Strain Name:

STOCK Rxratm1Rev/HsvJ

Stock Number:

024089

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Availability:

Repository- Live

This Rxra knockout strain is useful in studies of cardiac development, and the role of retinoic acid receptors in cellular processes.

Description

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemWild-type x Heterozygote         (Female x Male)   02-JUL-14
Mating SystemHeterozygote x Wild-type         (Female x Male)   02-JUL-14
Specieslaboratory mouse
Generation?+pN1 (12-AUG-14)
Generation Definitions
 
Donating Investigator Henry Sucov,   University of Southern California

Description
The Rxra, retinoid X receptor alpha, gene encodes for a nuclear receptor of retinoic acid. The retinoid X receptors regulate gene expression via both ligand-dependent and ligand-independent mechanisms. These mice carry a targeted mutation for the Rxra gene in which a NEO cassette replaced part of exon 3 and intron 3. Mice that are heterozygous for the targeted mutation are viable and fertile. Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic day 15.5 due to congestive heart failure. Abberant non-functional gene product (mRNA) is detected by Northern analysis of homozygous embryos, embryonic day 13.5. Homozygous embryos exhibit impaired placental, eye, cardiac and hepatic (transient delay in fetal erythropopiesis) development as well as subdermal edema. Heterozygotes exhibit cardiac and myocardial defects.

Development
A targeting vector containing PGK-NEO cassette was used to disrupt part of exon 3 and intron 3. The construct was electroporated into 129S4/SvJae derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6 mice. The mice are on a STOCK background that includes C57BL/6, ICR (CD-1), 129, and other backgrounds. Upon arrival at The Jackson Laboratory, the mice were crossed to C57BL/6J (Stock No. 000664) at least once to establish the colony.

Control Information

  Control
   Wild-type siblings from the colony
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Rxra
013086   STOCK Rxratm1Krc/J
View Strains carrying other alleles of Rxra     (1 strain)

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.

Rxratm1Rev/Rxra+

        involves: 129S4/SvJae * C57BL/6
  • cardiovascular system phenotype
  • abnormal atrioventricular valve morphology
    • atrioventricular cushion defects range from absent fusion (3%) and hypoplasia (8%) to abnormalities of mature valvular structures   (MGI Ref ID J:35363)
    • abnormal mitral valve morphology
      • 17% show cleft mitral valve   (MGI Ref ID J:35363)
      • mitral valve stenosis
        • 2% show mitral valve stenosis   (MGI Ref ID J:35363)
    • abnormal tricuspid valve morphology
      • 8% show tricuspid valve abnormalities   (MGI Ref ID J:35363)
  • abnormal heart development
    • 15% exhibit conotruncal defects, with severity ranging from absent conotruncal ridges (3%) to a shortened conotruncal septum (7%)   (MGI Ref ID J:35363)
  • abnormal heart ventricle morphology   (MGI Ref ID J:35363)
    • abnormal interventricular septum morphology   (MGI Ref ID J:35363)
    • abnormal ventricle papillary muscle morphology
      • 86% show papillary muscle defects   (MGI Ref ID J:35363)
    • thin ventricular wall
      • severe thinning of the ventricular wall is seen in both the left (2%) and right (2%) ventricles, but never simultaneously   (MGI Ref ID J:35363)
      • thin left ventricle wall is associated with mitral valve stenosis yet a normal right ventricle and semilunar valves   (MGI Ref ID J:35363)
      • thin right ventricle is associated with dysmorphic tricuspid valve yet normal left-sided and semilunar structures   (MGI Ref ID J:35363)
  • abnormal myocardium layer morphology   (MGI Ref ID J:35363)
    • abnormal myocardial trabeculae morphology
      • 49% show trabecular defects with less organized trabecular arrangement   (MGI Ref ID J:35363)
    • abnormal myocardium compact layer morphology
      • intermediate thickness of compact layer compared to homozygotes and wild-type, especially prominent at E13.5 and 14.5   (MGI Ref ID J:35363)
    • abnormal ventricle papillary muscle morphology
      • 86% show papillary muscle defects   (MGI Ref ID J:35363)
  • double outlet right ventricle
    • seen in 5% of heterozygotes   (MGI Ref ID J:35363)
  • pulmonary artery stenosis
    • one heterozygote shows pulmonary artery stenosis   (MGI Ref ID J:35363)
  • muscle phenotype
  • abnormal myocardial trabeculae morphology
    • 49% show trabecular defects with less organized trabecular arrangement   (MGI Ref ID J:35363)

Rxratm1Rev/Rxratm1Rev

        involves: 129S4/SvJae * C57BL/6
  • mortality/aging
  • complete lethality throughout fetal growth and development
    • homozygotes die between E13.5 and E16.5, with most embryos still viable at E14.5 but dead by E15.5   (MGI Ref ID J:18047)
  • cardiovascular system phenotype
  • abnormal heart morphology
    • at E13.5, upon color fluorescent imaging, the mutant heart appears much more translucent than the wild-type heart   (MGI Ref ID J:65904)
    • abnormal atrioventricular cushion morphology
      • exhibit a wide spectrum of atrioventricular cushion defects   (MGI Ref ID J:35363)
      • 67% show partial fusion of the atrioventricular cushions   (MGI Ref ID J:35363)
      • failure of atrioventricular cushion closure
        • complete lack of fusion of the superior and inferior atroioventricular cushions   (MGI Ref ID J:35363)
    • abnormal conotruncal ridge morphology
      • 100% have abnormalities of conotruncal ridges ranging from mild deficiency of conotruncal tissue (6%) to complete absence of cushion tissue (66%)   (MGI Ref ID J:35363)
    • abnormal heart left atrium morphology
      • at E14.5, homozygotes exhibit normal atrial structure and function with no differences in overall position of heart and major vessels; however, the left atrium appears small   (MGI Ref ID J:65904)
    • abnormal heart ventricle morphology
      • at E11.5 or later, homozygotes exhibit an uneven ventricular contour   (MGI Ref ID J:18047)
      • at E14.5, both ventricles exhibit a globular rather than elliptical shape, suggesting a dilated form of congestive heart failure   (MGI Ref ID J:65904)
      • abnormal ventricle papillary muscle morphology
        • 56% exhibit dysmorphic papillary muscles   (MGI Ref ID J:35363)
      • dilated heart right ventricle
        • at E14.5, some homozygotes display dilated right ventricles   (MGI Ref ID J:18047)
      • muscular ventricular septal defect   (MGI Ref ID J:65904)
        • at E14.5, homozygotes display a poorly developed ventricular septum   (MGI Ref ID J:18047)
        • 94% exhibit a ventricular septal defect, with all defects being muscular   (MGI Ref ID J:35363)
        • by E14.5, 9 of 10 homozygotes display obvious ventricular septal defects at the septal-cushion fusion   (MGI Ref ID J:18047)
      • thin ventricular wall   (MGI Ref ID J:35363)
        • at E14.5, all (10 of 10) homozygotes exhibit a thinned ventricular wall   (MGI Ref ID J:18047)
        • at E13.5, the relatively thin-walled "atrial-like" phenotype of mutant ventricular muscle cells is shown to correlate with the aberrant, persistent expression of an atrial marker   (MGI Ref ID J:18047)
      • ventricular hypoplasia
        • by E14.5, all (10 of 10) homozygotes show ventricular chamber hypoplasia   (MGI Ref ID J:18047)
    • abnormal mitral valve morphology
      • 17% show cleft mitral valve   (MGI Ref ID J:35363)
      • mitral valve atresia
        • by E14.4, 1 of 10 homozygotes displays mitral atresia; no tricuspid atresia is observed   (MGI Ref ID J:18047)
    • abnormal myocardium layer morphology
      • all homozygotes display impaired differentiation or maturation of the ventricular cardiac myocytes   (MGI Ref ID J:18047)
      • spongy layer of the myocardium is generally thicker   (MGI Ref ID J:35363)
      • abnormal myocardial trabeculae morphology
        • 67% show attenuated trabeculae and contain an unusual, random branching pattern   (MGI Ref ID J:35363)
        • trabecula carnea hypoplasia
          • by E14.5, ventricular trabeculation is present but reduced and appears disorganized at the muscular septum   (MGI Ref ID J:18047)
      • abnormal myocardium compact layer morphology
        • by E14.5, homozygotes show absence of myocyte proliferation at the ventricular epicardial surface ("compact layer")   (MGI Ref ID J:18047)
        • ventricular myocardium compact layer hypoplasia
          • 94% exhibit a hypoplastic compact zone of the ventricular myocardium   (MGI Ref ID J:35363)
      • abnormal ventricle papillary muscle morphology
        • 56% exhibit dysmorphic papillary muscles   (MGI Ref ID J:35363)
    • abnormal pericardial cavity morphology
      • by E14.5, most homozygotes show a prominent pericardial space   (MGI Ref ID J:18047)
    • abnormal pericardium morphology
      • at E11.5 and E12.5, homozygotes exhibit a loosely apposed pericardium; however, the pericardium appears relatively normal at E14.5   (MGI Ref ID J:18047)
    • abnormal tricuspid valve morphology
      • 17% show cleft tricuspid valve   (MGI Ref ID J:35363)
    • aortopulmonary window
      • 28% show incomplete aorticopulmonary septum/aorticopulmonary window   (MGI Ref ID J:35363)
    • complete atrioventricular septal defect
      • 39% show a common atrioventricular canal   (MGI Ref ID J:35363)
    • dilated heart atrium
      • at E14.5, 5 of 10 homozygotes display dilation of the right atrial chambers   (MGI Ref ID J:18047)
    • double outlet right ventricle
      • portion of embryos with shortened conotruncal ridges exhibit double outlet right ventricle (17%)   (MGI Ref ID J:35363)
    • persistent truncus arteriosis
      • seen in 11% of homozygotes   (MGI Ref ID J:35363)
  • abnormal truncus arteriosus septation
    • at E14.5, only 1 of 10 homozygotes displays an abnormal aortic pulmonary septum; both aortic and pulmonary valves appear unaffected   (MGI Ref ID J:18047)
    • aortopulmonary window
      • 28% show incomplete aorticopulmonary septum/aorticopulmonary window   (MGI Ref ID J:35363)
    • persistent truncus arteriosis
      • seen in 11% of homozygotes   (MGI Ref ID J:35363)
  • congestive heart failure   (MGI Ref ID J:65904)
    • homozygotes appear to die in utero as a result of congestive heart failure   (MGI Ref ID J:18047)
  • decreased cardiac output   (MGI Ref ID J:65904)
  • decreased heart rate
    • at E13.5, homozygotes show normal AV synchrony and display heart rates comparable to those of wild-type mice; however, mutant heart rates are slightly decreased at E14.5   (MGI Ref ID J:65904)
  • decreased ventricle muscle contractility
    • at E13.5 and E14.5, left ventricular area ejection fractions of mutant hearts average 14% vs 50% in wild-type hearts, indicating ventricular dysfunction   (MGI Ref ID J:65904)
    • at E14.5, depressed ejection fraction is related to thinned left ventricular wall and impaired shortening of the mutant myocardium   (MGI Ref ID J:65904)
  • heart block
    • at E14.5, 2 of 10 homozygotes display a complete heart block   (MGI Ref ID J:65904)
    • atrioventricular block
      • by E14.5, homozygotes with slightly reduced heart rates exhibit an intermittent partial AV block (not quantified)   (MGI Ref ID J:65904)
  • homeostasis/metabolism phenotype
  • skin edema
    • at E14.5, homozygotes display a dramatic subdermal edema, that is most prominent along the back and in the folds of skin around the eye   (MGI Ref ID J:18047)
    • however, most major organ systems, including the intestine, skin, kidney and eye, appear normal   (MGI Ref ID J:18047)
  • liver/biliary system phenotype
  • decreased hepatocyte proliferation
    • at E12.5, homozygotes exhibit a marked reduction in hepatocyte proliferation with substantial recovery to ~60% of wild-type values noted at E14.5   (MGI Ref ID J:18047)
  • delayed hepatic development   (MGI Ref ID J:18047)
  • small liver
    • at E12.5, homozygotes display a liver mass that is ~30% of wild-type mice in the absence of morphological defects   (MGI Ref ID J:18047)
  • muscle phenotype
  • abnormal myocardial trabeculae morphology
    • 67% show attenuated trabeculae and contain an unusual, random branching pattern   (MGI Ref ID J:35363)
    • trabecula carnea hypoplasia
      • by E14.5, ventricular trabeculation is present but reduced and appears disorganized at the muscular septum   (MGI Ref ID J:18047)
  • decreased ventricle muscle contractility
    • at E13.5 and E14.5, left ventricular area ejection fractions of mutant hearts average 14% vs 50% in wild-type hearts, indicating ventricular dysfunction   (MGI Ref ID J:65904)
    • at E14.5, depressed ejection fraction is related to thinned left ventricular wall and impaired shortening of the mutant myocardium   (MGI Ref ID J:65904)
  • integument phenotype
  • skin edema
    • at E14.5, homozygotes display a dramatic subdermal edema, that is most prominent along the back and in the folds of skin around the eye   (MGI Ref ID J:18047)
    • however, most major organ systems, including the intestine, skin, kidney and eye, appear normal   (MGI Ref ID J:18047)
  • translucent skin   (MGI Ref ID J:18047)
  • cellular phenotype
  • decreased hepatocyte proliferation
    • at E12.5, homozygotes exhibit a marked reduction in hepatocyte proliferation with substantial recovery to ~60% of wild-type values noted at E14.5   (MGI Ref ID J:18047)
View Research Applications

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

Cardiovascular Research
Heart Abnormalities

Developmental Biology Research
Embryonic Lethality (Homozygous)
Internal/Organ Defects
      heart
      liver

Internal/Organ Research
Heart Abnormalities
Liver Defects

Research Tools
Cardiovascular Research

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Rxratm1Rev
Allele Name targeted mutation 1, Ronald M Evans
Allele Type Targeted (Null/Knockout)
Common Name(s) RXRalpha-;
Strain of Origin129S4/SvJae
Gene Symbol and Name Rxra, retinoid X receptor alpha
Chromosome 2
Gene Common Name(s) 9530071D11Rik; NR2B1; RIKEN cDNA 9530071D11 gene; RXR alpha 1; RXRalpha1;
General Note Heterozygotes display Phenotypic Similarity to Human Syndrome: congenital heart disease (J:35363).
Molecular Note A genomic fragment containing part of exon 3 and intron 3 was replaced with a neomycin resistance cassette. RT-PCR analysis on RNA derived from E13.5 embryos indicated that no normal transcript was produced from this allele in homozygous embryos. [MGI Ref ID J:18047]

Genotyping

Genotyping Information

Genotyping Protocols

Rxratm1Rev-alternate 1, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Sucov HM; Dyson E; Gumeringer CL; Price J; Chien KR; Evans RM. 1994. RXR alpha mutant mice establish a genetic basis for vitamin A signaling in heart morphogenesis. Genes Dev 8(9):1007-18. [PubMed: 7926783]  [MGI Ref ID J:18047]

Additional References

Rxratm1Rev related

Bruneau BG; Bao ZZ; Tanaka M; Schott JJ; Izumo S; Cepko CL; Seidman JG; Seidman CE. 2000. Cardiac expression of the ventricle-specific homeobox gene Irx4 is modulated by Nkx2-5 and dHand. Dev Biol 217(2):266-77. [PubMed: 10625552]  [MGI Ref ID J:59924]

Cai Y; Dai T; Ao Y; Konishi T; Chuang KH; Lue Y; Chang C; Wan YJ. 2003. Cytochrome P450 genes are differentially expressed in female and male hepatocyte retinoid X receptor alpha-deficient mice. Endocrinology 144(6):2311-8. [PubMed: 12746291]  [MGI Ref ID J:115718]

Chen TH; Chang TC; Kang JO; Choudhary B; Makita T; Tran CM; Burch JB; Eid H; Sucov HM. 2002. Epicardial induction of fetal cardiomyocyte proliferation via a retinoic acid-inducible trophic factor. Dev Biol 250(1):198-207. [PubMed: 12297106]  [MGI Ref ID J:107701]

Dyson E; Sucov HM; Kubalak SW; Schmid-Schonbein GW; DeLano FA; Evans RM; Ross J Jr; Chien KR. 1995. Atrial-like phenotype is associated with embryonic ventricular failure in retinoid X receptor alpha -/- mice. Proc Natl Acad Sci U S A 92(16):7386-90. [PubMed: 7638202]  [MGI Ref ID J:65904]

Gruber PJ; Kubalak SW; Pexieder T; Sucov HM; Evans RM; Chien KR. 1996. RXR alpha deficiency confers genetic susceptibility for aortic sac, conotruncal, atrioventricular cushion, and ventricular muscle defects in mice. J Clin Invest 98(6):1332-43. [PubMed: 8823298]  [MGI Ref ID J:35363]

Gyamfi MA; Kocsis MG; He L; Dai G; Mendy AJ; Wan YJ. 2006. The role of retinoid X receptor alpha in regulating alcohol metabolism. J Pharmacol Exp Ther 319(1):360-8. [PubMed: 16829625]  [MGI Ref ID J:144689]

Gyamfi MA; Wan YJ. 2009. Mechanisms of resistance of hepatocyte retinoid X receptor alpha-null mice to WY-14,643-induced hepatocyte proliferation and cholestasis. J Biol Chem 284(14):9321-30. [PubMed: 19176532]  [MGI Ref ID J:148814]

Hoover LL; Burton EG; O'Neill ML; Brooks BA; Sreedharan S; Dawson NA; Kubalak SW. 2008. Retinoids regulate TGFbeta signaling at the level of Smad2 phosphorylation and nuclear accumulation. Biochim Biophys Acta 1783(12):2279-86. [PubMed: 18773928]  [MGI Ref ID J:142429]

Jenkins SJ; Hutson DR; Kubalak SW. 2005. Analysis of the proepicardium-epicardium transition during the malformation of the RXRalpha(-/-) epicardium. Dev Dyn 233(3):1091-1101. [PubMed: 15861408]  [MGI Ref ID J:98794]

Kubalak SW; Hutson DR; Scott KK; Shannon RA. 2002. Elevated transforming growth factor beta2 enhances apoptosis and contributes to abnormal outflow tract and aortic sac development in retinoic X receptor alpha knockout embryos. Development 129(3):733-46. [PubMed: 11830573]  [MGI Ref ID J:74237]

Li P; Pashmforoush M; Sucov HM. 2010. Retinoic acid regulates differentiation of the secondary heart field and TGFbeta-mediated outflow tract septation. Dev Cell 18(3):480-5. [PubMed: 20230754]  [MGI Ref ID J:159110]

Makita T; Duncan SA; Sucov HM. 2005. Retinoic acid, hypoxia, and GATA factors cooperatively control the onset of fetal liver erythropoietin expression and erythropoietic differentiation. Dev Biol 280(1):59-72. [PubMed: 15766748]  [MGI Ref ID J:98265]

Makita T; Hernandez-Hoyos G; Chen TH; Wu H; Rothenberg EV; Sucov HM. 2001. A developmental transition in definitive erythropoiesis: erythropoietin expression is sequentially regulated by retinoic acid receptors and HNF4. Genes Dev 15(7):889-901. [PubMed: 11297512]  [MGI Ref ID J:111472]

Martin LJ; Tremblay JJ. 2010. Nuclear receptors in leydig cell gene expression and function. Biol Reprod 83(1):3-14. [PubMed: 20375256]  [MGI Ref ID J:161974]

Nugent P; Sucov HM; Pisano MM; Greene RM. 1999. The role of RXR-alpha in retinoic acid-induced cleft palate as assessed with the RXR-alpha knockout mouse. Int J Dev Biol 43(6):567-70. [PubMed: 10610030]  [MGI Ref ID J:106284]

Ruiz-Lozano P; Smith SM; Perkins G; Kubalak SW; Boss GR; Sucov HM ; Evans RM ; Chien KR. 1998. Energy deprivation and a deficiency in downstream metabolic target genes during the onset of embryonic heart failure in RXRalpha-/- embryos. Development 125(3):533-44. [PubMed: 9425147]  [MGI Ref ID J:46220]

Shalom-Barak T; Nicholas JM; Wang Y; Zhang X; Ong ES; Young TH; Gendler SJ; Evans RM; Barak Y. 2004. Peroxisome proliferator-activated receptor gamma controls Muc1 transcription in trophoblasts. Mol Cell Biol 24(24):10661-9. [PubMed: 15572671]  [MGI Ref ID J:95115]

Tran CM; Sucov HM. 1998. The RXRalpha gene functions in a non-cell-autonomous manner during mouse cardiac morphogenesis. Development 125(10):1951-6. [PubMed: 9550727]  [MGI Ref ID J:48373]

Wan YJ; An D; Cai Y; Repa JJ; Hung-Po Chen T; Flores M; Postic C; Magnuson MA; Chen J; Chien KR; French S; Mangelsdorf DJ; Sucov HM. 2000. Hepatocyte-specific mutation establishes retinoid X receptor alpha as a heterodimeric integrator of multiple physiological processes in the liver. Mol Cell Biol 20(12):4436-44. [PubMed: 10825207]  [MGI Ref ID J:62594]

Wan YJ; Han G; Cai Y; Dai T; Konishi T; Leng AS. 2003. Hepatocyte retinoid X receptor-alpha-deficient mice have reduced food intake, increased body weight, and improved glucose tolerance. Endocrinology 144(2):605-11. [PubMed: 12538623]  [MGI Ref ID J:81482]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, heterozygous mice may be bred together, to wildtype siblings, or to C57BL/6J inbred mice (Stock No. 000664). Homozygotes are not viable.
Mating SystemWild-type x Heterozygote         (Female x Male)   02-JUL-14
Heterozygote x Wild-type         (Female x Male)   02-JUL-14

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 $232.00Female or MaleHeterozygous for Rxratm1Rev  
Price per Pair (US dollars $)Pair Genotype
$304.00Heterozygous for Rxratm1Rev x Wild-type for Rxratm1Rev  
$304.00Wild-type for Rxratm1Rev x Heterozygous for Rxratm1Rev  

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 $301.60Female or MaleHeterozygous for Rxratm1Rev  
Price per Pair (US dollars $)Pair Genotype
$395.20Heterozygous for Rxratm1Rev x Wild-type for Rxratm1Rev  
$395.20Wild-type for Rxratm1Rev x Heterozygous for Rxratm1Rev  

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 siblings from the colony
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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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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.


(6.8)