Strain Name:

B6(Cg)-Htra2mnd2/J

Stock Number:

004608

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Availability:

Cryopreserved - Ready for recovery

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 STOCK Htra2mnd2/J    (Changed: 14-DEC-05 )
STOCK Prss25mnd2/J    (Changed: 06-SEP-05 )
STOCK mnd2/J    (Changed: 15-DEC-04 )
Type Mutant Stock; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse

Description
Mice homozygous for the recessive Htra2mnd2 mutation have a basal ganglia disorder initially described as an early onset motor neuron disease. This is first outwardly evident by 21 to 24 days of age as an unsteady gait with extended hind limbs, repetitive movements and episodes of sudden arrests. This progresses to include severe muscle atrophy, hunched posture, increased imbalance, chorea, dystonia, and progressive akinesis. A failure to gain weight becomes evident shortly after the onset of the other symptoms and by 35 days of age wildtype littermates are twice as heavy as the mutants. Body fat is not detectable at necropsy. Both the spleen and the thymus drop from normal weights at 23 days of age to 10% of normal at 30 days of age and the thymic corticomedullary junction is lost. Death usually occurs within two weeks of disease onset, by 40 days of age. The growth retardation is not the primary cause since disease is not delayed by intragastric feeding.

Although the initial assessment of the Htra2mnd2 phenotype described a primary motor neuron disease, it has been characterized subsequently as a basal ganglia disorder. Neurodegeneration is first detected in the striatum around 23 days of age and progresses such that mid-striatum sections at 39 days of age show a loss of approximately 50% of the neurons. Neuronal degeneration that is much less severe is also found after 30 days of age in the N. amygdaloides corticalis, N. subthalamicus, Globus pallidus, claustrum, amygdala, and brain stem, in addition to the motor neuron degeneration found in the spinal cord which led to the initial characterization of motor neuron degeneration. No neurodegeneration is detected in the cerebellum, and myelin staining is normal. Astrogliosis and microgliosis are detected only in the striatum and N. amygdaloides, and progress parallel with neurodegeneration. There is an upregulation of Il1b, Il6, Il10, Il12, Csf1 and Tnfa in the central nervous system, an upregulation of Csf2, Il1b and Tnfa in the lungs, and an upregulation of Il1b and Tnfa in spleen as well. The dying neurons have characteristics consistent with both apoptotic and necrotic death. Transgenic expression of human BCL2 under the control of a neuron-specific enolase promoter fails to prevent disease in Htra2mnd2 homozygotes.

Histochemistry of spinal chords taken from 34-38 day old homozygotes shows that the motoneurons in both the cervical and lumbar regions are swollen, spherical, and show weaker staining with cresyl violet. Abnormal spontaneous activity with fibrillation potentials and positive waves is detected in needle electromyography of hind limb muscles, indicating denervation. However, unlike surgical and other models of denervation, Htra2mnd2 homozygotes do not have an increase in transcription of the acetylcholine receptor alpha subunit in affected muscle. Although motor nerve conduction velocities are normal, indicating normal axon function, the compound muscle action potential amplitudes are less than half of normal.

Development
mnd2 was first identified in the progeny of a transgenic founder. The transgene had been injected into (C3H/HeJ x C57BL/6J)F2 fertilized eggs. The mnd2 mutation was bred away from the transgene through outcrossing to C57BL/6J with progeny testing to identify mnd2 carriers. Carriers were later bred to CAST/Ei and fine mapping of the mnd2 congenic interval showed that this mutation arose in the chromosomal segment from C57BL/6J. More recently this stock was crossed once to C57BL/6J and subsequently crossed once to SJL/J before being intercrossed and then backcrossed 4 times to C57BL/6J. It was then imported into The Jackson Laboratory in February 2005 where it was backcrossed by in vitro fertilization for re-derivation using an N4 heterozygous male and C57BL/6J females. The N5 insipient congenic offspring were then intercrossed.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls

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View Parkinson's Disease Models     (112 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 13, Autosomal Dominant, Susceptibility To; PARK13
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Htra2mnd2/Htra2mnd2

        involves: C57BL/6J
  • behavior/neurological phenotype
  • abnormal behavior
    • neural phenotype is stated to be identical to that of Hax1 tm1Jni homozygotes; however no data are presented   (MGI Ref ID J:132627)
  • nervous system phenotype
  • abnormal nervous system morphology   (MGI Ref ID J:132627)
  • immune system phenotype
  • abnormal immune system morphology
    • loss of lymphocytes is stated to be identical to that of Hax1 tm1Jni homozygotes, and shows greater severity than Hax1 homozygotes   (MGI Ref ID J:132627)
    • decreased double-positive T cell number   (MGI Ref ID J:132627)
    • decreased pre-B cell number   (MGI Ref ID J:132627)
    • decreased pro-B cell number   (MGI Ref ID J:132627)
    • decreased single-positive T cell number   (MGI Ref ID J:132627)
  • hematopoietic system phenotype
  • abnormal bone marrow cell morphology/development   (MGI Ref ID J:132627)
  • decreased double-positive T cell number   (MGI Ref ID J:132627)
  • decreased pre-B cell number   (MGI Ref ID J:132627)
  • decreased pro-B cell number   (MGI Ref ID J:132627)
  • decreased single-positive T cell number   (MGI Ref ID J:132627)

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

Htra2mnd2/Htra2mnd2

        involves: C3H/He * C57BL/6J
  • mortality/aging
  • premature death
    • animals die within two weeks of onset, usually prior to 40 days of age   (MGI Ref ID J:12780)
  • behavior/neurological phenotype
  • abnormal gait
    • affected animals between 21 and 24 days of age walk with an unsteady gait with extended hind limbs, as if they are walking on tiptoe.   (MGI Ref ID J:12780)
  • hunched posture   (MGI Ref ID J:12780)
  • hypoactivity
    • resulting from the continued atrophy of the hind leg muscle   (MGI Ref ID J:12780)
  • impaired balance
    • caused by atrophy of the hind leg muscle   (MGI Ref ID J:12780)
  • growth/size/body phenotype
  • postnatal growth retardation
    • during disease progression mice fail to gain weight; and their growth falls significantly behind that of unaffected littermates   (MGI Ref ID J:12780)
  • muscle phenotype
  • dystrophic muscle
    • continued atrophy of the hind leg muscle results in a hunched posture, loss of balance, difficulty in recovering from a reclining position, and decline in mobility   (MGI Ref ID J:12780)

Htra2mnd2/Htra2mnd2

        involves: C3H/HeJ * C57BL/6J * CAST/Ei
  • mortality/aging
  • premature death
    • mice die within 2 weeks of onset, usually prior to 40 days of age   (MGI Ref ID J:12780)
  • adipose tissue phenotype
  • decreased total body fat amount
    • no body fat was detected on necropsy   (MGI Ref ID J:50420)
  • behavior/neurological phenotype
  • abnormal gait
    • unsteady gait apparent by 2-3 weeks of age   (MGI Ref ID J:50420)
  • hunched posture
    • in later stages of disease   (MGI Ref ID J:50420)
  • impaired balance
    • apparent by 2-3 weeks of age   (MGI Ref ID J:50420)
  • seizures
    • increased frequency of generalized seizures in later stages of disease   (MGI Ref ID J:50420)
  • growth/size/body phenotype
  • decreased total body fat amount
    • no body fat was detected on necropsy   (MGI Ref ID J:50420)
  • postnatal growth retardation
    • wasted appearance by 2-3 weeks of age   (MGI Ref ID J:50420)
  • hematopoietic system phenotype
  • abnormal thymus morphology
    • significant regression of lymphoid cells at 30 days of age, although specific classes of cells were present in normal frequencies   (MGI Ref ID J:12780)
  • spleen atrophy
    • atrophy of both lymphoid and hematopoetic tissue in spleen by 30 days of age   (MGI Ref ID J:12780)
    • positive cells were present in normal frequencies for all antigens examined   (MGI Ref ID J:12780)
  • immune system phenotype
  • abnormal thymus morphology
    • significant regression of lymphoid cells at 30 days of age, although specific classes of cells were present in normal frequencies   (MGI Ref ID J:12780)
  • spleen atrophy
    • atrophy of both lymphoid and hematopoetic tissue in spleen by 30 days of age   (MGI Ref ID J:12780)
    • positive cells were present in normal frequencies for all antigens examined   (MGI Ref ID J:12780)
  • muscle phenotype
  • muscular atrophy
    • in later stages of disease   (MGI Ref ID J:50420)
  • nervous system phenotype
  • abnormal action potential
    • abnormal spontaneous activity in sciatic-tibial innervated hind limb muscle, consisting of fibrillation potentials and positive waves   (MGI Ref ID J:12780)
  • abnormal spinal cord morphology
    • while the degree of cellularity in the spinal cord appeared normal, motoneurons in cervical and lumbar regions of the spinal cord were swollen and stained weakly for myelin   (MGI Ref ID J:12780)
  • seizures
    • increased frequency of generalized seizures in later stages of disease   (MGI Ref ID J:50420)
  • endocrine/exocrine gland phenotype
  • abnormal thymus morphology
    • significant regression of lymphoid cells at 30 days of age, although specific classes of cells were present in normal frequencies   (MGI Ref ID J:12780)

Htra2mnd2/Htra2mnd2

        B6.Cg-Htra2mnd2
  • behavior/neurological phenotype
  • akinesia
    • increasingly evident by 26 days of age, complete by 30-35 days of age   (MGI Ref ID J:76481)
  • bradykinesia
    • episodes of sudden arrest begin around 3 weeks of age   (MGI Ref ID J:76481)
    • increasingly frequent episodes of random, involuntary movements by 26 days of age   (MGI Ref ID J:76481)
  • dystonia
    • by 26 days of age, demonstrated as abnormal stretching of the limbs   (MGI Ref ID J:76481)
  • impaired balance
    • severe balancing problems begin around 3 weeks of age   (MGI Ref ID J:76481)
  • increased stereotypic behavior
    • repetitive movements begin around 3 weeks of age   (MGI Ref ID J:76481)
  • growth/size/body phenotype
  • postnatal growth retardation
    • mice did not gain weight after day 20, and by day 35, their weight was less than half that of unaffected littermates   (MGI Ref ID J:76481)
  • immune system phenotype
  • abnormal interleukin level
    • mice have elevated expression of Il1b, Il6, Il10, Il12 in the CNS, with highest expression in regions that exhibit neurodegeneration   (MGI Ref ID J:76481)
  • abnormal tumor necrosis factor level
    • mice have elevated expression of Tnf in the CNS, with highest expression in regions that exhibit neurodegeneration   (MGI Ref ID J:76481)
  • muscle phenotype
  • dystonia
    • by 26 days of age, demonstrated as abnormal stretching of the limbs   (MGI Ref ID J:76481)
  • muscle spasm
    • increased frequency of episodes of sudden involuntary limb movements by 26 days of age   (MGI Ref ID J:76481)
  • nervous system phenotype
  • abnormal astrocyte morphology   (MGI Ref ID J:76481)
  • abnormal brain morphology   (MGI Ref ID J:76481)
  • gliosis
    • astrogliosis and microglia activation in the striatum at 23 days of age   (MGI Ref ID J:76481)
    • in the N. amygdaloides corticalis, astrogliosis beginning at 26 days and microglia activation beginning at 31 days   (MGI Ref ID J:76481)
    • gliosis of cervical spinal cord motoneurons after day 30   (MGI Ref ID J:76481)
  • neurodegeneration
    • coronal sections from mice between the ages of 20 to 40 days showed progressive neurodegeneration, with the most extensive degeneration in the striatal neurons beginning around 23 days   (MGI Ref ID J:76481)
    • ~50% reduction in midstriatal neurons at 39 days of age   (MGI Ref ID J:76481)
    • clumps of chromatin exhibited a "bulls eye profile" in striatal neurodegeneration at 39 days   (MGI Ref ID J:76481)
    • laddering degradation of striatal DNA at 23 days and 39 days   (MGI Ref ID J:76481)
    • nuclear morphology of affected neurons showed characteristics of apoptosis   (MGI Ref ID J:76481)
    • cytoplasmic vacuoles and early disintegration of mitochondria in degenerating striatal neurons   (MGI Ref ID J:76481)
    • neuronal cell death was not detected in the cerebellum   (MGI Ref ID J:76481)
    • transgenic overexpression of human BCL2 in neurons did not prevent striatal cell loss   (MGI Ref ID J:76481)
    • motor neuron degeneration
      • sporadic degeneration and gliosis of cervical spinal cord motoneurons were observed after day 30   (MGI Ref ID J:76481)
  • homeostasis/metabolism phenotype
  • abnormal interleukin level
    • mice have elevated expression of Il1b, Il6, Il10, Il12 in the CNS, with highest expression in regions that exhibit neurodegeneration   (MGI Ref ID J:76481)
  • abnormal tumor necrosis factor level
    • mice have elevated expression of Tnf in the CNS, with highest expression in regions that exhibit neurodegeneration   (MGI Ref ID J:76481)
View Research Applications

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

Neurobiology Research
Parkinson's Disease
      Htra2 (PARK13) mutants

Htra2mnd2 related

Immunology, Inflammation and Autoimmunity Research
Lymphoid Tissue Defects

Internal/Organ Research
Lymphoid Tissue Defects
Spleen Defects
Thymus Defects

Neurobiology Research
Ataxia (Movement) Defects
Neurodegeneration
Parkinson's Disease

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Htra2mnd2
Allele Name motor neuron degeneration 2
Allele Type Spontaneous
Common Name(s) mnd2;
Strain of OriginC57BL/6J
Gene Symbol and Name Htra2, HtrA serine peptidase 2
Chromosome 6
Gene Common Name(s) AI481710; OMI; PARK13; PRSS25; Prss25; expressed sequence AI481710; mnd2; motor neuron degeneration 2; protease, serine, 25;
Molecular Note The mutation in the mnd2 mouse has been identified as an A to T transversion that predicts a Ser276Cys change in the protease domain of the protein. This mutation has no effect on mRNA or protein concentrations. However, enzyme assays reveal that the serine protease activity of this protein is lost. [MGI Ref ID J:85268]

Genotyping

Genotyping Information

Genotyping Protocols

Htra2mnd2, Restriction Enzyme Digest


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Jones JM; Albin RL; Feldman EL; Simin K; Schuster TG; Dunnick WA; Collins JT; Chrisp CE; Taylor BA; Meisler MH. 1993. mnd2: a new mouse model of inherited motor neuron disease. Genomics 16(3):669-77. [PubMed: 8325640]  [MGI Ref ID J:12780]

Additional References

Rathke-Hartlieb S; Schlomann U; Heimann P; Meisler MH; Jockusch H; Bartsch JW. 2002. Progressive loss of striatal neurons causes motor dysfunction in MND2 mutant mice and is not prevented by Bcl-2. Exp Neurol 175(1):87-97. [PubMed: 12009762]  [MGI Ref ID J:76481]

Htra2mnd2 related

Chao JR; Parganas E; Boyd K; Hong CY; Opferman JT; Ihle JN. 2008. Hax1-mediated processing of HtrA2 by Parl allows survival of lymphocytes and neurons. Nature 452(7183):98-102. [PubMed: 18288109]  [MGI Ref ID J:132627]

Goo HG; Jung MK; Han SS; Rhim H; Kang S. 2013. HtrA2/Omi deficiency causes damage and mutation of mitochondrial DNA. Biochim Biophys Acta 1833(8):1866-75. [PubMed: 23542127]  [MGI Ref ID J:202412]

Ideguchi K; Shimizu S; Okumura M; Tsujimoto Y. 2010. Cyclophilin D-dependent mitochondrial permeability transition is not involved in neurodegeneration in mnd2 mutant mice. Biochem Biophys Res Commun 393(2):264-7. [PubMed: 20123086]  [MGI Ref ID J:158830]

Jang W; Hua A; Spilson SV; Miller W; Roe BA; Meisler MH. 1999. Comparative sequence of human and mouse BAC clones from the mnd2 region of chromosome 2p13. Genome Res 9(1):53-61. [PubMed: 9927484]  [MGI Ref ID J:52798]

Jones JM; Datta P; Srinivasula SM; Ji W; Gupta S; Zhang Z; Davies E; Hajnoczky G; Saunders TL; Van Keuren ML; Fernandes-Alnemri T; Alnemri ES; Meisler MH. 2003. Loss of Omi mitochondrial protease activity causes the neuromuscular disorder of mnd2 mutant mice. Nature 425(6959):721-7. [PubMed: 14534547]  [MGI Ref ID J:85268]

Kang S; Louboutin JP; Datta P; Landel CP; Martinez D; Zervos AS; Strayer DS; Fernandes-Alnemri T; Alnemri ES. 2013. Loss of HtrA2/Omi activity in non-neuronal tissues of adult mice causes premature aging. Cell Death Differ 20(2):259-69. [PubMed: 22976834]  [MGI Ref ID J:205541]

Li B; Hu Q; Wang H; Man N; Ren H; Wen L; Nukina N; Fei E; Wang G. 2010. Omi/HtrA2 is a positive regulator of autophagy that facilitates the degradation of mutant proteins involved in neurodegenerative diseases. Cell Death Differ 17(11):1773-84. [PubMed: 20467442]  [MGI Ref ID J:186355]

Liu ML; Liu MJ; Shen YF; Ryu H; Kim HJ; Klupsch K; Downward J; Hong ST. 2009. Omi is a mammalian heat-shock protein that selectively binds and detoxifies oligomeric amyloid-beta. J Cell Sci 122(Pt 11):1917-26. [PubMed: 19435805]  [MGI Ref ID J:150584]

Rathke-Hartlieb S; Budde P; Ewert S; Schlomann U; Staege MS; Jockusch H; Bartsch JW; Frey J. 2000. Elevated expression of membrane type 1 metalloproteinase (MT1-MMP) in reactive astrocytes following neurodegeneration in mouse central nervous system. FEBS Lett 481(3):227-34. [PubMed: 11007969]  [MGI Ref ID J:115115]

Rathke-Hartlieb S; Schlomann U; Heimann P; Meisler MH; Jockusch H; Bartsch JW. 2002. Progressive loss of striatal neurons causes motor dysfunction in MND2 mutant mice and is not prevented by Bcl-2. Exp Neurol 175(1):87-97. [PubMed: 12009762]  [MGI Ref ID J:76481]

Strauss KM; Martins LM; Plun-Favreau H; Marx FP; Kautzmann S; Berg D; Gasser T; Wszolek Z; Muller T; Bornemann A; Wolburg H; Downward J; Riess O; Schulz JB; Kruger R. 2005. Loss of function mutations in the gene encoding Omi/HtrA2 in Parkinson's disease. Hum Mol Genet 14(15):2099-111. [PubMed: 15961413]  [MGI Ref ID J:125616]

Weber JS; Jang W; Simin K; Lu W; Yu J; Meisler MH. 1998. High-resolution genetic, physical, and transcript map of the mnd2 region of mouse chromosome 6. Genomics 54(1):107-15. [PubMed: 9806835]  [MGI Ref ID J:50420]

Yoshida T; Mizuta T; Shimizu S. 2010. Neurodegeneration in mnd2 mutant mice is not prevented by parkin transgene. Biochem Biophys Res Commun 402(4):676-9. [PubMed: 20971077]  [MGI Ref ID J:167568]

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 & HusbandryHomozygotes die between 3-4 weeks of age and are not available for distribution.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2140.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2782.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

General Supply Notes

  • View the complete collection of spontaneous mutants in the Mouse Mutant Resource.

Control Information

  Control
   Wild-type from the colony
 
  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


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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