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- Description
- Disease & phenotype
- Genes & alleles
- Genotyping
- Health & care
- References
- Pricing & purchasing
- 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
Former Names B6C3FeF1 a/A-Eya1bor/J (Changed: 18-FEB-05 ) Type Mutant Strain; Additional information on Genetically Engineered and Mutant Mice. Type *F1 Hybrid; Additional information on Hybrid Strains. Visit our online Nomenclature tutorial. Species laboratory mouse Description
The human Branchio-Oto-Renal Syndrome is generally a dominant disorder with incomplete penetrance and variable expressivity resulting from null mutations in the EYA1 gene. The mouse Eya1bor allele is primarily a recessive hypomorphic mutation. Nevertheless, homozygous mice with this hypomorphic allele offer a good model for Branchio-Oto-Renal Syndrome. The phenotype of Eya1bor/Eya1bor mice parallels that of the human Branchio-Oto-Renal Syndrome and both are thought to result from reduced gene dosage. The Eya1bor/Eya1bor mice are deaf and their behavior is marked by circling and head-bobbing. They lack all but the most basal one-quarter of the cochlea, and the organ of Corti is completely absent. They have foreshortened, narrower semicircular canals and in some the common crus is incomplete. Their kidneys are absent or dysmorphic with greater severity generally on the left side. Fewer homozygotes than expected are born. During mapping crosses using CAST/Ei and C3H/HeJ, it was found that genetic background impacts both the kidney and inner ear phenotypes, and modifier genes in humans also may impact the severity of Branchio-Oto-Renal-Syndrome. (Johnson et al., 1999)Mice heterozygous for a targeted mutation of Eya1 display a phenotype with hearing loss, renal defects (at low penetrance), and developmental disorders, paralleling the phenotype of mice homozygous for Eya1bor. TUNEL analysis on developing ears of the Eya1 targeted mutant mice revealed an increase in apoptotic cells in the otic vesicle at embryonic day 10.5. (Xu et al., 1999.)
Development
The branchio otorenal syndrome mutation (Bor) arose spontaneously on the C3HeB/FeJ inbred strain at The Jackson Laboratory in 1984, when that inbred was at generation F123. This mutant subline was maintained by sibling inbreeding heterozgyotes with wild type siblings for over a decade then, at F29, backcrossed once to a C3HeB/FeJ male and again maintained by sibling intercrossing. Subsequently this coisogenic mutant subline was backcrossed to a C3HeB/FeJ female at F29N1F5 and maintained by sibling inbreeding. A third backcross to C3HeB/FeJ was done with a male heterozygote at generation F29N1F5N1F3 and the offspring were sibling bred. Between 1998 and 1999 embryos were cryopreserved from C57BL/6J females outcrossed to C3HeB/FeJ heterozygous males at generation F29N3F7 or less. These F1 embryos were subsequently revived and sperm was cryopreserved from heterozygous males.
Related Strains
Strains carrying A allele
002083 B6 x B6EiC3 a/A-T(7;16)235Dn/J 000507 B6 x B6EiC3 a/A-Otcspf/J 000628 B6.CE-A Amy1b Amy2a5b/J 004200 B6;CBACa Aw-J/A-Npr2cn-2J/GrsrJ 000604 B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J 000314 B6CBACa Aw-J/A-EdaTa/J-XO 006450 B6EiC3 a/A-Vss/GrsrJ 000557 B6EiC3-+ a/LnpUl A/J 000504 B6EiC3Sn a/A-Cacnb4lh/J 000553 B6EiC3Sn a/A-Egfrwa2 Wnt3avt/J 001811 B6EiC3Sn a/A-Otcspf-ash/J 002343 B6EiC3Sn a/A-Otcspf/J 001923 B6EiC3Sn a/A-Ts(417)2Lws TimT(4;17)3Lws/J 000638 C3FeB6 A/Aw-J-Sptbn4qv-J/J 000200 C3FeB6 A/Aw-J-Ankank/J 000283 LT.CAST-A/J 001759 STOCK A Tyrc Sha/J 001145 WSB/EiJ View Strains carrying A (18 strains)
002588 C3HeB/FeJ-Eya1bor/J
Phenotype
Phenotype Information
- 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).
Branchiootorenal Syndrome 1; BOR1
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Otofaciocervical Syndrome (EYA1)
Skin/Hair/Eye Pigmentation, Variation In, 9; SHEP9 (ASIP)
assigned by genotype
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Eya1bor/Eya1bor
C3HeB/FeJ-Eya1bor
- mortality/aging
- partial perinatal lethality
- reduced litter size suggests perinatal lethality occurs probably relating to bilateral kidney agenesis or severe hypoplasia (MGI Ref ID J:54408)
- behavior/neurological phenotype
- circling (MGI Ref ID J:54408)
- head bobbing (MGI Ref ID J:54408)
- hearing/vestibular/ear phenotype
- abnormal common crus morphology
- the common crus which is formed where the superior and posterior semicircular canals meet is incomplete (MGI Ref ID J:54408)
- absent organ of Corti
- the organ of Corti is absent however the pharyngeal pouches are normal (MGI Ref ID J:54408)
- deafness (MGI Ref ID J:54408)
- decreased cochlear coiling
- only the basal quarter turn of the cochlea is seen in adults (MGI Ref ID J:54408)
- decreased lateral semicircular canal size
- the lateral semicircular canal is foreshortened with a smaller diameter compared to wild-type mice (MGI Ref ID J:54408)
- increased or absent threshold for auditory brainstem response
- homozygotes show no response to sound pressures less than 95 dB at 3-4 weeks of age (MGI Ref ID J:54408)
- homeostasis/metabolism phenotype
- increased blood urea nitrogen level
- increased BUN indicates functional stress from reduced kidney size (MGI Ref ID J:54408)
- renal/urinary system phenotype
- renal hypoplasia
- single kidney
- unilateral kidney agenesis is sometimes seen (MGI Ref ID J:54408)
- reproductive system phenotype
- female infertility
- females do not breed, however homozygous males will sometimes breed (MGI Ref ID J:54408)
Eya1bor/Eya1bor
involves: C3HeB/FeJ
- hearing/vestibular/ear phenotype
- abnormal cochlea morphology (MGI Ref ID J:140027)
- abnormal orientation of cochlear hair cell stereociliary bundles
- adult mice exhibit short and disorganized stereocilia bundles that have a loss of polarity (MGI Ref ID J:140027)
- decreased cochlear coiling
- all mice have shortened cochlear (MGI Ref ID J:140027)
- decreased outer hair cell stereocilia number
- some of the outer hair cell bundles are missing in the middle and apical regions (MGI Ref ID J:140027)
- increased cochlear inner hair cell number
- increased cochlear outer hair cell number
- there is a significant increase in the number of outer hair cells compared to controls (MGI Ref ID J:140027)
- abnormal semicircular canal morphology (MGI Ref ID J:140027)
- abnormal semicircular canal ampulla morphology
- all mice at E18.5 have abnormal ampulla, either truncated or absent (MGI Ref ID J:140027)
- 13 of 20 mice have at least one ear with an absent anterior ampulla (MGI Ref ID J:140027)
- all mice have an absent ampulla in the posterior section (MGI Ref ID J:140027)
- all mice have a malformed ampulla in the lateral section (MGI Ref ID J:140027)
- decreased posterior semicircular canal size
- all mice at E18.5 have truncated posterior semicircular canals (MGI Ref ID J:140027)
- decreased superior semicircular canal size
- 13 of 20 mice at E18.5 have truncated anterior semicircular canals (MGI Ref ID J:140027)
- abnormal utricle morphology
- all mice have severely affected utricle (MGI Ref ID J:140027)
- abnormal vestibular saccule morphology
- all mice at E18.5 have malformed saccule (MGI Ref ID J:140027)
- decreased vestibular hair cell number
- short endolymphatic duct
- 16 mice of 20 mice at E18.5 have a truncated endolymphatic duct (MGI Ref ID J:140027)
- nervous system phenotype
- abnormal orientation of cochlear hair cell stereociliary bundles
- adult mice exhibit short and disorganized stereocilia bundles that have a loss of polarity (MGI Ref ID J:140027)
- decreased outer hair cell stereocilia number
- some of the outer hair cell bundles are missing in the middle and apical regions (MGI Ref ID J:140027)
- decreased vestibular hair cell number
- increased cochlear inner hair cell number
- increased cochlear outer hair cell number
- there is a significant increase in the number of outer hair cells compared to controls (MGI Ref ID J:140027)
This mouse can be used to support research in many areas including:Eya1bor related
Developmental Biology Research
Internal/Organ Defects
kidney
Internal/Organ Research
Kidney Defects
Mouse/Human Gene Homologs
branchiootorenal dysplasia, branchiootic syndrome
Neurobiology Research
Hearing Defects
Sensorineural Research
Hearing Defects
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | A | ||
|---|---|---|---|
| Allele Name | wild-type agouti | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | dark-bellied agouti; | ||
| Strain of Origin | various | ||
| Gene Symbol and Name | a, nonagouti | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | AGSW; AGTI; AGTIL; ASP; As; SHEP9; agouti; agouti signal protein; agouti suppressor; | ||
| General Note | The A allele is usually regarded as a wild-type allele. The C3H and CBA mouse sublines are homozygous for agouti. Hairs are black with a subapical yellow band. This black-yellow-black pattern is referred to as agouti. The general appearance is yellowish brown, slightly lighter on the belly than on the back. | ||
| Molecular Note | This allele, often referred to as wild-type, comprises a novel 131 amino acid protein encoded in a gene comprising four exons, three coding, spanning 18kb. Unique changes in this gene account for all other alleles that have been molecularly characterized. The expression of this allele is almost always dominant to other alleles of this gene. [MGI Ref ID J:3523] | ||
| Allele Symbol | Eya1bor | ||
| Allele Name | branchio otorenal syndrome | ||
| Allele Type | Spontaneous | ||
| Strain of Origin | C3HeB/FeJ | ||
| Gene Symbol and Name | Eya1, eyes absent 1 homolog (Drosophila) | ||
| Chromosome | 1 | ||
| Gene Common Name(s) | BOP; BOR; BOS1; bor; branchiootorenal dysplasia; | ||
| Molecular Note | Insertion of an intracisternal A particle (IAP) element in intron 7. The presence of the IAP insertion was associated with reduced expression of the normal mRNA and aberrant splicing. | ||
Genotyping
Genotyping Information
Genotyping Protocols
Eya1bor, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Additional References
Abdelhak S; Kalatzis V; Heilig R; Compain S; Samson D; Vincent C; Weil D; Cruaud C; Sahly I; Leibovici M; Bitner-Glindzicz M; Francis M; Lacombe D; Vigneron J; Charachon R; Boven K; Bedbeder P; Van Regemorter N; Weissenbach J; Petit C. 1997. A human homologue of the Drosophila eyes absent gene underlies branchio-oto-renal (BOR) syndrome and identifies a novel gene family. Nat Genet 15(2):157-64. [PubMed: 9020840] [MGI Ref ID J:38771]
Johnson KR; Cook SA; Erway LC; Matthews AN; Sanford LP; Paradies NE ; Friedman RA. 1999. Inner ear and kidney anomalies caused by IAP insertion in an intron of the Eya1 gene in a mouse model of BOR syndrome. Hum Mol Genet 8(4):645-53. [PubMed: 10072433] [MGI Ref ID J:54408]
Ohto H; Kamada S; Tago K; Tominaga SI; Ozaki H; Sato S; Kawakami K. 1999. Cooperation of six and eya in activation of their target genes through nuclear translocation of Eya. Mol Cell Biol 19(10):6815-24. [PubMed: 10490620] [MGI Ref ID J:113793]
Xu PX; Adams J; Peters H; Brown MC; Heaney S; Maas R. 1999. Eya1-deficient mice lack ears and kidneys and show abnormal apoptosis of organ primordia. Nat Genet 23(1):113-7. [PubMed: 10471511] [MGI Ref ID J:57313]
Xu PX; Cheng J; Epstein JA; Maas RL. 1997. Mouse Eya genes are expressed during limb tendon development and encode a transcriptional activation function. Proc Natl Acad Sci U S A 94(22):11974-9. [PubMed: 9342347] [MGI Ref ID J:43703]
Xu PX; Woo I; Her H; Beier DR; Maas RL. 1997. Mouse Eya homologues of the Drosophila eyes absent gene require Pax6 for expression in lens and nasal placode. Development 124(1):219-31. [PubMed: 9006082] [MGI Ref ID J:38379]
A relatedEya1bor relatedBlewitt ME; Vickaryous NK; Hemley SJ; Ashe A; Bruxner TJ; Preis JI; Arkell R; Whitelaw E. 2005. An N-ethyl-N-nitrosourea screen for genes involved in variegation in the mouse. Proc Natl Acad Sci U S A 102(21):7629-34. [PubMed: 15890782] [MGI Ref ID J:99816]
Bultman SJ; Michaud EJ; Woychik RP. 1992. Molecular characterization of the mouse agouti locus. Cell 71(7):1195-204. [PubMed: 1473152] [MGI Ref ID J:3523]
Bundschuh VG; Madry M. 1988. [atwp mutation in an albino mouse substrain (AB/Hum-1)] Z Versuchstierkd 31(6):249-54. [PubMed: 3227730] [MGI Ref ID J:16568]
Czyzyk TA; Sikorski MA; Yang L; McKnight GS. 2008. Disruption of the RIIbeta subunit of PKA reverses the obesity syndrome of Agouti lethal yellow mice. Proc Natl Acad Sci U S A 105(1):276-81. [PubMed: 18172198] [MGI Ref ID J:131039]
Dickie MM. 1969. Mutations at the agouti locus in the mouse. J Hered 60(1):20-5. [PubMed: 5798139] [MGI Ref ID J:30922]
Dry FW. 1928. The agouti coloration of the mouse (Mus Musculus) and the rat (Mus Norvegicus). J Genet 20:131-144. [MGI Ref ID J:46318]
Dunn LC. 1945. A New Eye Color Mutant in the Mouse with Asymmetrical Expression. Proc Natl Acad Sci U S A 31(11):343-6. [PubMed: 16578176] [MGI Ref ID J:13122]
Galbraith DB; Wolff GL; Brewer NL. 1979. Tissue microenvironment and the genetic control of hair pigment patterns in mice Dev Genet 1(2):167-179. [MGI Ref ID J:156092]
Guido V; and The Mouse Mutant Resource (MMR) at The Jackson Laboratory. 2002. Two new mutations of white bellied agouti, w-46J and w-47J MGI Direct Data Submission :. [MGI Ref ID J:77218]
Jackson IJ; Budd PS; Keighren M; McKie L. 2007. Humanized MC1R transgenic mice reveal human specific receptor function. Hum Mol Genet 16(19):2341-8. [PubMed: 17652101] [MGI Ref ID J:129904]
Kelly EM. 1957. Beige, bg Mouse News Lett 16:36. [MGI Ref ID J:29744]
Mather K; North SB. 1940. Umbrous: a case of dominance modification in mice. J Genet 40:229-41. [MGI Ref ID J:280]
MouseBookTM. 2005. Information obtained from MouseBook<sup>TM</sup>, Medical Research Council Mammalian Genetics Unit, Harwell, UK. Unpublished :. [MGI Ref ID J:169366]
Perry WL; Copeland NG; Jenkins NA. 1994. The molecular basis for dominant yellow agouti coat color mutations. Bioessays 16(10):705-7. [PubMed: 7980472] [MGI Ref ID J:21244]
Phillips RJS. 1966. A cis-trans position effect at the A locus of the house mouse. Genetics 54(2):485-95. [PubMed: 5968639] [MGI Ref ID J:5027]
Quevedo WC Jr.; Chase HB. 1958. An analysis of the light mutation of coat color in mice. J Morphol 102:329-345. [MGI Ref ID J:13094]
Silvers WK. 1979. The Coat Colors of Mice; A Model for Mammalian Gene Action and Interaction. In: The Coat Colors of Mice. Springer-Verlag, New York. [MGI Ref ID J:78801]
Siracusa LD; Washburn LL; Swing DA; Argeson AC; Jenkins NA; Copeland NG. 1995. Hypervariable yellow (Ahvy), a new murine agouti mutation: Ahvy displays the largest variation in coat color phenotypes of all known agouti alleles. J Hered 86(2):121-8. [PubMed: 7751596] [MGI Ref ID J:24247]
Floyd JA; Gold DA; Concepcion D; Poon TH; Wang X; Keithley E; Chen D; Ward EJ; Chinn SB; Friedman RA; Yu HT; Moriwaki K; Shiroishi T; Hamilton BA. 2003. A natural allele of Nxf1 suppresses retrovirus insertional mutations. Nat Genet 35(3):221-8. [PubMed: 14517553] [MGI Ref ID J:86371]
Friedman RA; Makmura L; Biesiada E; Wang X; Keithley EM. 2005. Eya1 acts upstream of Tbx1, Neurogenin 1, NeuroD and the neurotrophins BDNF and NT-3 during inner ear development. Mech Dev 122(5):625-34. [PubMed: 15817220] [MGI Ref ID J:98114]
Johnson KR; Cook SA; Erway LC; Matthews AN; Sanford LP; Paradies NE ; Friedman RA. 1999. Inner ear and kidney anomalies caused by IAP insertion in an intron of the Eya1 gene in a mouse model of BOR syndrome. Hum Mol Genet 8(4):645-53. [PubMed: 10072433] [MGI Ref ID J:54408]
Niu H; Li X; Makmura L; Friedman RA. 2008. Mapping of genetic modifiers of Eya1 ( bor/bor ) in CAST/EiJ and BALB/cJ that suppress cochlear aplasia and associated deafness. Mamm Genome 19(9):634-9. [PubMed: 18836772] [MGI Ref ID J:148630]
Niu H; Makmura L; Shen T; Sheth SS; Blair K; Friedman RA. 2006. Identification of two major loci that suppress hearing loss and cochlear dysmorphogenesis in Eya1bor/bor mice. Genomics 88(3):302-8. [PubMed: 16488112] [MGI Ref ID J:114904]
Sajithlal G; Zou D; Silvius D; Xu PX. 2005. Eya 1 acts as a critical regulator for specifying the metanephric mesenchyme. Dev Biol 284(2):323-36. [PubMed: 16018995] [MGI Ref ID J:100569]
The Jackson Laboratory Office of Genetic Resources. 1983. Registry of Remutation at The Jackson Laboratory, 1983-1984 MGI Direct Data Submission :. [MGI Ref ID J:79402]
Zou D; Erickson C; Kim EH; Jin D; Fritzsch B; Xu PX. 2008. Eya1 gene dosage critically affects the development of sensory epithelia in the mammalian inner ear. Hum Mol Genet 17(21):3340-56. [PubMed: 18678597] [MGI Ref ID J:140027]
Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $1980.00 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 of Strains Needing Progeny Testing.
At least two untested males and two untested females (two pairs) will be recovered (eight or more mice is typical). The total number of animals provided, their gender and genotype will vary. Untested animals typically are available to ship between 13 and 16 weeks from the date of your order. If the first recovery attempt is unsuccessful, a second recovery will be done, extending the overall recovery time to approximately 25 weeks.Progeny testing is required to identify the genotype of mice of this strain, as a genotyping assay is not available. This type of testing involves breeding the recovered animals and assessing the phenotype of the offspring in order to identify animals carrying the mutation of interest. We can perform the progeny testing for you as a service or we can ship all recovered animals to you for progeny testing at your facility. If you perform the progeny testing, there is NO guarantee that a carrier will be identified. If we perform progeny testing as a service, additional breeding time will be required. In this case, when a male and female (one pair) are identified that carry the mutation, they and their offspring will be shipped. Delivery time for strains requiring progeny testing often exceeds 25 weeks and may take 12 months or more due to the difficulties in breeding some strains. The progeny testing cost is in addition to the recovery cost and is based on the number of boxes used and the time taken to produce the mice identified as carrying the mutation. Please note that identified pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Please contact Customer Service for more information on the cost of progeny testing for a strain: Tel: 1-800-422-6423 (from U.S.A., Canada and Puerto Rico only) or 1-207-288-5845 (from any location). 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 |
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2574.00 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 of Strains Needing Progeny Testing.
At least two untested males and two untested females (two pairs) will be recovered (eight or more mice is typical). The total number of animals provided, their gender and genotype will vary. Untested animals typically are available to ship between 13 and 16 weeks from the date of your order. If the first recovery attempt is unsuccessful, a second recovery will be done, extending the overall recovery time to approximately 25 weeks.Progeny testing is required to identify the genotype of mice of this strain, as a genotyping assay is not available. This type of testing involves breeding the recovered animals and assessing the phenotype of the offspring in order to identify animals carrying the mutation of interest. We can perform the progeny testing for you as a service or we can ship all recovered animals to you for progeny testing at your facility. If you perform the progeny testing, there is NO guarantee that a carrier will be identified. If we perform progeny testing as a service, additional breeding time will be required. In this case, when a male and female (one pair) are identified that carry the mutation, they and their offspring will be shipped. Delivery time for strains requiring progeny testing often exceeds 25 weeks and may take 12 months or more due to the difficulties in breeding some strains. The progeny testing cost is in addition to the recovery cost and is based on the number of boxes used and the time taken to produce the mice identified as carrying the mutation. Please note that identified pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Please contact Customer Service for more information on the cost of progeny testing for a strain: Tel: 1-800-422-6423 (from U.S.A., Canada and Puerto Rico only) or 1-207-288-5845 (from any location). 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).
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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.Ordering Information
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