Strain Name:

FVB-Tg(Sod1*G86R)M1Jwg/J

Stock Number:

005110

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Availability:

Cryopreserved - Ready for recovery

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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 FVB-Tg(Sod1-G86R)M1Jwg/J    (Changed: 11-JUL-07 )
Type Mutant Strain; Transgenic;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
GenerationN?+6pN1
Generation Definitions
 
Donating InvestigatorDr. Jon W. Gordon,   Mount Sinai School of Medicine

Description
These transgenic mice express the missense mutant mouse Sod1 under the control of the endogenous promoter. The missense mutation is a point mutation in exon 4 resulting in a glycine-86 to arginine substitution,which corresponds to amino acid position 86 in the human SOD1 protein. Transgene expression is detected by RT-PCR analysis of brain, spinal cord, and other tissues. Onset of progressive loss of motor function begins at 3-4 months of age with hind limb spastic paralysis and muscle wasting. Transgenic mice do not survive beyond 4 months of age. Histological analysis of spinal cord ventral horns, brain stem and neocortex reveals neurodegeneration and abnormal neurites. Affected mice do not exhibit diminished SOD1 activity. This mutant mouse strain may be useful in studies of amyotrophic lateral sclerosis.

Development
A transgenic construct containing 1.5kb sequence of the modified mouse Sod1 gene with the missense mutation in exon 4, and flanking regions was injected into fertilized FVB/N mouse eggs. Founder animals were bred to wildtype FVB/N mice.

Control Information

  Control
   Noncarrier
   001800 FVB/NJ
 
  Considerations for Choosing Controls

Related Strains

View Amyotrophic Lateral Sclerosis (ALS)     (30 strains)

Strains carrying other alleles of Sod1
003881   B6.129S7-Sod1tm1Leb/DnJ
004140   B6.SOD1-Sod1c/CjeDnJ
002972   B6;129S-Sod1tm1Leb/J
View Strains carrying other alleles of Sod1     (3 strains)

Additional Web Information

Working with ALS Mice manual [.pdf]
This resource was prepared by scientists with Prize4Life and The Jackson Laboratory.

Visit the Amyotrophic Lateral Sclerosis (ALS) Mouse Model Resource site for helpful information on ALS Disease and research resources.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.
Amyotrophic Lateral Sclerosis 1; ALS1
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Tg(Sod1*G86R)M1Jwg/0

        involves: FVB/N
  • mortality/aging
  • premature death
    • none survive past 4 months of age   (MGI Ref ID J:22628)
    • compensating the energetic imbalance with a highly energetic diet extends the mean survival by 20% and improves motor neuronal function   (MGI Ref ID J:91800)
  • behavior/neurological phenotype
  • abnormal motor capabilities/coordination/movement
    • exhibit an age-related rapidly progressive decline of motor function   (MGI Ref ID J:22628)
    • decreased grip strength
      • progressive decrease in grip strength is observed starting at around 15 weeks of age   (MGI Ref ID J:131028)
    • impaired balance
      • animals show increased incidence of falling   (MGI Ref ID J:131028)
    • impaired coordination
      • mice show reduced ability with aging to remain on rotating rod   (MGI Ref ID J:131028)
    • paralysis
      • develop a spastic paralysis, initially involving the hindlimbs but progressing to the forelimb, that is associated with profound muscle wasting   (MGI Ref ID J:22628)
    • weakness
      • at 3-4 months of age, develop a generalized weakness that progresses within 72 hours to total immobility   (MGI Ref ID J:22628)
  • aphagia
    • cease food and water intake   (MGI Ref ID J:22628)
  • nervous system phenotype
  • abnormal cranial nerve morphology
    • within the brain stem and neocortex, show degenerative changes in the motor components of cranial nerve nuclei   (MGI Ref ID J:22628)
  • abnormal facial motor nucleus morphology
    • exhibit a variable (16-72%) decrease in neuron number in the facial nucleus and a smaller nuclear volume   (MGI Ref ID J:58733)
  • abnormal hypoglossal nucleus morphology
    • neuron loss is also seen in the hypoglossal nucleus but it is more variable and much milder than the loss in the facial nucleus   (MGI Ref ID J:58733)
  • abnormal oculomotor nucleus morphology
    • consistent neuronal loss in the oculomotor nucleus is seen only in the two most severely affected mice   (MGI Ref ID J:58733)
  • abnormal spinal cord dorsal horn morphology
    • exhibit a few dystrophic neurites in the dorsal horn, however do not detect any argyrophilic perikarya   (MGI Ref ID J:22628)
  • abnormal spinal cord ventral horn morphology
    • exhibit moderate to severe degenerative changes within the ventral horns   (MGI Ref ID J:22628)
    • exhibit numerous dystrophic neurites in the ventral horn gray matter, large and small argyrophilic perikarya, and swollen fragmented processes   (MGI Ref ID J:22628)
  • abnormal trigeminal motor nucleus morphology
    • exhibit a moderate deletion of neurons in the trigeminal motor nucleus   (MGI Ref ID J:58733)
  • neurodegeneration
    • exhibit neurodegeneration of motorneurons within the spinal cord, brain stem, and neocortex and show some degenerative changes in the hypothalamus, deep layers of the superior colliculus, deep cerebellar nuclei, basal ganglia, and thalamus   (MGI Ref ID J:22628)
    • motor neuron degeneration
      • exhibit pronounced loss of large spinal motorneurons, with remaining motorneurons showing pyknosis and karyorrhexis   (MGI Ref ID J:22628)
      • exhibit degeneration of a few cortical motorneurons in layer V   (MGI Ref ID J:22628)
  • muscle phenotype
  • abnormal muscle physiology
    • exhibit skeletal muscle hypermetabolism as indicated by increased muscle expression of genes involved in lipid and carbohydrate metabolism   (MGI Ref ID J:91800)
  • muscle degeneration
    • exhibit progressive muscle wasting   (MGI Ref ID J:22628)
  • adipose tissue phenotype
  • abnormal adipose tissue morphology
    • exhibit reduced adipose tissue accumulation   (MGI Ref ID J:91800)
    • abnormal fat pad morphology
      • epididymal and retroperitoneal white adipose tissue is markedly reduced or almost nonexistent in the asymptomatic phase of the disease   (MGI Ref ID J:91800)
    • decreased white adipose tissue amount
      • seen in both asymptomatic and symptomatic homozygotes   (MGI Ref ID J:91800)
  • growth/size/body phenotype
  • decreased body weight
    • body mass and body weight is lower in symptomatic (75 days of age) and early symptomatic (105 days of age) mutants   (MGI Ref ID J:91800)
    • weight loss
      • mice show decrease in body weight compared to controls from 14-16 weeks after birth onwards   (MGI Ref ID J:131028)
  • homeostasis/metabolism phenotype
  • abnormal circulating hormone level   (MGI Ref ID J:91800)
    • decreased circulating insulin level   (MGI Ref ID J:91800)
    • decreased circulating leptin level
      • plasma leptin levels are diminished   (MGI Ref ID J:91800)
    • decreased circulating triiodothyronine level
      • plasma T3 levels are decreased in older early symptomatic (105 days old) mutants   (MGI Ref ID J:91800)
    • increased circulating corticosterone level   (MGI Ref ID J:91800)
  • abnormal energy expenditure
    • exhibit increased energy expenditure at rest   (MGI Ref ID J:91800)
  • abnormal gas homeostasis   (MGI Ref ID J:91800)
    • decreased respiratory quotient
      • respiratory quotient is lower   (MGI Ref ID J:91800)
    • increased oxygen consumption
      • exhibit higher rates of total oxygen consumption   (MGI Ref ID J:91800)
  • abnormal glucose homeostasis
    • fasted homozygotes clear glucose more efficiently than wild-type when injected with glucose   (MGI Ref ID J:91800)
    • fasted mutants incorporate a nonmetabolizable glucose analog in white adipose tissue and skeletal muscle   (MGI Ref ID J:91800)
    • decreased circulating insulin level   (MGI Ref ID J:91800)
    • increased circulating glucose level
      • exhibit a higher fasting glycemia than wild-type, although no differences are seen under normal feeding conditions   (MGI Ref ID J:91800)
  • abnormal lipid homeostasis   (MGI Ref ID J:91800)
    • abnormal glycerol level
      • norepinephrine-stimulated glycerol release is higher in white adipose tissue transplants than in wild-type, indicating an increase of activated lipolysis   (MGI Ref ID J:91800)
    • enhanced lipolysis   (MGI Ref ID J:91800)
    • increased circulating corticosterone level   (MGI Ref ID J:91800)
    • increased circulating ketone body level
      • levels of circulating ketone bodies, an indicator of fatty acid oxidation, increase with age   (MGI Ref ID J:91800)
  • impaired adaptive thermogenesis
    • unable to maintain body temperature when placed under conditions in which adaptive thermogenesis is challenged; show lower rectal temperature than wild-type when fasted for 24 hours or exposed to 4 degrees C   (MGI Ref ID J:91800)

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Tg(Sod1*G86R)M1Jwg/0

        involves: C57BL/6 * FVB/N
  • mortality/aging
  • premature death
    • die between 105 and 140 days of age   (MGI Ref ID J:59356)
  • behavior/neurological phenotype
  • paralysis
    • limb paralysis   (MGI Ref ID J:59356)
  • vision/eye phenotype
  • abnormal eye electrophysiology
    • exposure to constant bright light for 20 days causes a diminution of electroretinographic activity   (MGI Ref ID J:59356)
  • abnormal retinal rod cell outer segment morphology
    • light exposed eyes show shortening of the rod outer segments relative to the rod inner segments   (MGI Ref ID J:59356)
  • retinal photoreceptor degeneration
    • exposure to constant bright light for 20 days causes specific degeneration of photoreceptor cells   (MGI Ref ID J:59356)
  • thin retinal outer nuclear layer
    • light exposed eyes show a decrease in the thickness of the retinal outer nuclear layer due to loss of photoreceptor cells compared to controls   (MGI Ref ID J:59356)
  • nervous system phenotype
  • abnormal retinal rod cell outer segment morphology
    • light exposed eyes show shortening of the rod outer segments relative to the rod inner segments   (MGI Ref ID J:59356)
  • retinal photoreceptor degeneration
    • exposure to constant bright light for 20 days causes specific degeneration of photoreceptor cells   (MGI Ref ID J:59356)
View Research Applications

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

Neurobiology Research
Amyotrophic Lateral Sclerosis (ALS)

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tg(Sod1*G86R)M1Jwg
Allele Name transgene insertion M1, Jon W Gordon
Allele Type Transgenic (random, expressed)
Common Name(s) M1; Tg(Sod1*G85R)M1Jwg; Tg(Sod1-G86R)M1Jwg;
Mutation Made ByDr. Jon Gordon,   Mount Sinai School of Medicine
Strain of OriginFVB/N
Expressed Gene Sod1, superoxide dismutase 1, soluble, mouse, laboratory
Promoter Sod1, superoxide dismutase 1, soluble, mouse, laboratory
Molecular Note The entire mouse Sod1 gene with an engineered point mutation in exon 4 resulting in a glycine to arginine substitution at residue 86 (G86R) was used as the transgene. Mutation G86R corresponds to the SOD1 G86R mutation found in some cases of human amyotrophic lateral sclerosis (ALS) patients. RT-PCR analysis detected expression of the transgene in brain, spinal cord, and other tissues. The missense mutation is a point mutation in exon 4 resulting in a glycine-86 to arginine substitution, which corresponds to amino acid position 86 in the human SOD1 protein. Transgenics exhibit widespread high expression of the transgene and do not exhibit diminished SOD1 activity. . [MGI Ref ID J:22628]
 

Genotyping

Genotyping Information

Genotyping Protocols

Tg(Sod1*G86R)M1Jwg, Pyrosequencing
Tg(Sod1*G86R)M1Jwg, Restriction Enzyme Digest


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Ripps ME; Huntley GW; Hof PR; Morrison JH; Gordon JW. 1995. Transgenic mice expressing an altered murine superoxide dismutase gene provide an animal model of amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A 92(3):689-93. [PubMed: 7846037]  [MGI Ref ID J:22628]

Additional References

Kiaei M; Bush AI; Morrison BM; Morrison JH; Cherny RA; Volitakis I; Beal MF; Gordon JW. 2004. Genetically decreased spinal cord copper concentration prolongs life in a transgenic mouse model of amyotrophic lateral sclerosis. J Neurosci 24(36):7945-50. [PubMed: 15356208]  [MGI Ref ID J:92633]

Tg(Sod1*G86R)M1Jwg related

Audet JN; Gowing G; Julien JP. 2010. Wild-type human SOD1 overexpression does not accelerate motor neuron disease in mice expressing murine Sod1(G86R). Neurobiol Dis 40(1):245-250. [PubMed: 20573565]  [MGI Ref ID J:163019]

Dupuis L; Fergani A; Braunstein KE; Eschbach J; Holl N; Rene F; Gonzalez De Aguilar JL; Zoerner B; Schwalenstocker B; Ludolph AC; Loeffler JP. 2009. Mice with a mutation in the dynein heavy chain 1 gene display sensory neuropathy but lack motor neuron disease. Exp Neurol 215(1):146-52. [PubMed: 18952079]  [MGI Ref ID J:144868]

Dupuis L; Oudart H; Rene F; Gonzalez de Aguilar JL; Loeffler JP. 2004. Evidence for defective energy homeostasis in amyotrophic lateral sclerosis: benefit of a high-energy diet in a transgenic mouse model. Proc Natl Acad Sci U S A 101(30):11159-64. [PubMed: 15263088]  [MGI Ref ID J:91800]

Dupuis L; di Scala F; Rene F; de Tapia M; Oudart H; Pradat PF; Meininger V; Loeffler JP. 2003. Up-regulation of mitochondrial uncoupling protein 3 reveals an early muscular metabolic defect in amyotrophic lateral sclerosis. FASEB J 17(14):2091-3. [PubMed: 14500553]  [MGI Ref ID J:127918]

Fergani A; Oudart H; Gonzalez De Aguilar JL; Fricker B; Rene F; Hocquette JF; Meininger V; Dupuis L; Loeffler JP. 2007. Increased peripheral lipid clearance in an animal model of amyotrophic lateral sclerosis. J Lipid Res 48(7):1571-80. [PubMed: 17438338]  [MGI Ref ID J:122493]

Gonzalez de Aguilar JL; Gordon JW; Rene F; de Tapia M; Lutz-Bucher B; Gaiddon C; Loeffler JP. 2000. Alteration of the bcl-x/Bax ratio in a transgenic mouse model of amyotrophic lateral sclerosis: evidence for the implication of the p53 signaling pathway Neurobiol Dis 7(4):406-15. [PubMed: 10964611]  [MGI Ref ID J:64355]

Halter B; Gonzalez de Aguilar JL; Rene F; Petri S; Fricker B; Echaniz-Laguna A; Dupuis L; Larmet Y; Loeffler JP. 2010. Oxidative stress in skeletal muscle stimulates early expression of Rad in a mouse model of amyotrophic lateral sclerosis. Free Radic Biol Med 48(7):915-23. [PubMed: 20079427]  [MGI Ref ID J:158020]

Hetz C; Lee AH; Gonzalez-Romero D; Thielen P; Castilla J; Soto C; Glimcher LH. 2008. Unfolded protein response transcription factor XBP-1 does not influence prion replication or pathogenesis. Proc Natl Acad Sci U S A 105(2):757-62. [PubMed: 18178615]  [MGI Ref ID J:131028]

Hetz C; Thielen P; Matus S; Nassif M; Court F; Kiffin R; Martinez G; Cuervo AM; Brown RH; Glimcher LH. 2009. XBP-1 deficiency in the nervous system protects against amyotrophic lateral sclerosis by increasing autophagy. Genes Dev 23(19):2294-306. [PubMed: 19762508]  [MGI Ref ID J:153047]

Hussain G; Schmitt F; Henriques A; Lequeu T; Rene F; Bindler F; Dirrig-Grosch S; Oudart H; Palamiuc L; Metz-Boutigue MH; Dupuis L; Marchioni E; Gonzalez De Aguilar JL; Loeffler JP. 2013. Systemic down-regulation of delta-9 desaturase promotes muscle oxidative metabolism and accelerates muscle function recovery following nerve injury. PLoS One 8(6):e64525. [PubMed: 23785402]  [MGI Ref ID J:204219]

Jokic N; Gonzalez de Aguilar JL; Dimou L; Lin S; Fergani A; Ruegg MA; Schwab ME; Dupuis L; Loeffler JP. 2006. The neurite outgrowth inhibitor Nogo-A promotes denervation in an amyotrophic lateral sclerosis model. EMBO Rep 7(11):1162-7. [PubMed: 17039253]  [MGI Ref ID J:116078]

Kao TJ; Palmesino E; Kania A. 2009. SRC family kinases are required for limb trajectory selection by spinal motor axons. J Neurosci 29(17):5690-700. [PubMed: 19403835]  [MGI Ref ID J:148253]

Karch CM; Borchelt DR. 2008. A limited role for disulfide cross-linking in the aggregation of mutant SOD1 linked to familial amyotrophic lateral sclerosis. J Biol Chem 283(20):13528-37. [PubMed: 18316367]  [MGI Ref ID J:137090]

Kariya S; Re DB; Jacquier A; Nelson K; Przedborski S; Monani UR. 2012. Mutant superoxide dismutase 1 (SOD1), a cause of amyotrophic lateral sclerosis, disrupts the recruitment of SMN, the spinal muscular atrophy protein to nuclear Cajal bodies. Hum Mol Genet 21(15):3421-34. [PubMed: 22581780]  [MGI Ref ID J:185362]

Kiaei M; Bush AI; Morrison BM; Morrison JH; Cherny RA; Volitakis I; Beal MF; Gordon JW. 2004. Genetically decreased spinal cord copper concentration prolongs life in a transgenic mouse model of amyotrophic lateral sclerosis. J Neurosci 24(36):7945-50. [PubMed: 15356208]  [MGI Ref ID J:92633]

Kunst CB; Messer L; Gordon J; Haines J; Patterson D. 2000. Genetic mapping of a mouse modifier gene that can prevent ALS onset Genomics 70(2):181-9. [PubMed: 11112346]  [MGI Ref ID J:66226]

Matus S; Lopez E; Valenzuela V; Nassif M; Hetz C. 2013. Functional contribution of the transcription factor ATF4 to the pathogenesis of amyotrophic lateral sclerosis. PLoS One 8(7):e66672. [PubMed: 23874395]  [MGI Ref ID J:204414]

Milane A; Fernandez C; Dupuis L; Buyse M; Loeffler JP; Farinotti R; Meininger V; Bensimon G. 2010. P-glycoprotein expression and function are increased in an animal model of amyotrophic lateral sclerosis. Neurosci Lett 472(3):166-70. [PubMed: 20138122]  [MGI Ref ID J:159919]

Mittag TW; Bayer AU; La VAIL MM. 1999. Light-induced retinal damage in mice carrying a mutated SOD I gene. Exp Eye Res 69(6):677-83. [PubMed: 10620397]  [MGI Ref ID J:59356]

Nimchinsky EA; Young WG; Yeung G; Shah RA; Gordon JW; Bloom FE; Morrison JH; Hof PR. 2000. Differential vulnerability of oculomotor, facial, and hypoglossal nuclei in G86R superoxide dismutase transgenic mice. J Comp Neurol 416(1):112-25. [PubMed: 10578106]  [MGI Ref ID J:58733]

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 is maintained as a hemizgyote. The Donating Investigator reports that female transgenic mice have reduced fertility, small litters and poor milk production.

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.

Control Information

  Control
   Noncarrier
   001800 FVB/NJ
 
  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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