Strain Name:

B6.129-Xrcc5tm1Nus/J

Stock Number:

004361

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Availability:

Cryopreserved - Ready for recovery

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 Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
 
Donating Investigator Andre Nussenzweig,   CCR, NCI, National Institutes of Health

Description
Mice that are homozygous for the targeted mutation are viable, fertile, but are 40-60% the size of normal mice. No Xrcc5 protein product is detected. The growth deficiency phenotype is exhibited as early as E15.5. Organ weights, excepting lymphoid organs, are proportional to total body weight. Histological analysis shows decreased size of spleen, lymph nodes and thymus. T cell and B cell development is arrested at early precursor stages and a deficiency in V(D)J rearrangement is exhibited. B cell maturation stops at the B220+CD43+ stage. Only CD4-CD8- cells are found in the thymus. Primary embryonic fibroblasts (MEFs) have slower growth and early loss of proliferating cells. Early appearance of non-dividing cells in MEF cultures suggest early onset senescence. Karyotypes reveal increased chromosomal aberrations. Breaks or translocations occur in 83% of metaphases, polyploidy in 15%. Although cells from the mutant mice display chromosomal instability, these mice do not display early tumorgenesis. Litters must be fostered because homozygous mutant female mice are unable to sustain newborn pups. Survival of homozygous mutant mice is 80% when the larger heterozygous mutant and wildtype littermates are removed. This mutant mouse strain represents a model that may be useful in studies related to DNA repair and aging.

Development
A targeting vector containing a neomycin resistance gene driven by the phosphoglycerate kinase promoter was used to disrupt 3.4 kb of the targeted gene, including 100 bp of the promoter and first 2 exons. The construct was electroporated into 129 derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were backcrossed to C57BL/6 mice.

Phenotype

Phenotype Information

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.

Xrcc5tm1Nus/Xrcc5tm1Nus

        involves: 129S1/Sv * 129X1/SvJ
  • mortality/aging
  • partial postnatal lethality
    • 50% of homozygotes fail to thrive and die within 3 days of birth; survival improves to 80% when the larger wild-type and heterozygous littermates are removed   (MGI Ref ID J:81484)
  • growth/size/body phenotype
  • decreased body size
    • homozygotes are smaller than wild-type or heterozygous littermates   (MGI Ref ID J:81484)
    • proportional dwarf
      • newborns are 40-60% smaller than wild-type and heterozygous littermates and during 6-month observation grew but maintained a body weight of 40-60% that of controls; Xrcc5-null mice are proportional dwarfs   (MGI Ref ID J:81484)
  • fetal growth retardation
    • growth retardation is noted first at E15.5 and size difference is significant at E17.5, increasing to ~40% at birth   (MGI Ref ID J:81484)
  • cellular phenotype
  • abnormal double-strand DNA break repair
    • cells from null mice show a reduced ability to rejoin DNA double-strand breaks than wild-type   (MGI Ref ID J:108657)
  • increased cellular sensitivity to ionizing radiation
    • after exposure to ionizing radiation, bone marrow cells display less colony formation compared to wild-type   (MGI Ref ID J:108657)
  • immune system phenotype
  • abnormal class switch recombination
    • class switching recombination (CSR)-induced Smu internal deletion is impaired   (MGI Ref ID J:120658)
  • abnormal humoral immune response
    • B cell proliferation and apoptosis following LSP or Il-4 treatment was severely impaired even in cells that had undergone several rounds of cell division   (MGI Ref ID J:120658)
  • spleen hypoplasia
    • spleen contains over 50-fold less cells than wild-type   (MGI Ref ID J:108657)
  • thymus hypoplasia
    • thymus has over 100-fold less cells than wild-type   (MGI Ref ID J:108657)
  • behavior/neurological phenotype
  • abnormal maternal nurturing
    • Xrcc-deficient females are unable to sustain their pups which die in a few days unless nursed by a foster mother   (MGI Ref ID J:81484)
  • hematopoietic system phenotype
  • abnormal bone marrow cell morphology/development
    • bone marrow reduced lymphoid cellularity compared to wild-type   (MGI Ref ID J:108657)
  • abnormal class switch recombination
    • class switching recombination (CSR)-induced Smu internal deletion is impaired   (MGI Ref ID J:120658)
  • spleen hypoplasia
    • spleen contains over 50-fold less cells than wild-type   (MGI Ref ID J:108657)
  • thymus hypoplasia
    • thymus has over 100-fold less cells than wild-type   (MGI Ref ID J:108657)
  • reproductive system phenotype
  • decreased litter size   (MGI Ref ID J:81484)
  • homeostasis/metabolism phenotype
  • abnormal double-strand DNA break repair
    • cells from null mice show a reduced ability to rejoin DNA double-strand breaks than wild-type   (MGI Ref ID J:108657)
View Research Applications

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

Xrcc5tm1Nus related

Developmental Biology Research
Growth Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Xrcc5tm1Nus
Allele Name targeted mutation 1, Andre Nussenzweig
Allele Type Targeted (knock-out)
Common Name(s) Ku80-; Ku86-; Xrcc5tm1Gcl;
Mutation Made By Andre Nussenzweig,   CCR, NCI, National Institutes of Health
Strain of Origin(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
ES Cell Line NameR1
ES Cell Line Strain(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name Xrcc5, X-ray repair complementing defective repair in Chinese hamster cells 5
Chromosome 1
Gene Common Name(s) AI314015; KARP-1; KARP1; KU80; KUB2; Ku86; Kup80; NFIV; expressed sequence AI314015;
Molecular Note A neomycin resistance cassette replaced 3.4 kb of the gene, including 100 bp of the promoter region. [MGI Ref ID J:72368]

Genotyping

Genotyping Information

Genotyping Protocols

Xrcc5tm1Nus, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Nussenzweig A; Chen C; da Costa Soares V; Sanchez M; Sokol K; Nussenzweig MC; Li GC. 1996. Requirement for Ku80 in growth and immunoglobulin V(D)J recombination. Nature 382(6591):551-5. [PubMed: 8700231]  [MGI Ref ID J:72368]

Additional References

Difilippantonio MJ; Petersen S; Chen HT; Johnson R; Jasin M; Kanaar R; Ried T; Nussenzweig A. 2002. Evidence for replicative repair of DNA double-strand breaks leading to oncogenic translocation and gene amplification. J Exp Med 196(4):469-80. [PubMed: 12186839]  [MGI Ref ID J:78496]

Difilippantonio MJ; Zhu J; Chen HT; Meffre E; Nussenzweig MC; Max EE; Ried T; Nussenzweig A. 2000. DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation. Nature 404(6777):510-4. [PubMed: 10761921]  [MGI Ref ID J:72312]

Xrcc5tm1Nus 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; 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]

Brugmans L; Kanaar R; Essers J. 2007. Analysis of DNA double-strand break repair pathways in mice. Mutat Res 614(1-2):95-108. [PubMed: 16797606]  [MGI Ref ID J:118077]

Bunting SF; Callen E; Kozak ML; Kim JM; Wong N; Lopez-Contreras AJ; Ludwig T; Baer R; Faryabi RB; Malhowski A; Chen HT; Fernandez-Capetillo O; D'Andrea A; Nussenzweig A. 2012. BRCA1 Functions Independently of Homologous Recombination in DNA Interstrand Crosslink Repair. Mol Cell 46(2):125-35. [PubMed: 22445484]  [MGI Ref ID J:183455]

Casellas R; Nussenzweig A; Wuerffel R; Pelanda R; Reichlin A; Suh H; Qin XF; Besmer E; Kenter A; Rajewsky K; Nussenzweig MC. 1998. Ku80 is required for immunoglobulin isotype switching. EMBO J 17(8):2404-11. [PubMed: 9545251]  [MGI Ref ID J:127088]

Couedel C; Mills KD; Marco B; Shen L; Olshen A; Johnson RD; Nussenzweig A; Essers J; Kanaar R; Li GC; Alt FW; Jasin M. 2004. Collaboration of homologous recombination and nonhomologous end-joining factors for the survival and integrity of mice and cells. Genes Dev 18(11):1293-304. [PubMed: 15175261]  [MGI Ref ID J:90441]

Difilippantonio MJ; Zhu J; Chen HT; Meffre E; Nussenzweig MC; Max EE; Ried T; Nussenzweig A. 2000. DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation. Nature 404(6777):510-4. [PubMed: 10761921]  [MGI Ref ID J:72312]

Dmitrieva NI; Celeste A; Nussenzweig A; Burg MB. 2005. Ku86 preserves chromatin integrity in cells adapted to high NaCl. Proc Natl Acad Sci U S A 102(30):10730-5. [PubMed: 16027367]  [MGI Ref ID J:100182]

Henrie MS; Kurimasa A; Burma S; Menissier-de Murcia J; de Murcia G; Li GC; Chen DJ. 2003. Lethality in PARP-1/Ku80 double mutant mice reveals physiological synergy during early embryogenesis. DNA Repair (Amst) 2(2):151-8. [PubMed: 12531386]  [MGI Ref ID J:81484]

Hurd YL; Yakovleva T; Nussenzweig A; Li GC; Terenius L; Bakalkin G. 1999. A novel neuron-specific DNA end-binding factor in the murine brain. Mol Cell Neurosci 14(3):213-24. [PubMed: 10576891]  [MGI Ref ID J:57758]

Ishii KJ; Takeshita F; Gursel I; Gursel M; Conover J; Nussenzweig A; Klinman DM. 2002. Potential role of phosphatidylinositol 3 kinase, rather than DNA-dependent protein kinase, in CpG DNA-induced immune activation. J Exp Med 196(2):269-74. [PubMed: 12119352]  [MGI Ref ID J:120697]

Liebe B; Petukhova G; Barchi M; Bellani M; Braselmann H; Nakano T; Pandita TK; Jasin M; Fornace A; Meistrich ML; Baarends WM; Schimenti J; de Lange T; Keeney S; Camerini-Otero RD; Scherthan H. 2006. Mutations that affect meiosis in male mice influence the dynamics of the mid-preleptotene and bouquet stages. Exp Cell Res 312(19):3768-81. [PubMed: 17010969]  [MGI Ref ID J:147391]

McConnell MJ; Kaushal D; Yang AH; Kingsbury MA; Rehen SK; Treuner K; Helton R; Annas EG; Chun J; Barlow C. 2004. Failed clearance of aneuploid embryonic neural progenitor cells leads to excess aneuploidy in the Atm-deficient but not the Trp53-deficient adult cerebral cortex. J Neurosci 24(37):8090-6. [PubMed: 15371510]  [MGI Ref ID J:109775]

Nussenzweig A; Sokol K; Burgman P; Li L; Li GC. 1997. Hypersensitivity of Ku80-deficient cell lines and mice to DNA damage: the effects of ionizing radiation on growth, survival, and development. Proc Natl Acad Sci U S A 94(25):13588-93. [PubMed: 9391070]  [MGI Ref ID J:78648]

Ouyang H; Nussenzweig A; Kurimasa A; Soares VC; Li X; Cordon-Cardo C; Li W; Cheong N; Nussenzweig M; Iliakis G; Chen DJ; Li GC. 1997. Ku70 is required for DNA repair but not for T cell antigen receptor gene recombination In vivo. J Exp Med 186(6):921-9. [PubMed: 9294146]  [MGI Ref ID J:108657]

Ramiro AR; Jankovic M; Callen E; Difilippantonio S; Chen HT; McBride KM; Eisenreich TR; Chen J; Dickins RA; Lowe SW; Nussenzweig A; Nussenzweig MC. 2006. Role of genomic instability and p53 in AID-induced c-myc-Igh translocations. Nature 440(7080):105-9. [PubMed: 16400328]  [MGI Ref ID J:106450]

Reina-San-Martin B; Chen HT; Nussenzweig A; Nussenzweig MC. 2004. ATM is required for efficient recombination between immunoglobulin switch regions. J Exp Med 200(9):1103-10. [PubMed: 15520243]  [MGI Ref ID J:94913]

Reina-San-Martin B; Difilippantonio S; Hanitsch L; Masilamani RF; Nussenzweig A; Nussenzweig MC. 2003. H2AX is required for recombination between immunoglobulin switch regions but not for intra-switch region recombination or somatic hypermutation. J Exp Med 197(12):1767-78. [PubMed: 12810694]  [MGI Ref ID J:120658]

Reliene R; Bishop AJ; Li G; Schiestl RH. 2004. Ku86 deficiency leads to reduced intrachromosomal homologous recombination in vivo in mice. DNA Repair (Amst) 3(2):103-11. [PubMed: 14706343]  [MGI Ref ID J:87471]

Reliene R; Goad ME; Schiestl RH. 2006. Developmental cell death in the liver and newborn lethality of Ku86 deficient mice suppressed by antioxidant N-acetyl-cysteine. DNA Repair (Amst) 5(11):1392-7. [PubMed: 16916625]  [MGI Ref ID J:115982]

Rockwood LD; Nussenzweig A; Janz S. 2003. Paradoxical decrease in mutant frequencies and chromosomal rearrangements in a transgenic lacZ reporter gene in Ku80 null mice deficient in DNA double strand break repair. Mutat Res 529(1-2):51-8. [PubMed: 12943919]  [MGI Ref ID J:126991]

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]

Seminotti B; da Rosa MS; Fernandes CG; Amaral AU; Braga LM; Leipnitz G; de Souza DO; Woontner M; Koeller DM; Goodman S; Wajner M. 2012. Induction of oxidative stress in brain of glutaryl-CoA dehydrogenase deficient mice by acute lysine administration. Mol Genet Metab 106(1):31-8. [PubMed: 22445450]  [MGI Ref ID J:183456]

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]

Touvrey C; Couedel C; Soulas P; Couderc R; Jasin M; de Villartay JP; Marche PN; Jouvin-Marche E; Candeias SM. 2008. Distinct effects of DNA-PKcs and Artemis inactivation on signal joint formation in vivo. Mol Immunol 45(12):3383-91. [PubMed: 18501428]  [MGI Ref ID J:137712]

Zhao B; Benson EK; Qiao R; Wang X; Kim S; Manfredi JJ; Lee SW; Aaronson SA. 2009. Cellular senescence and organismal ageing in the absence of p21(CIP1/WAF1) in ku80(-/-) mice. EMBO Rep 10(1):71-8. [PubMed: 19079133]  [MGI Ref ID J:143043]

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 & HusbandryThis strain originated on a B6;129 background, has been backcrossed for 9 generations on the C57BL/6 background and is maintained as a heterozygote.

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* $2085.00
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 11 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* $2710.50
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 11 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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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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