Strain Name:

B6;129X1-Sncatm1Rosl/J

Stock Number:

003692

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Homozygous null mice suffer from a reduction in total striatal dopamine and exhibit an attenuated locomotor response when given amphetamine. Observed phenotype suggests that Snca is an activity-dependent negative regulator of dopamine neurotransmission. These mice may be useful in studies relating to Parkinson's disease.

Description

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHomozygote x Homozygote         (Female x Male)   26-DEC-06
Specieslaboratory mouse
Generation[F8p]+F14 (11-DEC-13)
Generation Definitions
 
Donating InvestigatorDr. Arnon Rosenthal,   Rinat Neuroscience Corporation

Description
Homozygous null mice are viable, fertile, normal in size and do not display any gross abnormalities. No gene product (mRNA or protein) is detected in brain tissue. A wild-type complement of dopamine neurons, fibers and synaptic terminals is present and the overall brain architecture appears to be intact. They suffer from a reduction in total striatal dopamine and exhibit an attenuated locomotor response when given amphetamine. Normal dopamine release is observed upon stimulation of the nigrostriatal terminal with a single electrical pulse. When multiple stimuli are applied however, null mice exhibit an accelerated recovery of dopamine release. A similar acceleration is seen in wildtype mice in the presence of increased extracellular calcium. The phenotype observed in homozygous Snca-null mice suggests that Snca is an activity-dependent negative regulator of dopamine neurotransmission.

Development
A targeting vector containing a neomycin resistance gene driven by a phosphoglycerate 1 promoter was used to disrupt Snca exons 1-2 in RW-4 embryonic stem (ES) cells. These two exons encode amino acids 1-41. Correctly targeted ES cells were injected into C57BL/6 blastocysts and chimeric animals were obtained.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls

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View Parkinson's Disease Models     (112 strains)

View Strains carrying other alleles of Snca     (6 strains)

Additional Web Information

Visit the Parkinson's Disease Resource site for helpful information on Parkinson's and research resources.

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).
Parkinson Disease 1, Autosomal Dominant; PARK1
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Dementia, Lewy Body; DLB   (SNCA)
Parkinson Disease 4, Autosomal Dominant; PARK4   (SNCA)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Sncatm1Rosl/Sncatm1Rosl

        involves: 129X1/SvJ * C57BL/6
  • nervous system phenotype
  • abnormal dopaminergic neuron morphology
    • when exposed to paired electrical stimuli, striatal brain slices (containing dopamine terminals) from homozygous mice exhibit a faster dopamine release recovery as compared to wild-type   (MGI Ref ID J:60151)
    • dopamine discharge and reuptake in response to a single electrical pulse or a train of pulses is comparable to wild-type   (MGI Ref ID J:60151)
  • decreased dopamine level
    • dopamine content is reduced by 18% in the striatum, however, dopamine content in the ventral midbrain and nucleus accumbens is similar to wild-type   (MGI Ref ID J:60151)
  • behavior/neurological phenotype
  • abnormal locomotor activation
    • homozygous mice exhibit an attenuated locomotor response after administration of amphetamine as compared to wild-type   (MGI Ref ID J:60151)
    • in the absence of amphetamine, locomotor activity in the open field test is comparable to wild-type   (MGI Ref ID J:60151)
  • homeostasis/metabolism phenotype
  • decreased dopamine level
    • dopamine content is reduced by 18% in the striatum, however, dopamine content in the ventral midbrain and nucleus accumbens is similar to wild-type   (MGI Ref ID J:60151)

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

Sncatm1Rosl/Sncatm1Rosl

        involves: 129X1/SvJ
  • immune system phenotype
  • decreased susceptibility to bacterial infection
    • mice do not exhibit as much dopamine neuron loss following injection of LPS into the substantia nigra as similarly treated wild-type mice   (MGI Ref ID J:138194)

Sncatm1Rosl/Sncatm1Rosl

        B6.129X1-Sncatm1Rosl
  • nervous system phenotype
  • *normal* nervous system phenotype
    • at P2, homozygotes display normal numbers of sensory neurons in trigeminal ganglia and L6 lumbar dorsal root ganglia relative to wild-type controls   (MGI Ref ID J:86439)
    • homozygotes exhibit normal morphology and numbers of myelinated A-fibers and unmyelinated C-fibers in adult saphenous nerves relative to wild-type controls   (MGI Ref ID J:86439)
    • in culture, neurons from P2 peripheral (trigeminal and superior cervical) ganglia of mutant mice display the same survival rate as wild-type neurons in the presence of nerve growth factor and, as expected, fail to survive in its absence   (MGI Ref ID J:86439)
    • homozygotes display no gross abnormalities of the nervous system relative to wild-type controls   (MGI Ref ID J:92213)
    • no significant differences in dopamine or its metabolite (DOPAC, 5-HIAA and HVA) levels are noted in the striatum at 9 months of age   (MGI Ref ID J:92213)
    • decreased dopaminergic neuron number
      • adult homozygotes show a ~20% reduction in the number of tyrosine hydroxylase (TH)-positive dopaminergic neurons in substantia nigra pars compacta (SNpc) but not in ventral tegmental area (VTA) relative to wild-type controls, similar to that observed in adult Sncgtm1Vlb homozygotes   (MGI Ref ID J:92213)
      • however, no significant decrease in the number of TH-positive dopaminergic neurons is observed in SNpc after methyl-phenyl-tetrahydropyridine (MPTP) treatment relative to controls   (MGI Ref ID J:92213)
    • decreased susceptibility to dopaminergic neuron neurotoxicity
      • homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity   (MGI Ref ID J:92213)
  • homeostasis/metabolism phenotype
  • decreased susceptibility to dopaminergic neuron neurotoxicity
    • homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity   (MGI Ref ID J:92213)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • homozygotes are behaviorally normal and show no detectable motor dysfunction in either constant speed or accelerating rotarod tests   (MGI Ref ID J:92213)
  • cellular phenotype
  • decreased susceptibility to dopaminergic neuron neurotoxicity
    • homozygotes display resistance of SNpc dopaminergic neurons to MPTP neurotoxicity   (MGI Ref ID J:92213)
View Research Applications

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

Neurobiology Research
Parkinson's Disease
      resistance to MPTP
      synuclein mutants

Sncatm1Rosl related

Neurobiology Research
Astrocyte Defects
Behavioral and Learning Defects
Neurodegeneration
Neurotransmitter Receptor and Synaptic Vesicle Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Sncatm1Rosl
Allele Name targeted mutation 1, Arnon Rosenthal
Allele Type Targeted (knock-out)
Common Name(s) alpha-Syn-; alpha-Synko;
Strain of Origin129X1/SvJ
ES Cell Line NameRW-4
ES Cell Line Strain129X1/SvJ
Gene Symbol and Name Snca, synuclein, alpha
Chromosome 6
Gene Common Name(s) NACP; PARK1; PARK4; PD1; alpha-synuclein; alphaSYN;
Molecular Note A PGK-neo cassette was used to delete exons 1 and 2, encoding amino acids 1 through 41 as well as a 5' untranslated region. RT-PCR analysis of extracts from the brains of homozygous mutant mice, using probes for both the deleted 5' region as well the untargeted 3' region, showed an absence of transcript. Western blot analysis, immunohistochemical analysis, and in situ hybridization confirmed a lack of encoded protein in homozygous mutant mice. [MGI Ref ID J:60151]

Genotyping

Genotyping Information

Genotyping Protocols

Sncatm1Rosl,

SEPARATED MELT


Sncatm1Rosl, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Abeliovich A; Schmitz Y; Farinas I; Choi-Lundberg D; Ho WH; Castillo PE; Shinsky N; Verdugo JM; Armanini M; Ryan A; Hynes M; Phillips H; Sulzer D; Rosenthal A. 2000. Mice lacking alpha-synuclein display functional deficits in the nigrostriatal dopamine system. Neuron 25(1):239-52. [PubMed: 10707987]  [MGI Ref ID J:60151]

Additional References

Sncatm1Rosl related

Akil O; Weber CM; Park SN; Ninkina N; Buchman V; Lustig LR. 2008. Localization of synucleins in the Mammalian cochlea. J Assoc Res Otolaryngol 9(4):452-63. [PubMed: 18665422]  [MGI Ref ID J:141972]

Al-Wandi A; Ninkina N; Millership S; Williamson SJ; Jones PA; Buchman VL. 2010. Absence of alpha-synuclein affects dopamine metabolism and synaptic markers in the striatum of aging mice. Neurobiol Aging 31(5):796-804. [PubMed: 19097673]  [MGI Ref ID J:159589]

Alvarez-Fischer D; Henze C; Strenzke C; Westrich J; Ferger B; Hoglinger GU; Oertel WH; Hartmann A. 2008. Characterization of the striatal 6-OHDA model of Parkinson's disease in wild type and alpha-synuclein-deleted mice. Exp Neurol 210(1):182-93. [PubMed: 18053987]  [MGI Ref ID J:134020]

Anwar S; Peters O; Millership S; Ninkina N; Doig N; Connor-Robson N; Threlfell S; Kooner G; Deacon RM; Bannerman DM; Bolam JP; Chandra SS; Cragg SJ; Wade-Martins R; Buchman VL. 2011. Functional alterations to the nigrostriatal system in mice lacking all three members of the synuclein family. J Neurosci 31(20):7264-74. [PubMed: 21593311]  [MGI Ref ID J:173360]

Cano-Jaimez M; Perez-Sanchez F; Milan M; Buendia P; Ambrosio S; Farinas I. 2010. Vulnerability of peripheral catecholaminergic neurons to MPTP is not regulated by alpha-synuclein. Neurobiol Dis 38(1):92-103. [PubMed: 20079841]  [MGI Ref ID J:159933]

Chadchankar H; Ihalainen J; Tanila H; Yavich L. 2011. Decreased reuptake of dopamine in the dorsal striatum in the absence of alpha-synuclein. Brain Res 1382:37-44. [PubMed: 21276428]  [MGI Ref ID J:170114]

Chadchankar H; Yavich L. 2011. Sub-regional differences and mechanisms of the short-term plasticity of dopamine overflow in striatum in mice lacking alpha-synuclein. Brain Res 1423:67-76. [PubMed: 22000591]  [MGI Ref ID J:179023]

Duka T; Rusnak M; Drolet RE; Duka V; Wersinger C; Goudreau JL; Sidhu A. 2006. Alpha-synuclein induces hyperphosphorylation of Tau in the MPTP model of parkinsonism. FASEB J 20(13):2302-12. [PubMed: 17077307]  [MGI Ref ID J:129746]

Ebadi M; Sharma S. 2006. Metallothioneins 1 and 2 attenuate peroxynitrite-induced oxidative stress in Parkinson disease. Exp Biol Med (Maywood) 231(9):1576-83. [PubMed: 17018883]  [MGI Ref ID J:129277]

Gao HM; Kotzbauer PT; Uryu K; Leight S; Trojanowski JQ; Lee VM. 2008. Neuroinflammation and oxidation/nitration of alpha-synuclein linked to dopaminergic neurodegeneration. J Neurosci 28(30):7687-98. [PubMed: 18650345]  [MGI Ref ID J:138194]

Garcia-Reitboeck P; Anichtchik O; Dalley JW; Ninkina N; Tofaris GK; Buchman VL; Spillantini MG. 2013. Endogenous alpha-synuclein influences the number of dopaminergic neurons in mouse substantia nigra. Exp Neurol 248:541-5. [PubMed: 23933574]  [MGI Ref ID J:203866]

Geng X; Lou H; Wang J; Li L; Swanson AL; Sun M; Beers-Stolz D; Watkins S; Perez RG; Drain P. 2011. alpha-Synuclein binds the K(ATP) channel at insulin-secretory granules and inhibits insulin secretion. Am J Physiol Endocrinol Metab 300(2):E276-86. [PubMed: 20858756]  [MGI Ref ID J:172332]

Janezic S; Threlfell S; Dodson PD; Dowie MJ; Taylor TN; Potgieter D; Parkkinen L; Senior SL; Anwar S; Ryan B; Deltheil T; Kosillo P; Cioroch M; Wagner K; Ansorge O; Bannerman DM; Bolam JP; Magill PJ; Cragg SJ; Wade-Martins R. 2013. Deficits in dopaminergic transmission precede neuron loss and dysfunction in a new Parkinson model. Proc Natl Acad Sci U S A 110(42):E4016-25. [PubMed: 24082145]  [MGI Ref ID J:201991]

Klivenyi P; Siwek D; Gardian G; Yang L; Starkov A; Cleren C; Ferrante RJ; Kowall NW; Abeliovich A; Beal MF. 2006. Mice lacking alpha-synuclein are resistant to mitochondrial toxins. Neurobiol Dis 21(3):541-8. [PubMed: 16298531]  [MGI Ref ID J:106226]

Kokhan VS; Afanasyeva MA; Van'kin GI. 2012. alpha-Synuclein knockout mice have cognitive impairments. Behav Brain Res 231(1):226-30. [PubMed: 22469626]  [MGI Ref ID J:185435]

Lou H; Montoya SE; Alerte TN; Wang J; Wu J; Peng X; Hong CS; Friedrich EE; Mader SA; Pedersen CJ; Marcus BS; McCormack AL; Di Monte DA; Daubner SC; Perez RG. 2010. Serine 129 phosphorylation reduces the ability of alpha-synuclein to regulate tyrosine hydroxylase and protein phosphatase 2A in vitro and in vivo. J Biol Chem 285(23):17648-61. [PubMed: 20356833]  [MGI Ref ID J:164560]

Luk KC; Kehm V; Carroll J; Zhang B; O'Brien P; Trojanowski JQ; Lee VM. 2012. Pathological alpha-synuclein transmission initiates Parkinson-like neurodegeneration in nontransgenic mice. Science 338(6109):949-53. [PubMed: 23161999]  [MGI Ref ID J:191204]

Luk KC; Kehm VM; Zhang B; O'Brien P; Trojanowski JQ; Lee VM. 2012. Intracerebral inoculation of pathological alpha-synuclein initiates a rapidly progressive neurodegenerative alpha-synucleinopathy in mice. J Exp Med 209(5):975-86. [PubMed: 22508839]  [MGI Ref ID J:185142]

Martin ED; Gonzalez-Garcia C; Milan M; Farinas I; Cena V. 2004. Stressor-related impairment of synaptic transmission in hippocampal slices from alpha-synuclein knockout mice. Eur J Neurosci 20(11):3085-91. [PubMed: 15579163]  [MGI Ref ID J:101275]

Martin-Clemente B; Alvarez-Castelao B; Mayo I; Sierra AB; Diaz V; Milan M; Farinas I; Gomez-Isla T; Ferrer I; Castano JG. 2004. alpha-Synuclein expression levels do not significantly affect proteasome function and expression in mice and stably transfected PC12 cell lines. J Biol Chem 279(51):52984-90. [PubMed: 15466467]  [MGI Ref ID J:118517]

Mosharov EV; Larsen KE; Kanter E; Phillips KA; Wilson K; Schmitz Y; Krantz DE; Kobayashi K; Edwards RH; Sulzer D. 2009. Interplay between cytosolic dopamine, calcium, and alpha-synuclein causes selective death of substantia nigra neurons. Neuron 62(2):218-29. [PubMed: 19409267]  [MGI Ref ID J:155071]

Ninkina N; Papachroni K; Robertson DC; Schmidt O; Delaney L; O'Neill F; Court F; Rosenthal A; Fleetwood-Walker SM; Davies AM; Buchman VL. 2003. Neurons expressing the highest levels of gamma-synuclein are unaffected by targeted inactivation of the gene. Mol Cell Biol 23(22):8233-45. [PubMed: 14585981]  [MGI Ref ID J:86439]

Paine SM; Anderson G; Bedford K; Lawler K; Mayer RJ; Lowe J; Bedford L. 2013. Pale body-like inclusion formation and neurodegeneration following depletion of 26S proteasomes in mouse brain neurones are independent of alpha-synuclein. PLoS One 8(1):e54711. [PubMed: 23382946]  [MGI Ref ID J:195914]

Papachroni K; Ninkina N; Wanless J; Kalofoutis AT; Gnuchev NV; Buchman VL. 2005. Peripheral sensory neurons survive in the absence of alpha- and gamma-synucleins. J Mol Neurosci 25(2):157-64. [PubMed: 15784963]  [MGI Ref ID J:121324]

Pelkonen A; Yavich L. 2011. Neuromuscular pathology in mice lacking alpha-synuclein. Neurosci Lett 487(3):350-3. [PubMed: 21029764]  [MGI Ref ID J:168149]

Pena-Oliver Y; Buchman VL; Dalley JW; Robbins TW; Schumann G; Ripley TL; King SL; Stephens DN. 2012. Deletion of alpha-synuclein decreases impulsivity in mice. Genes Brain Behav 11(2):137-46. [PubMed: 22142176]  [MGI Ref ID J:198106]

Rappley I; Myers DS; Milne SB; Ivanova PT; Lavoie MJ; Brown HA; Selkoe DJ. 2009. Lipidomic profiling in mouse brain reveals differences between ages and genders, with smaller changes associated with alpha-synuclein genotype. J Neurochem 111(1):15-25. [PubMed: 19627450]  [MGI Ref ID J:153557]

Reznichenko L; Cheng Q; Nizar K; Gratiy SL; Saisan PA; Rockenstein EM; Gonzalez T; Patrick C; Spencer B; Desplats P; Dale AM; Devor A; Masliah E. 2012. In vivo alterations in calcium buffering capacity in transgenic mouse model of synucleinopathy. J Neurosci 32(29):9992-8. [PubMed: 22815513]  [MGI Ref ID J:186464]

Robertson DC; Schmidt O; Ninkina N; Jones PA; Sharkey J; Buchman VL. 2004. Developmental loss and resistance to MPTP toxicity of dopaminergic neurones in substantia nigra pars compacta of gamma-synuclein, alpha-synuclein and double alpha/gamma-synuclein null mutant mice. J Neurochem 89(5):1126-36. [PubMed: 15147505]  [MGI Ref ID J:92213]

Scott D; Roy S. 2012. alpha-Synuclein Inhibits Intersynaptic Vesicle Mobility and Maintains Recycling-Pool Homeostasis. J Neurosci 32(30):10129-35. [PubMed: 22836248]  [MGI Ref ID J:186545]

Senior SL; Ninkina N; Deacon R; Bannerman D; Buchman VL; Cragg SJ; Wade-Martins R. 2008. Increased striatal dopamine release and hyperdopaminergic-like behaviour in mice lacking both alpha-synuclein and gamma-synuclein. Eur J Neurosci 27(4):947-57. [PubMed: 18333965]  [MGI Ref ID J:132938]

Sharon R; Bar-Joseph I; Mirick GE; Serhan CN; Selkoe DJ. 2003. Altered fatty acid composition of dopaminergic neurons expressing alpha-synuclein and human brains with alpha-synucleinopathies. J Biol Chem 278(50):49874-81. [PubMed: 14507911]  [MGI Ref ID J:118570]

Shimshek DR; Schweizer T; Schmid P; van der Putten PH. 2012. Excess alpha-synuclein worsens disease in mice lacking ubiquitin carboxy-terminal hydrolase L1. Sci Rep 2:262. [PubMed: 22355774]  [MGI Ref ID J:207278]

Taylor TN; Potgieter D; Anwar S; Senior SL; Janezic S; Threlfell S; Ryan B; Parkkinen L; Deltheil T; Cioroch M; Livieratos A; Oliver PL; Jennings KA; Davies KE; Ansorge O; Bannerman DM; Cragg SJ; Wade-Martins R. 2013. Region-specific deficits in dopamine, but not norepinephrine, signaling in a novel A30P alpha-synuclein BAC transgenic mouse. Neurobiol Dis 62C:193-207. [PubMed: 24121116]  [MGI Ref ID J:201961]

Tomas-Zapico C; Diez-Zaera M; Ferrer I; Gomez-Ramos P; Moran MA; Miras-Portugal MT; Diaz-Hernandez M; Lucas JJ. 2012. alpha-Synuclein accumulates in huntingtin inclusions but forms independent filaments and its deficiency attenuates early phenotype in a mouse model of Huntington's disease. Hum Mol Genet 21(3):495-510. [PubMed: 22045698]  [MGI Ref ID J:179713]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryThis strain arose on a B6;129X background. It is maintained on a B6;129X background. Coat color expected from breeding:Black or Agouti
Mating SystemHomozygote x Homozygote         (Female x Male)   26-DEC-06
Diet Information LabDiet® 5K52/5K67

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 $195.00Female or MaleHomozygous for Sncatm1Rosl  
Price per Pair (US dollars $)Pair Genotype
$390.00Homozygous for Sncatm1Rosl x Homozygous for Sncatm1Rosl  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $253.50Female or MaleHomozygous for Sncatm1Rosl  
Price per Pair (US dollars $)Pair Genotype
$507.00Homozygous for Sncatm1Rosl x Homozygous for Sncatm1Rosl  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

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
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

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.


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