Strain Name:

B6;129-Fzd4tm1Nat/J

Stock Number:

012823

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Homozygous Fzd4 (frizzled homolog 4 (Drosophila)) mice have a congenital retinal hypovascularization, a progressive inner ear vascular atrophy, a defect in the blood brain barrier in the cerebellum, and a progressive cerebellar degeneration associated with severe ataxia. Mice also show an absence of a skeletal muscle sheath around the lower esophagus associated with progressive esophageal distension.

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
GenerationF24pN1
Generation Definitions
 
Donating Investigator Jeremy Nathans,   Johns Hopkins University

Description
Homozygous Fzd4 (frizzled homolog 4 (Drosophila)) mice have a congenital retinal hypovascularization, a progressive inner ear vascular atrophy, a defect in the blood brain barrier in the cerebellum, and a progressive cerebellar degeneration associated with severe ataxia. Mice also show an absence of a skeletal muscle sheath around the lower esophagus associated with progressive esophageal distension.

Development
The coding region for beta-galactosidase (LacZ) and a PGK-neomycin selectable marker were used to replace the coding region of the targeted gene. The mutation was created in (129X1/SvJ x 129S1/Sv)F1- Kitl+-derived R1 embryonic stem (ES) cells. This strain was maintained on a mixed C57BL/6 and 129 background by the donating laboratory.

Related Strains

Strains carrying other alleles of Fzd4
011078   B6;129-Fzd4tm2.1Nat/J
View Strains carrying other alleles of Fzd4     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- 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).
Exudative Vitreoretinopathy 1; EVR1
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Norrie Disease; ND
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Fzd4tm1Nat/Fzd4tm1Nat

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6
  • mortality/aging
  • premature death
    • 50% die within the first 4-5 months of life   (MGI Ref ID J:70078)
  • growth/size/body phenotype
  • weight loss
    • weight is normal during the first week after birth   (MGI Ref ID J:70078)
    • weight gain is slower from the second week on   (MGI Ref ID J:70078)
  • behavior/neurological phenotype
  • abnormal gait
    • minimal alternation between right and left side   (MGI Ref ID J:70078)
    • frequently fail to fully lift each foot between steps   (MGI Ref ID J:70078)
    • short stride length
      • in older animals   (MGI Ref ID J:70078)
  • abnormal posture
    • widened stance   (MGI Ref ID J:70078)
    • hunched posture   (MGI Ref ID J:70078)
  • absent startle reflex
    • eventually absent   (MGI Ref ID J:70078)
  • ataxia
    • cerebellar ataxia possibly causing the observed abnormal gait   (MGI Ref ID J:70078)
  • decreased startle reflex
    • normal at 1-2 months of age but diminishing thereafter and eventually disappears   (MGI Ref ID J:70078)
  • hearing/vestibular/ear phenotype
  • abnormal organ of Corti morphology   (MGI Ref ID J:107732)
    • cochlear hair cell degeneration
      • eventually the near complete loss of hair cells, first the outer hair cells and then the inner hair cells   (MGI Ref ID J:107732)
      • cochlear inner hair cell degeneration   (MGI Ref ID J:107732)
      • cochlear outer hair cell degeneration   (MGI Ref ID J:107732)
  • abnormal stria vascularis morphology   (MGI Ref ID J:107732)
    • abnormal stria vascularis vasculature morphology
      • enlarged blood vessels in the stria vascularis   (MGI Ref ID J:107732)
      • no identifiable blood vessels at 11 months of age   (MGI Ref ID J:107732)
    • stria vascularis degeneration
      • almost completely degenerated by 11 months of age   (MGI Ref ID J:107732)
  • impaired hearing
    • hearing loss does not require loss of primary sensory cells, either the outer or inner hair cells   (MGI Ref ID J:70078)
  • increased or absent threshold for auditory brainstem response
    • elevated auditory thresholds are observed; in one case, the auditory brainstem response threshold is at least 40 dB higher than the average control value of ~60 dB   (MGI Ref ID J:70078)
  • nervous system phenotype
  • abnormal astrocyte physiology
    • abnormal astroglial activation in adults   (MGI Ref ID J:70078)
  • abnormal cerebellum morphology
    • vasculature of the cerebellum is noticeably sparser than controls at 30 days of age and very sparse and irregular at 6 months   (MGI Ref ID J:107732)
    • progressive cerebellar degeneration starting around 3rd postnatal week   (MGI Ref ID J:107732)
    • abnormal cerebellar granule layer morphology
      • dramatic loss of granule cells and vacuolization   (MGI Ref ID J:70078)
      • massive apoptosis of granule cells starting between 14 and 19 days of age   (MGI Ref ID J:70078)
      • 50X more apoptosis in the cerebellum at 19 days of age   (MGI Ref ID J:70078)
      • apoptosis drops off greatly at 30 days of age   (MGI Ref ID J:70078)
    • cerebellum hypoplasia
      • hypocellular cerebellum but cerebellar architecture normal   (MGI Ref ID J:70078)
    • decreased Purkinje cell number
      • dramatic loss of Purkinje cells and vacuolization   (MGI Ref ID J:70078)
      • apoptosis not observed in Purkinje cells but cells are lost progressively through adulthood   (MGI Ref ID J:70078)
  • cochlear hair cell degeneration
    • eventually the near complete loss of hair cells, first the outer hair cells and then the inner hair cells   (MGI Ref ID J:107732)
    • cochlear inner hair cell degeneration   (MGI Ref ID J:107732)
    • cochlear outer hair cell degeneration   (MGI Ref ID J:107732)
  • cardiovascular system phenotype
  • abnormal retinal vasculature morphology
    • the two intraretinal capillary beds fail to develop   (MGI Ref ID J:107732)
    • major arteries and veins on the retina are enlarged and tortuous   (MGI Ref ID J:107732)
    • arteriolar arborization is diminished   (MGI Ref ID J:107732)
    • increased density of small vessels in nerve fiber layer   (MGI Ref ID J:107732)
    • many retinal blood vessels are fenestrated   (MGI Ref ID J:107732)
  • abnormal stria vascularis vasculature morphology
    • enlarged blood vessels in the stria vascularis   (MGI Ref ID J:107732)
    • no identifiable blood vessels at 11 months of age   (MGI Ref ID J:107732)
  • abnormal vascular development
    • female homozygotes display disrupted vascular development of the corpora luteum   (MGI Ref ID J:115734)
    • markers of vascular cell function are reduced in ovaries of mutant female mice following natural mating   (MGI Ref ID J:115734)
  • hemorrhage
    • small hemorrhages frequent in cerebellum   (MGI Ref ID J:107732)
    • retinal hemorrhage
      • small hemorrhages frequent in retina   (MGI Ref ID J:107732)
  • vision/eye phenotype
  • abnormal retinal vasculature morphology
    • the two intraretinal capillary beds fail to develop   (MGI Ref ID J:107732)
    • major arteries and veins on the retina are enlarged and tortuous   (MGI Ref ID J:107732)
    • arteriolar arborization is diminished   (MGI Ref ID J:107732)
    • increased density of small vessels in nerve fiber layer   (MGI Ref ID J:107732)
    • many retinal blood vessels are fenestrated   (MGI Ref ID J:107732)
  • persistence of hyaloid vascular system
    • hyaloid blood vessels fail to regress or regression is delayed 1-2 weeks   (MGI Ref ID J:107732)
  • retinal hemorrhage
    • small hemorrhages frequent in retina   (MGI Ref ID J:107732)
  • digestive/alimentary phenotype
  • abnormal digestion
    • defective esophageal peristalsis   (MGI Ref ID J:70078)
    • defective function of the gastric sphincter   (MGI Ref ID J:70078)
  • abnormal esophagus morphology
    • loss of skeletal muscle on lower 1/4 of esophagous to as much as the entire esophagus   (MGI Ref ID J:70078)
    • no motor end plates along the lower portion of the esophagus   (MGI Ref ID J:70078)
    • abnormal esophageal squamous epithelium morphology
      • desquamination of the esophageal epithelium   (MGI Ref ID J:70078)
    • enlarged esophagus
      • progressive enlargement of the esophagus apparent at 8 days of age but not at birth   (MGI Ref ID J:70078)
  • muscle phenotype
  • decreased skeletal muscle fiber diameter
    • muscle fibers with smaller diameter but otherwise normal   (MGI Ref ID J:70078)
  • pigmentation phenotype
  • diluted coat color
    • light black or silver coat color   (MGI Ref ID J:70078)
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • adult female homozygotes exhibit normal mating behavior relative to wild-type and heterozygous littermates   (MGI Ref ID J:115734)
    • following superovulation, female homozygotes produce an equal number of fertilized oocytes as their wild-type and heterozygous littermates   (MGI Ref ID J:115734)
    • immature mutant ovaries show normal follicular development and normal responses to gonadotropin stimulation during development to the preovulatory stage   (MGI Ref ID J:115734)
    • abnormal corpus luteum morphology
      • at 8 weeks of age, corpora lutea are variably present or absent in ovaries of some female mutant mice   (MGI Ref ID J:115734)
      • analysis of mutant ovaries from timed mating pairs shows that by day 7.5 pc, corpora lutea are not discernible, indicating that formation of functional corpora lutea is impaired   (MGI Ref ID J:115734)
      • on day 1.5 pc, mutant corpora lutea exhibit a thick, dense collagen IV network that is significantly less filamentous and punctate than that observed in wild-type corpora lutea, suggesting that vessel arborization is reduced during luteinization   (MGI Ref ID J:115734)
      • on day 1.5 pc, mutant corpora lutea exhibit clear signs of apoptosis, as indicated by the presence of activated caspase 3   (MGI Ref ID J:115734)
      • absent corpus luteum
        • after natural mating, some female homozygotes exhibit absence of corpora lutea   (MGI Ref ID J:115734)
      • impaired luteal cell differentiation
        • whereas luteal cells in day 5.5 pregnant wild-type ovaries display cellular hypertrophy, luteal cells in day 5.5 non-pregnant mutant ovaries appear disorganized and display a lower cytoplasmic to nuclear ratio   (MGI Ref ID J:115734)
        • in mutant ovaries, expression of luteal cell-specific mRNAs is reduced as early as day 1.5 pc and remains low on day 5.5 pc   (MGI Ref ID J:115734)
    • failure of embryo implantation
      • analysis of ovaries from timed mating pairs indicates that female homozygotes exhibit no implantation sites on days 5.5 and 7.5 pc   (MGI Ref ID J:115734)
    • female infertility
      • when mated to wild-type males, female homozygotes fail to become pregnant and produce offspring   (MGI Ref ID J:115734)
    • impaired luteinization
      • mutant ovaries collected at days 1.5, 5.5, and 7.5 pc display an altered histological appearance, reduced expression luteal cell-specific mRNAs, and distinct structural abnormalities within the vascular network, indicative of impaired luteal cell function   (MGI Ref ID J:115734)
    • male infertility
      • preliminary observations suggest that male homozygotes appear to be infertile   (MGI Ref ID J:115734)
  • homeostasis/metabolism phenotype
  • decreased circulating progesterone level
    • on day 1.5 post-coitum (pc), serum progesterone levels are reduced by 50% in female mutant mice relative to wild-type females, and decrease dramatically on days 5.5 and 7.5 pc with no evidence of implantation   (MGI Ref ID J:115734)
    • in contrast, no significant differences are observed in serum prolactin levels between female mutant and wild-type mice on day 5.5 pc   (MGI Ref ID J:115734)
  • endocrine/exocrine gland phenotype
  • abnormal corpus luteum morphology
    • at 8 weeks of age, corpora lutea are variably present or absent in ovaries of some female mutant mice   (MGI Ref ID J:115734)
    • analysis of mutant ovaries from timed mating pairs shows that by day 7.5 pc, corpora lutea are not discernible, indicating that formation of functional corpora lutea is impaired   (MGI Ref ID J:115734)
    • on day 1.5 pc, mutant corpora lutea exhibit a thick, dense collagen IV network that is significantly less filamentous and punctate than that observed in wild-type corpora lutea, suggesting that vessel arborization is reduced during luteinization   (MGI Ref ID J:115734)
    • on day 1.5 pc, mutant corpora lutea exhibit clear signs of apoptosis, as indicated by the presence of activated caspase 3   (MGI Ref ID J:115734)
    • absent corpus luteum
      • after natural mating, some female homozygotes exhibit absence of corpora lutea   (MGI Ref ID J:115734)
    • impaired luteal cell differentiation
      • whereas luteal cells in day 5.5 pregnant wild-type ovaries display cellular hypertrophy, luteal cells in day 5.5 non-pregnant mutant ovaries appear disorganized and display a lower cytoplasmic to nuclear ratio   (MGI Ref ID J:115734)
      • in mutant ovaries, expression of luteal cell-specific mRNAs is reduced as early as day 1.5 pc and remains low on day 5.5 pc   (MGI Ref ID J:115734)
  • integument phenotype
  • diluted coat color
    • light black or silver coat color   (MGI Ref ID J:70078)
  • cellular phenotype
  • impaired luteal cell differentiation
    • whereas luteal cells in day 5.5 pregnant wild-type ovaries display cellular hypertrophy, luteal cells in day 5.5 non-pregnant mutant ovaries appear disorganized and display a lower cytoplasmic to nuclear ratio   (MGI Ref ID J:115734)
    • in mutant ovaries, expression of luteal cell-specific mRNAs is reduced as early as day 1.5 pc and remains low on day 5.5 pc   (MGI Ref ID J:115734)

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

Fzd4tm1Nat/Fzd4tm1Nat

        involves: 129S1/Sv * 129X1/SvJ
  • vision/eye phenotype
  • abnormal eye electrophysiology
    • electroretinogram a wave is relatively normal   (MGI Ref ID J:154020)
    • electroretinogram b wave is markedly reduced   (MGI Ref ID J:154020)
  • abnormal retinal vasculature morphology
    • vascular development on the vitreal face of the retina is retarded   (MGI Ref ID J:154020)
    • retinal mural cells are thinner and lower in density than in controls   (MGI Ref ID J:154020)
  • impaired pupillary reflex
    • rod and cone signals are not transmitted effectively   (MGI Ref ID J:154020)
  • behavior/neurological phenotype
  • abnormal optokinetic reflex
    • rod and cone signals are not transmitted effectively   (MGI Ref ID J:154020)
  • impaired pupillary reflex
    • rod and cone signals are not transmitted effectively   (MGI Ref ID J:154020)
  • nervous system phenotype
  • abnormal brain vasculature morphology
    • progressive reduction in vascular density in the cerebellum   (MGI Ref ID J:154020)
    • misshapen capillaries in the cerebellum   (MGI Ref ID J:154020)
    • endothelial projections into the capillary lumen in the cerebellum   (MGI Ref ID J:154020)
    • leakage of IgG into the cerebellum   (MGI Ref ID J:154020)
    • frequent cerebellar hemorrhage but not in cerebral cortex   (MGI Ref ID J:154020)
  • abnormal cerebellum morphology
    • cerebellar degeneration observed   (MGI Ref ID J:154020)
  • cardiovascular system phenotype
  • abnormal brain vasculature morphology
    • progressive reduction in vascular density in the cerebellum   (MGI Ref ID J:154020)
    • misshapen capillaries in the cerebellum   (MGI Ref ID J:154020)
    • endothelial projections into the capillary lumen in the cerebellum   (MGI Ref ID J:154020)
    • leakage of IgG into the cerebellum   (MGI Ref ID J:154020)
    • frequent cerebellar hemorrhage but not in cerebral cortex   (MGI Ref ID J:154020)
  • abnormal retinal vasculature morphology
    • vascular development on the vitreal face of the retina is retarded   (MGI Ref ID J:154020)
    • retinal mural cells are thinner and lower in density than in controls   (MGI Ref ID J:154020)
  • renal/urinary system phenotype
  • small kidney
View Research Applications

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

Cardiovascular Research
Vascular Defects

Internal/Organ Research
Gastrointestinal Defects

Neurobiology Research
Ataxia (Movement) Defects
Cerebellar Defects

Sensorineural Research
Eye Defects
Hearing Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Fzd4tm1Nat
Allele Name targeted mutation 1, Jeremy Nathans
Allele Type Targeted (Null/Knockout, Reporter)
Common Name(s) Fz4lacZ; fz4(-);
Mutation Made By Jeremy Nathans,   Johns Hopkins University
Strain of Origin(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name Fzd4, frizzled homolog 4 (Drosophila)
Chromosome 7
Gene Common Name(s) CD344; EVR1; FEVR; FZD4S; Fz-4; Fz4; FzE4; GPCR; hFz4;
Molecular Note A cassette containing lacZ and neo was inserted at the start codon of the endogenous locus via homologous recombination. The inserted sequences replaced all but the last 70 bp of the protein coding region. Expression of beta-galactosidase was visualized by X-gal staining. [MGI Ref ID J:70078]

Genotyping

Genotyping Information

Genotyping Protocols

Fzd4tm1Nat, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Wang Y; Huso D; Cahill H; Ryugo D; Nathans J. 2001. Progressive cerebellar, auditory, and esophageal dysfunction caused by targeted disruption of the frizzled-4 gene. J Neurosci 21(13):4761-71. [PubMed: 11425903]  [MGI Ref ID J:70078]

Additional References

Fzd4tm1Nat related

Descamps B; Sewduth R; Ferreira Tojais N; Jaspard B; Reynaud A; Sohet F; Lacolley P; Allieres C; Lamaziere JM; Moreau C; Dufourcq P; Couffinhal T; Duplaa C. 2012. Frizzled 4 regulates arterial network organization through noncanonical Wnt/planar cell polarity signaling. Circ Res 110(1):47-58. [PubMed: 22076635]  [MGI Ref ID J:192713]

Hsieh M; Boerboom D; Shimada M; Lo Y; Parlow AF; Luhmann UF; Berger W; Richards JS. 2005. Mice null for Frizzled4 (Fzd4-/-) are infertile and exhibit impaired corpora lutea formation and function. Biol Reprod 73(6):1135-46. [PubMed: 16093361]  [MGI Ref ID J:115734]

Lin SL; Li B; Rao S; Yeo EJ; Hudson TE; Nowlin BT; Pei H; Chen L; Zheng JJ; Carroll TJ; Pollard JW; McMahon AP; Lang RA; Duffield JS. 2010. Macrophage Wnt7b is critical for kidney repair and regeneration. Proc Natl Acad Sci U S A 107(9):4194-9. [PubMed: 20160075]  [MGI Ref ID J:158579]

Wang Y; Rattner A; Zhou Y; Williams J; Smallwood PM; Nathans J. 2012. Norrin/Frizzled4 signaling in retinal vascular development and blood brain barrier plasticity. Cell 151(6):1332-44. [PubMed: 23217714]  [MGI Ref ID J:193332]

Xu Q; Wang Y; Dabdoub A; Smallwood PM; Williams J; Woods C; Kelley MW; Jiang L; Tasman W; Zhang K; Nathans J. 2004. Vascular development in the retina and inner ear: control by Norrin and Frizzled-4, a high-affinity ligand-receptor pair. Cell 116(6):883-95. [PubMed: 15035989]  [MGI Ref ID J:107732]

Ye X; Wang Y; Cahill H; Yu M; Badea TC; Smallwood PM; Peachey NS; Nathans J. 2009. Norrin, frizzled-4, and Lrp5 signaling in endothelial cells controls a genetic program for retinal vascularization. Cell 139(2):285-98. [PubMed: 19837032]  [MGI Ref ID J:154020]

Ye X; Wang Y; Rattner A; Nathans J. 2011. Genetic mosaic analysis reveals a major role for frizzled 4 and frizzled 8 in controlling ureteric growth in the developing kidney. Development 138(6):1161-72. [PubMed: 21343368]  [MGI Ref ID J:170839]

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 maintained as a live colony, heterozygotes may be bred. Homozygotes show reduced fertility and decreased viability.

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 willfulfill 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 willfulfill 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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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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