Strain Name:

B6.Cg-Terctm1Rdp/J

Stock Number:

004132

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Progressive adverse effects on the reproductive and hematopoietic systems and progressive telomere shortening are observed in successive generations of breeding of mice that are homozygous null for the Terc gene . Germ cells exhibit decreased rates in proliferation and increased rates of apoptosis resulting in a general state of germ cell depletion; fertility is significantly diminished. Proliferative capacity of hematopoietic cells derived from bone marrow and spleen is significantly compromised.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHeterozygote x Heterozygote         (Female x Male)   01-MAR-06
Specieslaboratory mouse
GenerationN7+N6F5 (24-MAR-11)
Generation Definitions
 
Donating InvestigatorDr. Carol Greider,   Johns Hopkins Univ School of Medicine

Description
Early generation mice that are homozygous null for the Terc gene are phenotypically normal. No Terc transcript or telomerase activity is detected. If null mice are maintained as homozygotes, progressive adverse effects on the reproductive and hematopoietic systems are observed. By the fifth generation of homozygous intercrossing, fertility is significantly diminished. Testes size and weight is reduced by ~80%. Germ cells exhibit decreased rates in proliferation and increased rates of apoptosis resulting in a general state of germ cell depletion. Females exhibit smaller ovaries and diminished uterine horns. The proliferative capacity of hematopoietic cells derived from bone marrow and spleen is significantly compromised. Progressive generations of interbreeding the null mice results in progressive telomere shortening (4.8 +/- 2.4 kb per generation). Cells from the fourth generation onward possess chromosome ends lacking detectable telomere repeats, aneuploidy, and chromosomal abnormalities, including end-to-end fusions.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt the entire Terc gene. The construct was electroporated into WW6 embryonic stem (ES) cells. WW6 ES cells are derived from a mixed genetic background (C57BL/6J ,129/Sv and SJL). Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric animals were backcrossed to C57BL/6J mice. This strain has been backcrossed to C57BL/6J for at least seven generations.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Terctm1Rdp allele
023535   B6.Cg-Terctm1Rdp Dmdmdx-4Cv/BlauJ
018915   STOCK Terctm1Rdp Dmdmdx/J
View Strains carrying   Terctm1Rdp     (2 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Dyskeratosis Congenita, Autosomal Dominant, 1; DKCA1   (TERC)
Pulmonary Fibrosis and/or Bone Marrow Failure, Telomere-Related, 2;   (TERC)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Terctm1Rdp/Terctm1Rdp

        involves: 129/Sv * C57BL/6J * SJL
  • mortality/aging
  • partial prenatal lethality
    • a fraction of homozygous embryos from late generation homozygous matings do not survive gestation to completion or die immediately after birth   (MGI Ref ID J:53600)
    • only 74% of homozygous fetuses from late generation pregnant females are alive   (MGI Ref ID J:89751)
  • premature aging
    • late generation mutants exhibit accelerated degeneration as indicated by hair graying, alopecia, kyphosis, reduced body size and weight, and fragility   (MGI Ref ID J:120065)
  • premature death
    • older (6-8 months) fifth generation mutants that show sudden loss in body weight and activity die 7-12 hours after the manifestation of these phenotypes   (MGI Ref ID J:110900)
  • cellular phenotype
  • abnormal chromosome morphology
    • lack of perinuclear distribution of telomeres in fourth generation mutants   (MGI Ref ID J:89751)
    • abnormal telomere length   (MGI Ref ID J:74001)
      • embryonic fibroblast cells derived from mutant mice after the fourth generation lacked detectable telomeric repeats and were often aneupolid with chromosomal abnormalities, including end to end fusions   (MGI Ref ID J:43517)
      • keratinocytes exhibit a significant decrease in average telomere length compared with wild-type cells   (MGI Ref ID J:96945)
      • splenocytes from non-immunized fifth generation mutants contain shorter telomere lengths than wild-type   (MGI Ref ID J:60223)
      • upon immunization with an antigen, proliferating splenocyte telomeres are shortened during germinal center formation, unlike in wildtype mice which show elongation of telomeres, however telomeres are longer than seen in non-immunized mutants   (MGI Ref ID J:60223)
      • cells from embryos that fail to close the neural tube have shorter telomeres and decreased viability than mutants with a closed neural tube   (MGI Ref ID J:53600)
      • cardiac myocytes of second and fifth generation mutants show telomere shortening, with cardiomyocytes from older mutants having shorter telomeres than in younger mutants   (MGI Ref ID J:110900)
      • telomere shortening occurs in both meiocytes with normal and abnormal synapsis   (MGI Ref ID J:89751)
      • the anaphase bridge index (ABI) is increased in late-generation (G4/G5) intestinal crypts indicating telomere dysfunction   (MGI Ref ID J:120065)
  • abnormal fetal cardiomyocyte proliferation
    • second and fifth generation mutants exhibit decreased cardiac myocyte proliferation   (MGI Ref ID J:110900)
  • abnormal male germ cell apoptosis
    • in response to telomere shortening, male germ cells undergo apoptosis   (MGI Ref ID J:89751)
    • apoptotic depletion of germ cells in late generation mutants   (MGI Ref ID J:120065)
  • increased apoptosis
    • E10.5 embryos with neural tube defects exhibit an increase in apoptosis   (MGI Ref ID J:53600)
    • apoptosis of male germ cells and in the GI crypts of late generation mutants   (MGI Ref ID J:120065)
    • increased B cell apoptosis
      • splenocytes from immunized fifth and sixth generation mice exhibit a small increase in apoptosis after mitogen treatment   (MGI Ref ID J:60223)
    • increased cardiomyocyte apoptosis
      • fifth generation mutants exhibit a 63% increase in cardiomyocyte apoptosis   (MGI Ref ID J:110900)
  • tumorigenesis
  • decreased incidence of induced tumors
    • fifth generation mutants show decreased tumor growth rate and lower tumor formation efficiency upon dermal or subcutaneous melanoma cell injection   (MGI Ref ID J:74001)
    • tumors that are induced in fifth generation mutants show decreased replication potential and increased apoptotic rates   (MGI Ref ID J:74001)
    • decreased incidence of tumors by chemical induction
      • first generation mutants are slightly less susceptible to DMBA + TPA induced skin tumorigenesis, with a delay in papilloma formation compared to wild-type and papillomas that do not progress to lesions bigger than 8 mm   (MGI Ref ID J:96945)
  • cardiovascular system phenotype
  • abnormal angiogenesis
    • late generation mutants show decreased angiogenic potential in a basement membrane matrix assay   (MGI Ref ID J:74001)
    • microvessel density is decreased in the induced tumors of fifth generation mutants   (MGI Ref ID J:74001)
    • large abnormal vessels are present in the induced tumors of fifth generation mutants   (MGI Ref ID J:74001)
  • abnormal cardiovascular system physiology
    • fifth generation, but not second generation, mutants suffer from a severe left ventricular failure   (MGI Ref ID J:110900)
    • abnormal cardiac muscle contractility
      • fifth generation, but not second generation, mutants exhibit a decrease in +dP/dt   (MGI Ref ID J:110900)
    • abnormal cardiac muscle relaxation
      • fifth generation mutants exhibit a decrease in -dP/dt   (MGI Ref ID J:110900)
    • abnormal fetal cardiomyocyte proliferation
      • second and fifth generation mutants exhibit decreased cardiac myocyte proliferation   (MGI Ref ID J:110900)
    • congestive heart failure
      • older fifth generation mutants die of heart failure   (MGI Ref ID J:110900)
    • decreased left ventricle developed pressure
      • fifth generation mutants exhibit a decrease in LV developed pressure   (MGI Ref ID J:110900)
    • dilated cardiomyopathy
      • dilated cardiomyopathy develops in fifth generation mutants   (MGI Ref ID J:110900)
    • increased cardiomyocyte apoptosis
      • fifth generation mutants exhibit a 63% increase in cardiomyocyte apoptosis   (MGI Ref ID J:110900)
    • increased left ventricle diastolic pressure
      • fifth generation mutants exhibit an elevation of LV end-diastolic pressure   (MGI Ref ID J:110900)
  • abnormal myocardial fiber morphology
    • the volume of binucleated cardiomyocytes is increased by 24% in second generation mutants and 52% in fifth generation mutants   (MGI Ref ID J:110900)
    • the volume of mononucleated cardiomyocytes is increased by 39% and 43% in second and fifth generation mutants, respectively   (MGI Ref ID J:110900)
    • decreased myocardial fiber number
      • cardiomyocyte number is decreased 16% and 49% in second and fifth generation mutants, respectively   (MGI Ref ID J:110900)
  • cardiac hypertrophy
    • fifth generation mutants exhibit cardiac myocyte hypertrophy   (MGI Ref ID J:110900)
    • heart left ventricle hypertrophy
      • fifth generation mutants show a reduction in left ventricle mass that is accompanied by a decrease in left ventricle mass:chamber volume ratio, indicating decompensated eccentric left ventricle hypertrophy in the absence of an absolute increase in ventricular weight   (MGI Ref ID J:110900)
  • decreased heart weight
    • heart weight is decreased in fifth generation mutants   (MGI Ref ID J:110900)
    • decreased heart left ventricle weight
      • left ventricle weight is decreased in fifth generation mutants   (MGI Ref ID J:110900)
  • hematopoietic system phenotype
  • abnormal spleen B cell follicle morphology
    • spleens from sixth generation mutants (but not earlier generations) show fewer follicles   (MGI Ref ID J:60223)
    • decreased spleen germinal center number
      • fifth and sixth generation homozygotes show a reduction in germinal centers following antigen (KLH) immunization   (MGI Ref ID J:60223)
  • decreased B cell proliferation
    • splenocytes (from both non-immunized and immunized) from sixth generation mutants show a decrease in the proliferative response to B and T cell mitogens   (MGI Ref ID J:60223)
  • decreased T cell proliferation
    • splenocytes (from both non-immunized and immunized) from sixth generation mutants show a decrease in the proliferative response to B and T cell mitogens   (MGI Ref ID J:60223)
  • increased B cell apoptosis
    • splenocytes from immunized fifth and sixth generation mice exhibit a small increase in apoptosis after mitogen treatment   (MGI Ref ID J:60223)
  • immune system phenotype
  • abnormal spleen B cell follicle morphology
    • spleens from sixth generation mutants (but not earlier generations) show fewer follicles   (MGI Ref ID J:60223)
    • decreased spleen germinal center number
      • fifth and sixth generation homozygotes show a reduction in germinal centers following antigen (KLH) immunization   (MGI Ref ID J:60223)
  • decreased B cell proliferation
    • splenocytes (from both non-immunized and immunized) from sixth generation mutants show a decrease in the proliferative response to B and T cell mitogens   (MGI Ref ID J:60223)
  • decreased T cell proliferation
    • splenocytes (from both non-immunized and immunized) from sixth generation mutants show a decrease in the proliferative response to B and T cell mitogens   (MGI Ref ID J:60223)
  • increased B cell apoptosis
    • splenocytes from immunized fifth and sixth generation mice exhibit a small increase in apoptosis after mitogen treatment   (MGI Ref ID J:60223)
  • embryogenesis phenotype
  • abnormal developmental patterning
    • a portion of embryos with open neural tube show absence of bilateral symmetry in the brain   (MGI Ref ID J:53600)
  • open neural tube
    • a percentage of embryos fail to close the neural tube, particularly in the forebrain and midbrain, at E10.5; penetrance of this defect increases with generation number, with 30% of fifth generation embryos showing an open neural tube   (MGI Ref ID J:53600)
  • nervous system phenotype
  • open neural tube
    • a percentage of embryos fail to close the neural tube, particularly in the forebrain and midbrain, at E10.5; penetrance of this defect increases with generation number, with 30% of fifth generation embryos showing an open neural tube   (MGI Ref ID J:53600)
  • reproductive system phenotype
  • abnormal male germ cell apoptosis
    • in response to telomere shortening, male germ cells undergo apoptosis   (MGI Ref ID J:89751)
    • apoptotic depletion of germ cells in late generation mutants   (MGI Ref ID J:120065)
  • abnormal meiosis
    • chromosome pairing, synapsis, and recombination are severely impaired in meiocytes with irregular telomeres   (MGI Ref ID J:89751)
    • abnormal female meiosis
      • in response to telomere shortening, female germ cells arrest in early meiosis   (MGI Ref ID J:89751)
      • meiocytes of fourth generation (G4) females with shortened telomeres bred with early generation males harboring relatively long telomeres, exhibit severely impaired chromosome pairing and synapsis and reduced meiotic recombination   (MGI Ref ID J:89751)
      • synaptonemal complex protein 3 (SCP3) elements are altered in G4 female meiotic cells   (MGI Ref ID J:89751)
    • abnormal male meiosis
      • the number of spermatocytes with synaptonemal complex protein 3 (SCP3) lateral elements is decreased in the fourth generation (G4) homozygotes   (MGI Ref ID J:89751)
  • abnormal oocyte morphology
    • the number of oocytes that form synaptonemal complexes is decreased   (MGI Ref ID J:89751)
  • abnormal spermatocyte morphology
    • apoptosis is increased 5-fold in seminiferous tubules of G4 homozygotes; apoptosis is found in the outer layers of spermatocytes whereas the inner layer of spermatogonia remains intact   (MGI Ref ID J:89751)
  • decreased litter size
    • mutants of late generations show a decrease in litter size   (MGI Ref ID J:53600)
  • infertility
    • mutants are infertile at the sixth generation (of interbreeding) and infertile at the fourth generation of backcrossing to C57BL/6J   (MGI Ref ID J:53600)
  • reduced female fertility
    • late generation pregnant females have fewer fetuses   (MGI Ref ID J:89751)
  • testicular atrophy
    • testicular atrophy and associated apoptotic depletion of germ cells in late generation mutants   (MGI Ref ID J:120065)
  • behavior/neurological phenotype
  • hypoactivity
    • older (6-8 months) fifth generation mutants often show a sudden decrease in activity   (MGI Ref ID J:110900)
  • growth/size/body phenotype
  • decreased body size
    • late generation mutants have reduced body size and are fragile   (MGI Ref ID J:120065)
    • decreased body weight
      • late generation mutants have reduced body weight   (MGI Ref ID J:120065)
      • weight loss
        • older (6-8 months) fifth generation mutants often show sudden losses in body weight   (MGI Ref ID J:110900)
  • decreased fetal size
    • 41% of homozygous fetuses from late generation pregnant females are reduced in size   (MGI Ref ID J:89751)
  • muscle phenotype
  • abnormal cardiac muscle contractility
    • fifth generation, but not second generation, mutants exhibit a decrease in +dP/dt   (MGI Ref ID J:110900)
  • abnormal cardiac muscle relaxation
    • fifth generation mutants exhibit a decrease in -dP/dt   (MGI Ref ID J:110900)
  • abnormal fetal cardiomyocyte proliferation
    • second and fifth generation mutants exhibit decreased cardiac myocyte proliferation   (MGI Ref ID J:110900)
  • abnormal myocardial fiber morphology
    • the volume of binucleated cardiomyocytes is increased by 24% in second generation mutants and 52% in fifth generation mutants   (MGI Ref ID J:110900)
    • the volume of mononucleated cardiomyocytes is increased by 39% and 43% in second and fifth generation mutants, respectively   (MGI Ref ID J:110900)
    • decreased myocardial fiber number
      • cardiomyocyte number is decreased 16% and 49% in second and fifth generation mutants, respectively   (MGI Ref ID J:110900)
  • dilated cardiomyopathy
    • dilated cardiomyopathy develops in fifth generation mutants   (MGI Ref ID J:110900)
  • increased cardiomyocyte apoptosis
    • fifth generation mutants exhibit a 63% increase in cardiomyocyte apoptosis   (MGI Ref ID J:110900)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • homozygotes exhibit normal wound healing   (MGI Ref ID J:96945)
    • decreased incidence of tumors by chemical induction
      • first generation mutants are slightly less susceptible to DMBA + TPA induced skin tumorigenesis, with a delay in papilloma formation compared to wild-type and papillomas that do not progress to lesions bigger than 8 mm   (MGI Ref ID J:96945)
  • digestive/alimentary phenotype
  • abnormal intestine morphology
    • the GI crypts of late generation mutants exhibit high levels of apoptosis   (MGI Ref ID J:120065)
  • skeleton phenotype
  • kyphosis
    • late generation mutants exhibit kyphosis   (MGI Ref ID J:120065)
  • integument phenotype
  • alopecia
    • late generation mutants exhibit alopecia   (MGI Ref ID J:120065)
  • endocrine/exocrine gland phenotype
  • testicular atrophy
    • testicular atrophy and associated apoptotic depletion of germ cells in late generation mutants   (MGI Ref ID J:120065)

Terctm1Rdp/Terctm1Rdp

        involves: FVB/N
  • cellular phenotype
  • abnormal telomere length
    • elongated spermatids from second generation (G2) homozygotes display variable telomere length, with some displaying long telomeres, while others have short telomeres   (MGI Ref ID J:98586)
  • reproductive system phenotype
  • abnormal spermatid morphology
    • at 8 months of age, second generation (G2) homozygotes exhibit fewer intact elongating spermatids containing extended telomeres than wild-type or heterozygous littermates   (MGI Ref ID J:98586)
    • however, fertility is preserved, suggesting that alternative telomere extension activity is capable of partially complementing the telomerase defect   (MGI Ref ID J:98586)

Terctm1Rdp/Terctm1Rdp

        involves: 129/Sv * C57BL/6 * C57BL/6J * SJL
  • mortality/aging
  • premature death
    • median survival is reduced in successive generations compared to in wild-type mice   (MGI Ref ID J:125218)
  • digestive/alimentary phenotype
  • abnormal enterocyte proliferation
    • intestinal cell proliferation is impaired compared to in wild-type mice   (MGI Ref ID J:125218)
  • abnormal intestine morphology
    • mice exhibit mild to severe intestinal atrophy unlike wild-type mice that worsens in successive generations   (MGI Ref ID J:125218)
  • increased enterocyte apoptosis
    • regardless of generation   (MGI Ref ID J:125218)
  • cellular phenotype
  • abnormal cell physiology
    • mouse embryonic fibroblasts (MEFs) from third generation mice exhibit decreased immortalization ability under a 3T3 cell passage protocol compared with similarly treated wild-type cells   (MGI Ref ID J:125218)
    • sister chromatid exchange in MEFs is increased compared to in wild-type cells   (MGI Ref ID J:125218)
    • abnormal DNA repair
      • cells from the small intestine exhibit an increase in gamma-H2AX foci, indicative of DNA damage, compared with cells from wild-type mice   (MGI Ref ID J:125218)
    • abnormal enterocyte proliferation
      • intestinal cell proliferation is impaired compared to in wild-type mice   (MGI Ref ID J:125218)
    • chromosomal instability
      • mouse embryonic fibroblasts (MEFs) exhibit in increase in microsatellite instability compared with wild-type cells   (MGI Ref ID J:125218)
      • end-to-end chromosome fusions in MEFs are increased compared to in wild-type cells   (MGI Ref ID J:125218)
      • MEFs from late generation mice exhibit an increase in chromosome breaks, fragments, bivalent recombination figures, and complex aberrations compared with wild-type cells   (MGI Ref ID J:125218)
    • increased enterocyte apoptosis
      • regardless of generation   (MGI Ref ID J:125218)
  • abnormal telomere length
    • telomeres become progressively shorter each generation unlike in wild-type mice   (MGI Ref ID J:125218)
  • tumorigenesis
  • increased lymphoma incidence
    • the incidence of lymphomas decreases in successive generation   (MGI Ref ID J:125218)
  • homeostasis/metabolism phenotype
  • abnormal DNA repair
    • cells from the small intestine exhibit an increase in gamma-H2AX foci, indicative of DNA damage, compared with cells from wild-type mice   (MGI Ref ID J:125218)
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Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Terctm1Rdp
Allele Name targeted mutation 1, Ronald DePinho
Allele Type Targeted (Null/Knockout)
Common Name(s) TR-; Terc-; mTR-; mTerc-;
Mutation Made ByDr. Carol Greider,   Johns Hopkins Univ School of Medicine
Strain of OriginSTOCK 129/Sv and C57BL/6J and SJL
ES Cell Line NameWW6
ES Cell Line StrainSTOCK 129/Sv and C57BL/6J and SJL
Gene Symbol and Name Terc, telomerase RNA component
Chromosome 3
Gene Common Name(s) mTER; mTR;
Molecular Note Replacement of the entire gene with a neomycin cassette. [MGI Ref ID J:43517]

Genotyping

Genotyping Information

Genotyping Protocols

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Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Blasco MA; Lee HW; Hande MP; Samper E; Lansdorp PM; DePinho RA ; Greider CW. 1997. Telomere shortening and tumor formation by mouse cells lacking telomerase RNA [see comments] Cell 91(1):25-34. [PubMed: 9335332]  [MGI Ref ID J:43517]

Additional References

Herrera E; Samper E; Blasco MA. 1999. Telomere shortening in mTR-/- embryos is associated with failure to close the neural tube. EMBO J 18(5):1172-81. [PubMed: 10064584]  [MGI Ref ID J:53600]

Terctm1Rdp related

Akbay EA; Contreras CM; Perera SA; Sullivan JP; Broaddus RR; Schorge JO; Ashfaq R; Saboorian H; Wong KK; Castrillon DH. 2008. Differential roles of telomere attrition in type I and II endometrial carcinogenesis. Am J Pathol 173(2):536-44. [PubMed: 18599611]  [MGI Ref ID J:138286]

Allsopp RC; Morin GB; DePinho R; Harley CB; Weissman IL. 2003. Telomerase is required to slow telomere shortening and extend replicative lifespan of HSCs during serial transplantation. Blood 102(2):517-20. [PubMed: 12663456]  [MGI Ref ID J:115695]

Argilla D; Chin K; Singh M; Hodgson JG; Bosenberg M; de Solorzano CO; Lockett S; DePinho RA; Gray J; Hanahan D. 2004. Absence of telomerase and shortened telomeres have minimal effects on skin and pancreatic carcinogenesis elicited by viral oncogenes. Cancer Cell 6(4):373-85. [PubMed: 15488760]  [MGI Ref ID J:94774]

Armanios M; Alder JK; Parry EM; Karim B; Strong MA; Greider CW. 2009. Short telomeres are sufficient to cause the degenerative defects associated with aging. Am J Hum Genet 85(6):823-32. [PubMed: 19944403]  [MGI Ref ID J:158466]

Artandi SE; Chang S; Lee SL; Alson S; Gottlieb GJ; Chin L; DePinho RA. 2000. Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice [see comments] Nature 406(6796):641-5. [PubMed: 10949306]  [MGI Ref ID J:63843]

Autexier C. 2008. POT of gold: modeling dyskeratosis congenita in the mouse. Genes Dev 22(13):1731-6. [PubMed: 18593874]  [MGI Ref ID J:137424]

Begus-Nahrmann Y; Hartmann D; Kraus J; Eshraghi P; Scheffold A; Grieb M; Rasche V; Schirmacher P; Lee HW; Kestler HA; Lechel A; Rudolph KL. 2012. Transient telomere dysfunction induces chromosomal instability and promotes carcinogenesis. J Clin Invest 122(6):2283-8. [PubMed: 22622037]  [MGI Ref ID J:190483]

Begus-Nahrmann Y; Lechel A; Obenauf AC; Nalapareddy K; Peit E; Hoffmann E; Schlaudraff F; Liss B; Schirmacher P; Kestler H; Danenberg E; Barker N; Clevers H; Speicher MR; Rudolph KL. 2009. p53 deletion impairs clearance of chromosomal-instable stem cells in aging telomere-dysfunctional mice. Nat Genet 41(10):1138-43. [PubMed: 19718028]  [MGI Ref ID J:155011]

Benetti R; Garcia-Cao M; Blasco MA. 2007. Telomere length regulates the epigenetic status of mammalian telomeres and subtelomeres. Nat Genet 39(2):243-50. [PubMed: 17237781]  [MGI Ref ID J:118330]

Bhattacharjee RN; Banerjee B; Akira S; Hande MP. 2010. Telomere-mediated chromosomal instability triggers TLR4 induced inflammation and death in mice. PLoS One 5(7):e11873. [PubMed: 20686699]  [MGI Ref ID J:163068]

Blanco R; Munoz P; Flores JM; Klatt P; Blasco MA. 2007. Telomerase abrogation dramatically accelerates TRF2-induced epithelial carcinogenesis. Genes Dev 21(2):206-20. [PubMed: 17234886]  [MGI Ref ID J:117418]

Bojovic B; Crowe DL. 2011. Telomere dysfunction promotes metastasis in a TERC null mouse model of head and neck cancer. Mol Cancer Res 9(7):901-13. [PubMed: 21593138]  [MGI Ref ID J:205225]

Bu DX; Johansson ME; Ren J; Xu DW; Johnson FB; Edfeldt K; Yan ZQ. 2010. Nuclear factor {kappa}B-mediated transactivation of telomerase prevents intimal smooth muscle cell from replicative senescence during vascular repair. Arterioscler Thromb Vasc Biol 30(12):2604-10. [PubMed: 20864668]  [MGI Ref ID J:183205]

Cayuela ML; Flores JM; Blasco MA. 2005. The telomerase RNA component Terc is required for the tumour-promoting effects of Tert overexpression. EMBO Rep 6(3):268-74. [PubMed: 15731767]  [MGI Ref ID J:96945]

Chamberlain JS. 2010. Duchenne muscular dystrophy models show their age. Cell 143(7):1040-2. [PubMed: 21183068]  [MGI Ref ID J:167707]

Chang S. 2005. Modeling aging and cancer in the telomerase knockout mouse. Mutat Res 576(1-2):39-53. [PubMed: 15927211]  [MGI Ref ID J:99987]

Chang S; Multani AS; Cabrera NG; Naylor ML; Laud P; Lombard D; Pathak S; Guarente L; DePinho RA. 2004. Essential role of limiting telomeres in the pathogenesis of Werner syndrome. Nat Genet 36(8):877-82. [PubMed: 15235603]  [MGI Ref ID J:91715]

Chiang YJ; Hemann MT; Hathcock KS; Tessarollo L; Feigenbaum L; Hahn WC; Hodes RJ. 2004. Expression of telomerase RNA template, but not telomerase reverse transcriptase, is limiting for telomere length maintenance in vivo. Mol Cell Biol 24(16):7024-31. [PubMed: 15282303]  [MGI Ref ID J:92243]

Chin L; Artandi SE; Shen Q; Tam A; Lee SL; Gottlieb GJ; Greider CW; DePinho RA. 1999. p53 deficiency rescues the adverse effects of telomere loss and cooperates with telomere dysfunction to accelerate carcinogenesis. Cell 97(4):527-38. [PubMed: 10338216]  [MGI Ref ID J:54988]

Choudhury AR; Ju Z; Djojosubroto MW; Schienke A; Lechel A; Schaetzlein S; Jiang H; Stepczynska A; Wang C; Buer J; Lee HW; von Zglinicki T; Ganser A; Schirmacher P; Nakauchi H; Rudolph KL. 2007. Cdkn1a deletion improves stem cell function and lifespan of mice with dysfunctional telomeres without accelerating cancer formation. Nat Genet 39(1):99-105. [PubMed: 17143283]  [MGI Ref ID J:117492]

Cosme-Blanco W; Shen MF; Lazar AJ; Pathak S; Lozano G; Multani AS; Chang S. 2007. Telomere dysfunction suppresses spontaneous tumorigenesis in vivo by initiating p53-dependent cellular senescence. EMBO Rep 8(5):497-503. [PubMed: 17396137]  [MGI Ref ID J:208249]

Denchi EL. 2009. Give me a break: How telomeres suppress the DNA damage response. DNA Repair (Amst) 8(9):1118-26. [PubMed: 19482563]  [MGI Ref ID J:151432]

Du X; Shen J; Kugan N; Furth EE; Lombard DB; Cheung C; Pak S; Luo G; Pignolo RJ; DePinho RA; Guarente L; Johnson FB. 2004. Telomere shortening exposes functions for the mouse werner and bloom syndrome genes. Mol Cell Biol 24(19):8437-46. [PubMed: 15367665]  [MGI Ref ID J:93016]

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Westhoff JH; Schildhorn C; Jacobi C; Homme M; Hartner A; Braun H; Kryzer C; Wang C; von Zglinicki T; Kranzlin B; Gretz N; Melk A. 2010. Telomere shortening reduces regenerative capacity after acute kidney injury. J Am Soc Nephrol 21(2):327-36. [PubMed: 19959722]  [MGI Ref ID J:185862]

Wiemann SU; Satyanarayana A; Buer J; Kamino K; Manns MP; Rudolph KL. 2005. Contrasting effects of telomere shortening on organ homeostasis, tumor suppression, and survival during chronic liver damage. Oncogene 24(9):1501-9. [PubMed: 15608677]  [MGI Ref ID J:96885]

Wong KK; Chang S; Weiler SR; Ganesan S; Chaudhuri J; Zhu C; Artandi SE; Rudolph KL; Gottlieb GJ; Chin L; Alt FW; DePinho RA. 2000. Telomere dysfunction impairs DNA repair and enhances sensitivity to ionizing radiation Nat Genet 26(1):85-8. [PubMed: 10973255]  [MGI Ref ID J:64366]

Wong KK; Maser RS; Bachoo RM; Menon J; Carrasco DR; Gu Y; Alt FW; DePinho RA. 2003. Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing. Nature 421(6923):643-8. [PubMed: 12540856]  [MGI Ref ID J:81552]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, heterozygous mice are bred together. The coat color expected from breeding is black.
Mating SystemHeterozygote x Heterozygote         (Female x Male)   01-MAR-06
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $239.00Female or MaleHeterozygous for Terctm1Rdp  
$239.00Female or MaleHomozygous for Terctm1Rdp  
Price per Pair (US dollars $)Pair Genotype
$478.00Heterozygous for Terctm1Rdp x Heterozygous for Terctm1Rdp  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $310.70Female or MaleHeterozygous for Terctm1Rdp  
$310.70Female or MaleHomozygous for Terctm1Rdp  
Price per Pair (US dollars $)Pair Genotype
$621.40Heterozygous for Terctm1Rdp x Heterozygous for Terctm1Rdp  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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.


See Terms of Use tab for General Terms and Conditions


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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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