Strain Name:

B6;129S6-Lig4tm1Fwa/Kvm

Stock Number:

006482

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Availability:

Cryopreserved - Ready for recovery

Use Restrictions Apply, see Terms of Use

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
Generation?pN1
Generation Definitions

Development
A targeting vector containing a loxP flanked neomycin resistance gene was used to disrupt the Lig4 exon. The construct was electroporated into 129S1/SvEvTac derived TC-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6 and maintained as an intercross. This strain was transferred to Dr. Kevin Mills at The Jackson Laboratory and backcrossed to C57BL/6 for an additional three generations. It was cryopreserved in 2007.

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.
LIG4 Syndrome   (LIG4)
Myeloma, Multiple   (LIG4)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Lig4tm1Fwa/Lig4+

        involves: 129S6/SvEvTac * C57BL/6
  • cellular phenotype
  • chromosome breakage
    • cultured fibroblasts display chromosomal instability at a level of ~32%   (MGI Ref ID J:80467)

Lig4tm1Fwa/Lig4tm1Fwa

        involves: 129S6/SvEvTac * C57BL/6
  • mortality/aging
  • complete prenatal lethality
    • no live-born mice Lig4-null mice are generated from Lig4tm1Fwa/+, Xrcc5+/+ crosses (0/153 total offspring)   (MGI Ref ID J:80467)
  • partial lethality throughout fetal growth and development
    • homozygotes are obtained at the expected Mendelian frequency at E15.0-E16.0; however, a significant number of homozygotes are found dead at E16.5-E17.5   (MGI Ref ID J:50865)
  • growth/size/body phenotype
  • decreased fetal size
    • at E13.5-E14.5, mutant embryos are ~12% smaller than wild-type embryos   (MGI Ref ID J:50865)
    • by E15.0-E16.0, mutant embryos are ~25% smaller than wild-type embryos   (MGI Ref ID J:50865)
  • cellular phenotype
  • abnormal cell physiology
    • in culture, mutant MEFs show defective repair of ionizing radiation-induced DNA damage   (MGI Ref ID J:50865)
    • in culture, mutant MEFs show impaired V(D)J recombination, as shown by both recombination signal sequence (RSS) and coding-joining deficiencies   (MGI Ref ID J:50865)
    • impaired V(D)J recombination accounts for the blocked lymphopoiesis observed in older mutant embryos   (MGI Ref ID J:50865)
    • chromosome breakage
      • cultured fibroblasts display chromosomal instability at a level of ~55%   (MGI Ref ID J:80467)
    • decreased cell proliferation
      • in culture, MEFs isolated from E13.5 homozygotes display significantly increased doubling times (55 hrs) relative to heterozygous (24 hrs) or wild-type MEFs (27 hrs)   (MGI Ref ID J:50865)
      • BrdU-labeling indicates a 23-34% reduction in the number of mutant MEFs found in the S phase of the cell cycle   (MGI Ref ID J:50865)
      • continuous BrdU-labeling of day 10 mutant MEFs and subsequent replating at low density shows impaired proliferative capacity and premature senescence   (MGI Ref ID J:50865)
    • increased cellular sensitivity to gamma-irradiation
      • mutant MEFs show significantly increased sensitivity to ionizing radiation relative to wild-type MEFs   (MGI Ref ID J:50865)
      • in contrast, sensitivity to ultraviolet irradiation remains unaffected   (MGI Ref ID J:50865)
  • immune system phenotype
  • abnormal lymphopoiesis   (MGI Ref ID J:50865)
    • abnormal B cell differentiation
      • in culture, fetal liver cells from E15-E17.5 mutant embryos show a significant reduction in IgM+ B220+ B cells, indicating defective B-cell development   (MGI Ref ID J:50865)
      • nucleotide sequencing of potential rearrangements in DNA from mutant B-cell cultures revealed grossly abnormal DJ and V(D)J joins, with large deletions extending from one or both sides of the recombining segment   (MGI Ref ID J:50865)
      • arrested B cell differentiation
        • B cell development is arrested at the B220+ D43+ progenitor stage   (MGI Ref ID J:63078)
    • abnormal T cell differentiation
      • T lymphocyte development is arrested at the double negative (DN) stage   (MGI Ref ID J:63078)
      • arrested T cell differentiation
        • at E16.5-E17.5, mutant embryos exhibit an arrest of thymocyte development at the CD4-CD8-CD25+ stage, indicating a defect in productive rearrangement of T-cell antigen receptor beta genes   (MGI Ref ID J:50865)
  • decreased thymocyte number
    • total thymocyte cellularity is reduced ~100-fold compared to wild-type   (MGI Ref ID J:63078)
  • small thymus
    • at E15.0-E16.0, homozygotes exhibit a small thymus relative to wild-type embryos   (MGI Ref ID J:50865)
  • hematopoietic system phenotype
  • *normal* hematopoietic system phenotype
    • at E15.0-E16.0, homozygotes appear grossly normal with no apparent anemia   (MGI Ref ID J:50865)
    • abnormal lymphopoiesis   (MGI Ref ID J:50865)
      • abnormal B cell differentiation
        • in culture, fetal liver cells from E15-E17.5 mutant embryos show a significant reduction in IgM+ B220+ B cells, indicating defective B-cell development   (MGI Ref ID J:50865)
        • nucleotide sequencing of potential rearrangements in DNA from mutant B-cell cultures revealed grossly abnormal DJ and V(D)J joins, with large deletions extending from one or both sides of the recombining segment   (MGI Ref ID J:50865)
        • arrested B cell differentiation
          • B cell development is arrested at the B220+ D43+ progenitor stage   (MGI Ref ID J:63078)
      • abnormal T cell differentiation
        • T lymphocyte development is arrested at the double negative (DN) stage   (MGI Ref ID J:63078)
        • arrested T cell differentiation
          • at E16.5-E17.5, mutant embryos exhibit an arrest of thymocyte development at the CD4-CD8-CD25+ stage, indicating a defect in productive rearrangement of T-cell antigen receptor beta genes   (MGI Ref ID J:50865)
    • decreased thymocyte number
      • total thymocyte cellularity is reduced ~100-fold compared to wild-type   (MGI Ref ID J:63078)
    • small thymus
      • at E15.0-E16.0, homozygotes exhibit a small thymus relative to wild-type embryos   (MGI Ref ID J:50865)
  • endocrine/exocrine gland phenotype
  • decreased thymocyte number
    • total thymocyte cellularity is reduced ~100-fold compared to wild-type   (MGI Ref ID J:63078)
  • small thymus
    • at E15.0-E16.0, homozygotes exhibit a small thymus relative to wild-type embryos   (MGI Ref ID J:50865)

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

Lig4tm1Fwa/Lig4tm1Fwa

        involves: 129S6/SvEvTac
  • nervous system phenotype
  • abnormal brainstem morphology
    • large cavities   (MGI Ref ID J:110848)
  • abnormal diencephalon morphology
    • large cavities   (MGI Ref ID J:110848)
  • abnormal striatum morphology
    • large cavities   (MGI Ref ID J:110848)
  • thin cerebral cortex
    • at E12.5, mice exhibit increased apoptotic cells in the developing cerebral cortex, diencephalon, and spinal cord compared to in wild-type mice   (MGI Ref ID J:110848)
    • apoptosis in the cerebral cortex is more severe than in Xrcc6tm1Fwa   (MGI Ref ID J:110848)
  • cellular phenotype
  • abnormal cell physiology
    • mouse embryonic fibroblasts fail to produce RS joining in a transient V(D)J recombination end joining assay unlike wild-type cells   (MGI Ref ID J:110848)
    • chromosomal instability
      • mouse embryonic fibroblasts (MEFs) exhibit chromosome fragments with few gaps or breaks within single chromatids   (MGI Ref ID J:147247)
      • MEFs exhibit less chromosomal instability than in Mre11a deficient MEFs   (MGI Ref ID J:147247)
      • following exposure to gamma radiation, cre-exposed MEFs fail to exhibit a downward trend in frequency of chromosomal anomalies unlike similarly treated wild-type cells   (MGI Ref ID J:147247)
      • induced chromosome breakage
        • cre-treated mouse embryonic fibroblasts exhibit hypersensitivity to aphidicolin compared to similarly treated wild-type cells   (MGI Ref ID J:147247)
    • increased apoptosis
      • at E12.5, mice exhibit increased apoptotic cells in the developing cerebral cortex and diencephalon compared to in wild-type mice   (MGI Ref ID J:110848)
    • increased cellular sensitivity to ionizing radiation
View Research Applications

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

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency Associated with Other Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Lig4tm1Fwa
Allele Name targeted mutation 1, Frederick W Alt
Allele Type Targeted (Null/Knockout)
Common Name(s) Lig4-; LigIV-;
Strain of Origin129S6/SvEvTac
ES Cell Line NameTC1/TC-1
ES Cell Line Strain129S6/SvEvTac
Gene Symbol and Name Lig4, ligase IV, DNA, ATP-dependent
Chromosome 8
Gene Common Name(s) 5830471N16Rik; DNA ligase IV; LIG4S; RIKEN cDNA 5830471N16 gene; tiny;
Molecular Note A neomycin resistance cassette replaced more than 50% of the coding sequences for the gene, removing the nucleotide sequences that encode amino acids 143 - 608 of the protein. [MGI Ref ID J:50865]

Genotyping

Genotyping Information

Genotyping Protocols

Lig4tm1Fwa, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Frank KM; Sekiguchi JM; Seidl KJ; Swat W; Rathbun GA; Cheng HL; Davidson L; Kangaloo L; Alt FW. 1998. Late embryonic lethality and impaired V(D)J recombination in mice lacking DNA ligase IV. Nature 396(6707):173-7. [PubMed: 9823897]  [MGI Ref ID J:50865]

Additional References

Lig4tm1Fwa related

Boboila C; Jankovic M; Yan CT; Wang JH; Wesemann DR; Zhang T; Fazeli A; Feldman L; Nussenzweig A; Nussenzweig M; Alt FW. 2010. Alternative end-joining catalyzes robust IgH locus deletions and translocations in the combined absence of ligase 4 and Ku70. Proc Natl Acad Sci U S A 107(7):3034-9. [PubMed: 20133803]  [MGI Ref ID J:157537]

Boboila C; Oksenych V; Gostissa M; Wang JH; Zha S; Zhang Y; Chai H; Lee CS; Jankovic M; Saez LM; Nussenzweig MC; McKinnon PJ; Alt FW; Schwer B. 2012. Robust chromosomal DNA repair via alternative end-joining in the absence of X-ray repair cross-complementing protein 1 (XRCC1). Proc Natl Acad Sci U S A 109(7):2473-8. [PubMed: 22308491]  [MGI Ref ID J:182020]

Boboila C; Yan C; Wesemann DR; Jankovic M; Wang JH; Manis J; Nussenzweig A; Nussenzweig M; Alt FW. 2010. Alternative end-joining catalyzes class switch recombination in the absence of both Ku70 and DNA ligase 4. J Exp Med 207(2):417-27. [PubMed: 20142431]  [MGI Ref ID J:158825]

Buis J; Wu Y; Deng Y; Leddon J; Westfield G; Eckersdorff M; Sekiguchi JM; Chang S; Ferguson DO. 2008. Mre11 nuclease activity has essential roles in DNA repair and genomic stability distinct from ATM activation. Cell 135(1):85-96. [PubMed: 18854157]  [MGI Ref ID J:147247]

Celli GB; de Lange T. 2005. DNA processing is not required for ATM-mediated telomere damage response after TRF2 deletion. Nat Cell Biol 7(7):712-8. [PubMed: 15968270]  [MGI Ref ID J:105516]

Dimitrova N; Chen YC; Spector DL; de Lange T. 2008. 53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobility. Nature 456(7221):524-8. [PubMed: 18931659]  [MGI Ref ID J:143563]

Ferguson DO; Sekiguchi JM; Chang S; Frank KM; Gao Y; DePinho RA; Alt FW. 2000. The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations. Proc Natl Acad Sci U S A 97(12):6630-3. [PubMed: 10823907]  [MGI Ref ID J:62721]

Foster SS; De S; Johnson LK; Petrini JH; Stracker TH. 2012. Cell cycle- and DNA repair pathway-specific effects of apoptosis on tumor suppression. Proc Natl Acad Sci U S A 109(25):9953-8. [PubMed: 22670056]  [MGI Ref ID J:185501]

Frank KM; Sharpless NE; Gao Y; Sekiguchi JM; Ferguson DO; Zhu C; Manis JP; Horner J; DePinho RA; Alt FW. 2000. DNA ligase IV deficiency in mice leads to defective neurogenesis and embryonic lethality via the p53 pathway. Mol Cell 5(6):993-1002. [PubMed: 10911993]  [MGI Ref ID J:63078]

Gostissa M; Yan CT; Bianco JM; Cogne M; Pinaud E; Alt FW. 2009. Long-range oncogenic activation of Igh-c-myc translocations by the Igh 3' regulatory region. Nature 462(7274):803-7. [PubMed: 20010689]  [MGI Ref ID J:155801]

Green MR; Monti S; Dalla-Favera R; Pasqualucci L; Walsh NC; Schmidt-Supprian M; Kutok JL; Rodig SJ; Neuberg DS; Rajewsky K; Golub TR; Alt FW; Shipp MA; Manis JP. 2011. Signatures of murine B-cell development implicate Yy1 as a regulator of the germinal center-specific program. Proc Natl Acad Sci U S A 108(7):2873-8. [PubMed: 21282644]  [MGI Ref ID J:169063]

Gu Y; Sekiguchi J; Gao Y; Dikkes P; Frank K; Ferguson D; Hasty P; Chun J; Alt FW. 2000. Defective embryonic neurogenesis in Ku-deficient but not DNA-dependent protein kinase catalytic subunit-deficient mice. Proc Natl Acad Sci U S A 97(6):2668-73. [PubMed: 10716994]  [MGI Ref ID J:110848]

Gurley KE; Moser R; Gu Y; Hasty P; Kemp CJ. 2009. DNA-PK suppresses a p53-independent apoptotic response to DNA damage. EMBO Rep 10(1):87-93. [PubMed: 19057578]  [MGI Ref ID J:157375]

Karanjawala ZE; Adachi N; Irvine RA; Oh EK; Shibata D; Schwarz K; Hsieh CL; Lieber MR. 2002. The embryonic lethality in DNA ligase IV-deficient mice is rescued by deletion of Ku: implications for unifying the heterogeneous phenotypes of NHEJ mutants. DNA Repair (Amst) 1(12):1017-26. [PubMed: 12531011]  [MGI Ref ID J:80467]

Karanjawala ZE; Grawunder U; Hsieh CL; Lieber MR. 1999. The nonhomologous DNA end joining pathway is important for chromosome stability in primary fibroblasts. Curr Biol 9(24):1501-4. [PubMed: 10607596]  [MGI Ref ID J:76627]

Konishi A; de Lange T. 2008. Cell cycle control of telomere protection and NHEJ revealed by a ts mutation in the DNA-binding domain of TRF2. Genes Dev 22(9):1221-30. [PubMed: 18451109]  [MGI Ref ID J:134654]

Lottersberger F; Bothmer A; Robbiani DF; Nussenzweig MC; de Lange T. 2013. Role of 53BP1 oligomerization in regulating double-strand break repair. Proc Natl Acad Sci U S A 110(6):2146-51. [PubMed: 23345425]  [MGI Ref ID J:194338]

Maser RS; Wong KK; Sahin E; Xia H; Naylor M; Hedberg HM; Artandi SE; DePinho RA. 2007. DNA-dependent protein kinase catalytic subunit is not required for dysfunctional telomere fusion and checkpoint response in the telomerase-deficient mouse. Mol Cell Biol 27(6):2253-65. [PubMed: 17145779]  [MGI Ref ID J:118902]

Mills KD; Ferguson DO; Essers J; Eckersdorff M; Kanaar R; Alt FW. 2004. Rad54 and DNA Ligase IV cooperate to maintain mammalian chromatid stability. Genes Dev 18(11):1283-92. [PubMed: 15175260]  [MGI Ref ID J:90442]

Peuscher MH; Jacobs JJ. 2011. DNA-damage response and repair activities at uncapped telomeres depend on RNF8. Nat Cell Biol 13(9):1139-45. [PubMed: 21857671]  [MGI Ref ID J:176962]

Rommel PC; Bosque D; Gitlin AD; Croft GF; Heintz N; Casellas R; Nussenzweig MC; Kriaucionis S; Robbiani DF. 2013. Fate mapping for activation-induced cytidine deaminase (AID) marks non-lymphoid cells during mouse development. PLoS One 8(7):e69208. [PubMed: 23861962]  [MGI Ref ID J:204283]

Rucci F; Notarangelo LD; Fazeli A; Patrizi L; Hickernell T; Paganini T; Coakley KM; Detre C; Keszei M; Walter JE; Feldman L; Cheng HL; Poliani PL; Wang JH; Balter BB; Recher M; Andersson EM; Zha S; Giliani S; Terhorst C; Alt FW; Yan CT. 2010. Homozygous DNA ligase IV R278H mutation in mice leads to leaky SCID and represents a model for human LIG4 syndrome. Proc Natl Acad Sci U S A 107(7):3024-9. [PubMed: 20133615]  [MGI Ref ID J:157574]

Sekiguchi J; Ferguson DO; Chen HT; Yang EM; Earle J; Frank K; Whitlow S; Gu Y; Xu Y; Nussenzweig A; Alt FW. 2001. Genetic interactions between ATM and the nonhomologous end-joining factors in genomic stability and development. Proc Natl Acad Sci U S A 98(6):3243-8. [PubMed: 11248063]  [MGI Ref ID J:68074]

Sfeir A; Kosiyatrakul ST; Hockemeyer D; MacRae SL; Karlseder J; Schildkraut CL; de Lange T. 2009. Mammalian telomeres resemble fragile sites and require TRF1 for efficient replication. Cell 138(1):90-103. [PubMed: 19596237]  [MGI Ref ID J:157331]

Sfeir A; de Lange T. 2012. Removal of shelterin reveals the telomere end-protection problem. Science 336(6081):593-7. [PubMed: 22556254]  [MGI Ref ID J:184522]

Sharpless NE; Ferguson DO; O'Hagan RC; Castrillon DH; Lee C; Farazi PA; Alson S; Fleming J; Morton CC; Frank K; Chin L; Alt FW; DePinho RA. 2001. Impaired nonhomologous end-joining provokes soft tissue sarcomas harboring chromosomal translocations, amplifications, and deletions. Mol Cell 8(6):1187-96. [PubMed: 11779495]  [MGI Ref ID J:88792]

Tavana O; Puebla-Osorio N; Sang M; Zhu C. 2010. Absence of p53-dependent apoptosis combined with nonhomologous end-joining deficiency leads to a severe diabetic phenotype in mice. Diabetes 59(1):135-42. [PubMed: 19833883]  [MGI Ref ID J:164166]

Van Nguyen T; Puebla-Osorio N; Pang H; Dujka ME; Zhu C. 2007. DNA damage-induced cellular senescence is sufficient to suppress tumorigenesis: a mouse model. J Exp Med 204(6):1453-61. [PubMed: 17535972]  [MGI Ref ID J:123936]

Yan CT; Boboila C; Souza EK; Franco S; Hickernell TR; Murphy M; Gumaste S; Geyer M; Zarrin AA; Manis JP; Rajewsky K; Alt FW. 2007. IgH class switching and translocations use a robust non-classical end-joining pathway. Nature 449(7161):478-82. [PubMed: 17713479]  [MGI Ref ID J:126758]

Zhu C; Mills KD; Ferguson DO; Lee C; Manis J; Fleming J; Gao Y; Morton CC; Alt FW. 2002. Unrepaired DNA Breaks in p53-Deficient Cells Lead to Oncogenic Gene Amplification Subsequent to Translocations. Cell 109(7):811-21. [PubMed: 12110179]  [MGI Ref ID J:77972]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are bred as heterozygotes. Homozygotes are embryonic lethal.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2140.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2782.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

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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.


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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.
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