac-Atm x A.129S6-Atm)F1 or (A.129S6-Atm x 129S6/SvEvTac-Atm)F1

Genotype: Atm^tm1Awb/Atm^tm1Awb
A.129S6-Atm

Genotype: Atm^tm1Awb/Atm^tm1Awb
either: (A.129S6-Atm x B6.129S6-Atm)F1 or (B6.129S6-Atm x A.129S6-Atm)F1

Genotype: Atm^tm1Awb/Atm^tm1Awb
either: 129S6/SvEvTac-Atm or (involves: 129S6/SvEvTac * NIH Black Swiss)

Genotype: Atm^tm1Awb/Atm^tm1Awb
A.129S6-Atm/J

Genotype: Atm^tm1Awb/Atm^tm1Awb
B6.129S6-Atm

Genotype: Atm^tm1Awb/Atm^tm1Awb
either: (129S6/SvEvTac-Atm x B6.129S6-Atm)F1 or (B6.129S6-Atm x 129S6/SvEvTac-Atm)F1

Genotype: Atm^tm1Awb/Atm^tm1Awb
CByJ.129S6-Atm

Genotype: Atm^tm1Awb/Atm^tm1Awb
involves: 129S6/SvEvTac * C57BL/6

Genotype: Atm^tm1Awb/Atm^tm1Awb
129S6/SvEvTac-Atm

Genotype: Atm^tm1Awb/Atm^tm1Awb
involves: 129S6/SvEvTac

Genotype: Atm^tm1Awb/Atm^tm1Awb
129S6/SvEvTac-Atm/J

Additional - Atm^tm1Awb related