Strain Name:

B6.129X1-Fostm1Pa/J

Stock Number:

002099

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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

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain 129X1 via PJ1 ES cell line
 
Donating InvestigatorDr. Virginia E. Papaioannou,   Columbia University

Description
Mice homozygous for the Fostm1Pa mutation show reduced placental and fetal weights, lack teeth, and have a significant pre-weaning loss of viability. Survivors grow at a normal rate until about 11 days of age when they begin to develop a severe osteopetrosis. They may live as long as 5-7 months. Homozygous mice have delayed or absent gametogenesis and show lymphopenia. They also exhibit behavioral abnormalities, including hyperactivity and diminished response to external stimuli.

Development
The Fostm1Pa mutant strain was developed in the laboratory of Dr. Virginia E. Papaioannou at Columbia University. The 129-derived PJ5 ES cell line was used. The C57BL/6J strain was produced by backcrossing the Fostm1Pa mutation 5 times (N5) to C57BL/6J inbred mice. The strain is fixed at N5 for distribution. Recovery of homozygous mice at N10 is greatly reduced. Breeder pairs of heterozygous mice at N10 may be purchased as frozen embryos only.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Fostm1Pa allele
002293   B6;129X1-Fostm1Pa/J
View Strains carrying   Fostm1Pa     (1 strain)

View Strains carrying other alleles of Fos     (5 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Fostm1Pa/Fostm1Pa

        involves: 129X1/SvJ * C57BL/6J
  • mortality/aging
  • partial neonatal lethality
    • mutants display significantly reduced viability at birth; 60% of the expected numbers of mutants do not survive past birth   (MGI Ref ID J:3233)
  • premature death
    • 8/44 mutants weaned have died within a few weeks of weaning, showing a rapid decline   (MGI Ref ID J:3233)
  • embryogenesis phenotype
  • decreased placenta weight
    • at E15.5 placental weights are significantly lower than wild-type   (MGI Ref ID J:3233)
  • growth/size phenotype
  • decreased body size
    • at 5 weeks of age homozygotes are runted and less than half the size of wild-type or heterozygous littermates   (MGI Ref ID J:3233)
    • mutants remain ~1/3 to 1/2 the size of control littermates at 7 months of age   (MGI Ref ID J:3233)
    • slow postnatal weight gain
      • by P11 homozygotes begin to lag behind littermates in weight gain; mutants continue to gain weight slowly thereafter   (MGI Ref ID J:3233)
  • decreased fetal weight
    • at E15.5 fetal weights are significantly lower than wild-type   (MGI Ref ID J:64368)
  • endocrine/exocrine gland phenotype
  • abnormal ovarian follicle morphology
    • in adult females, atretic follicles predominate with no follicles more advanced than the antral stages were observed   (MGI Ref ID J:3233)
  • abnormal seminiferous tubule morphology
    • lumen is abnormally large and empty in mutants   (MGI Ref ID J:3233)
  • behavior/neurological phenotype
  • abnormal sexual interaction
    • homozygous males show a longer latency to the first mount and percentage of males mounting is lower than in wild-type   (MGI Ref ID J:18258)
    • mounting rates are lower in male mutants   (MGI Ref ID J:18258)
  • abnormal sleep pattern
    • homozygotes are awake more than wild-type and slept less during the light-on (day cycle) period   (MGI Ref ID J:64368)
    • intervening wake bouts are ~ 2-fold longer than those observed in wild-type   (MGI Ref ID J:64368)
    • after sleep deprivation, mice take longer to fall asleep   (MGI Ref ID J:64368)
    • abnormal frequency of paradoxical sleep
      • null mice have 1/3 fewer numbers of slightly longer REM sleep bouts than wild-type   (MGI Ref ID J:64368)
  • abnormal spatial learning
    • mutants show impairment in the visible platform portion of a Morris water maze test by not swimming directly to the platform by the end of the first day like wild-type do; mutants have longer escape latencies compared to wild-type   (MGI Ref ID J:19202)
    • mutant mice swim more slowly and take longer swim paths than controls in the Morris water maze test   (MGI Ref ID J:19202)
    • in a hidden-platform task one week after visible platform training homozygous mutants show impairment in finding the hidden platform   (MGI Ref ID J:19202)
  • absent startle reflex
    • homozygous mutants do not startle in response to higher frequency stimuli but wild-type and heterozygotes do   (MGI Ref ID J:19202)
  • decreased anxiety-related response
    • mice are less responsive to external stimuli that would induce stress   (MGI Ref ID J:3233)
  • hyperactivity
    • mutants display hyperactivity compared to controls   (MGI Ref ID J:3233)
  • craniofacial phenotype
  • absent teeth   (MGI Ref ID J:3233)
    • homozygous mice lack teeth   (MGI Ref ID J:64368)
  • domed cranium
    • homozygotes have a domed skull   (MGI Ref ID J:3233)
  • failure of tooth eruption
    • homozygotes display a lack of incisor eruption   (MGI Ref ID J:3233)
  • short snout
    • homzygotes have a foreshortened snout   (MGI Ref ID J:3233)
  • skeleton phenotype
  • abnormal long bone morphology
    • at 3 weeks the ends of the long bones are porous   (MGI Ref ID J:3233)
    • abnormal long bone diaphysis morphology
      • the diaphysus medullary cavity contains thick bone trabeculae with trapped chondrocytes and many associated osteoclasts   (MGI Ref ID J:3233)
    • decreased length of long bones
      • long bones are shortened and show increased density   (MGI Ref ID J:3233)
    • disorganized long bone epiphyseal plate
      • there is disorganization at the epiphyseal growth plate and a small ossified marrow cavity   (MGI Ref ID J:3233)
  • domed cranium
    • homozygotes have a domed skull   (MGI Ref ID J:3233)
  • hematopoietic system phenotype
  • abnormal lymphopoiesis
    • levels of circulating lymphocytes in 4/5 mutants is reduced by 75%, compared to wild-type; one animal had higher levels   (MGI Ref ID J:3233)
  • immune system phenotype
  • abnormal lymphopoiesis
    • levels of circulating lymphocytes in 4/5 mutants is reduced by 75%, compared to wild-type; one animal had higher levels   (MGI Ref ID J:3233)
  • limbs/digits/tail phenotype
  • kinked tail
    • animals have slightly kinked tail tips   (MGI Ref ID J:3233)
  • reproductive system phenotype
  • abnormal ovarian follicle morphology
    • in adult females, atretic follicles predominate with no follicles more advanced than the antral stages were observed   (MGI Ref ID J:3233)
  • abnormal seminiferous tubule morphology
    • lumen is abnormally large and empty in mutants   (MGI Ref ID J:3233)
  • abnormal sperm number
    • some mutant males have motile sperm in the epididymis but at lower levels than in wild-type   (MGI Ref ID J:3233)
  • abnormal spermatogenesis
    • in one of two adult males, spermatogenesis was very reduced with some abnormal spermatids but no spermatozoa   (MGI Ref ID J:3233)
  • nervous system phenotype
  • decreased retinal rod cell number
    • the number of rods in mutant mice is decreased by 22-24%   (MGI Ref ID J:60736)
  • vision/eye phenotype
  • abnormal eye electrophysiology
    • mice show a large variability in luminance-response functions of the a-, b- and c-waves with lower mean values   (MGI Ref ID J:60736)
    • curves of luminance-response functions of the a- and b-waves show a shift to the right indicating reduced retinal sensitivity   (MGI Ref ID J:60736)
    • mean values of the latencies of the b-waves are higher compared to control   (MGI Ref ID J:60736)
  • decreased retinal rod cell number
    • the number of rods in mutant mice is decreased by 22-24%   (MGI Ref ID J:60736)
  • thin retinal outer nuclear layer
    • thickness is decreased in the superior and the inferior hemisphere and in the central and peripheral retina   (MGI Ref ID J:60736)
  • hearing/vestibular/ear phenotype
  • impaired hearing
    • results from an acoustic startle test indicate that mutants have impaired hearing   (MGI Ref ID J:19202)
  • tumorigenesis
  • altered tumor morphology
    • TPA induced papillomas in mutants become very dry, elongated and hyperkeratinized whereas in wild-type tumors are vigorous and well vascularized although they eventually develop a similar morphology   (MGI Ref ID J:78834)
    • wild-type papillomas evolve into severely keatinized projections   (MGI Ref ID J:78834)
  • decreased metastatic potential
    • skin tumors in mutants do not become malignant as wild-type tumors do   (MGI Ref ID J:78834)
  • cellular phenotype
  • abnormal lymphopoiesis
    • levels of circulating lymphocytes in 4/5 mutants is reduced by 75%, compared to wild-type; one animal had higher levels   (MGI Ref ID J:3233)
View Research Applications

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

Developmental Biology Research
Skeletal Defects
      osteopetrosis

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency

Internal/Organ Research
Skeleton
      Bone

Reproductive Biology Research
Fertility Defects

Fostm1Pa related

Cancer Research
Oncogenes

Developmental Biology Research
Skeletal Defects

Neurobiology Research
Behavioral and Learning Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Fostm1Pa
Allele Name targeted mutation 1, Virginia E Papaioannou
Allele Type Targeted (knock-out)
Common Name(s) c-fos-;
Mutation Made ByDr. Virginia Papaioannou,   Columbia University
Strain of Origin129X1/SvJ
ES Cell Line NamePJ5
ES Cell Line Strain129X1/SvJ
Gene Symbol and Name Fos, FBJ osteosarcoma oncogene
Chromosome 12
Gene Common Name(s) AP-1; C-FOS; D12Rfj1; DNA segment, Chr 12, Russel F. Jacoby 1; cFos; p55;
Molecular Note Exon 1 was disrupted by the insertion of a neomycin selection cassette. Northern blot analysis showed an absence of transcript in homozygous mutant mice. [MGI Ref ID J:70953]

Genotyping

Genotyping Information

Genotyping Protocols

Fostm1Pa, Standard PCR
NEOTD (Generic Neo), Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Johnson RS; Spiegelman BM; Papaioannou V. 1992. Pleiotropic effects of a null mutation in the c-fos proto-oncogene. Cell 71(4):577-86. [PubMed: 1423615]  [MGI Ref ID J:3233]

Additional References

Hu E; Mueller E; Oliviero S; Papaioannou VE; Johnson R; Spiegelman BM. 1994. Targeted disruption of the c-fos gene demonstrates c-fos-dependent and -independent pathways for gene expression stimulated by growth factors or oncogenes. EMBO J 13(13):3094-103. [PubMed: 8039503]  [MGI Ref ID J:19605]

Jain J; Nalefski EA; McCaffrey PG; Johnson RS; Spiegelman BM; Papaioannou V; Rao A. 1994. Normal peripheral T-cell function in c-Fos-deficient mice. Mol Cell Biol 14(3):1566-74. [PubMed: 8114694]  [MGI Ref ID J:16901]

Paylor R; Johnson RS; Papaioannou V; Spiegelman BM; Wehner JM. 1994. Behavioral assessment of c-fos mutant mice. Brain Res 651(1-2):275-82. [PubMed: 7922576]  [MGI Ref ID J:19202]

Watanabe Y; Johnson RS; Butler LS; Binder DK; Spiegelman BM; Papaioannou VE; McNamara JO. 1996. Null mutation of c-fos impairs structural and functional plasticities in the kindling model of epilepsy. J Neurosci 16(12):3827-36. [PubMed: 8656277]  [MGI Ref ID J:33418]

Fostm1Pa related

Baum MJ; Brown JJ; Kica E; Rubin BS; Johnson RS; Papaioannou VE. 1994. Effect of a null mutation of the c-fos proto-oncogene on sexual behavior of male mice. Biol Reprod 50(5):1040-8. [PubMed: 8025159]  [MGI Ref ID J:18258]

Brown JR; Nigh E; Lee RJ; Ye H; Thompson MA; Saudou F; Pestell RG; Greenberg ME. 1998. Fos family members induce cell cycle entry by activating cyclin D1. Mol Cell Biol 18(9):5609-19. [PubMed: 9710644]  [MGI Ref ID J:111015]

Demiralp B; Chen HL; Koh AJ; Keller ET; McCauley LK. 2002. Anabolic actions of parathyroid hormone during bone growth are dependent on c-fos. Endocrinology 143(10):4038-47. [PubMed: 12239115]  [MGI Ref ID J:109785]

Deng X; Ladenheim B; Tsao LI; Cadet JL. 1999. Null mutation of c-fos causes exacerbation of methamphetamine-induced neurotoxicity. J Neurosci 19(22):10107-15. [PubMed: 10559418]  [MGI Ref ID J:109695]

Erlebacher A; Filvaroff EH; Ye JQ; Derynck R. 1998. Osteoblastic responses to TGF-beta during bone remodeling. Mol Biol Cell 9(7):1903-18. [PubMed: 9658179]  [MGI Ref ID J:134782]

Hafezi F; Abegg M; Grimm C; Wenzel A; Munz K; Sturmer J; Farber DB; Reme CE. 1998. Retinal degeneration in the rd mouse in the absence of c-fos. Invest Ophthalmol Vis Sci 39(12):2239-44. [PubMed: 9804131]  [MGI Ref ID J:112088]

Hobson AH; Donovan M; Humphries MM; Tuohy G; McNally N; Carmody R; Cotter T; Farrar GJ; Kenna PF; Humphries P. 2000. Apoptotic photoreceptor death in the rhodopsin knockout mouse in the presence and absence of c-fos. Exp Eye Res 71(3):247-54. [PubMed: 10973734]  [MGI Ref ID J:64875]

Honrado GI; Johnson RS; Golombek DA; Spiegelman BM; Papaioannou VE; Ralph MR. 1996. The circadian system of c-fos deficient mice. J Comp Physiol [A] 178(4):563-70. [PubMed: 8847666]  [MGI Ref ID J:32773]

Ito Y; Inoue D; Kido S; Matsumoto T. 2005. c-Fos degradation by the ubiquitin-proteasome proteolytic pathway in osteoclast progenitors. Bone 37(6):842-9. [PubMed: 16172035]  [MGI Ref ID J:104516]

Jain J; Nalefski EA; McCaffrey PG; Johnson RS; Spiegelman BM; Papaioannou V; Rao A. 1994. Normal peripheral T-cell function in c-Fos-deficient mice. Mol Cell Biol 14(3):1566-74. [PubMed: 8114694]  [MGI Ref ID J:16901]

Johnson RS; Sheng M; Greenberg ME; Kolodner RD; Papaioannou VE; Spiegelman BM. 1989. Targeting of nonexpressed genes in embryonic stem cells via homologous recombination. Science 245(4923):1234-6. [PubMed: 2506639]  [MGI Ref ID J:70953]

Koh AJ; Demiralp B; Neiva KG; Hooten J; Nohutcu RM; Shim H; Datta NS; Taichman RS; McCauley LK. 2005. Cells of the osteoclast lineage as mediators of the anabolic actions of parathyroid hormone in bone. Endocrinology 146(11):4584-96. [PubMed: 16081645]  [MGI Ref ID J:129838]

Kueng-Hitz N; Grimm C; Lansel N; Hafezi F; He L; Fox DA; Reme CE; Niemeyer G; Wenzel A. 2000. The retina of c-fos-/- mice: electrophysiologic, morphologic and biochemical aspects. Invest Ophthalmol Vis Sci 41(3):909-16. [PubMed: 10711713]  [MGI Ref ID J:60736]

Lackinger D; Kaina B. 2000. Primary mouse fibroblasts deficient for c-Fos, p53 or for both proteins are hypersensitive to UV light and alkylating agent-induced chromosomal breakage and apoptosis. Mutat Res 457(1-2):113-23. [PubMed: 11106803]  [MGI Ref ID J:119048]

Ortega N; Wang K; Ferrara N; Werb Z; Vu TH. 2010. Complementary interplay between matrix metalloproteinase-9, vascular endothelial growth factor and osteoclast function drives endochondral bone formation. Dis Model Mech 3(3-4):224-35. [PubMed: 20142327]  [MGI Ref ID J:160852]

Paylor R; Johnson RS; Papaioannou V; Spiegelman BM; Wehner JM. 1994. Behavioral assessment of c-fos mutant mice. Brain Res 651(1-2):275-82. [PubMed: 7922576]  [MGI Ref ID J:19202]

Roffler-Tarlov S; Brown JJ; Tarlov E; Stolarov J; Chapman DL; Alexiou M; Papaioannou VE. 1996. Programmed cell death in the absence of c-Fos and c-Jun. Development 122(1):1-9. [PubMed: 8565820]  [MGI Ref ID J:30818]

Saez E; Rutberg SE; Mueller E; Oppenheim H; Smoluk J; Yuspa SH; Spiegelman BM. 1995. c-fos is required for malignant progression of skin tumors. Cell 82(5):721-32. [PubMed: 7545543]  [MGI Ref ID J:78834]

Shearman LP; Weaver DR. 1997. Haloperidol regulates neurotensin gene expression in striatum of c-fos-deficient mice. Brain Res Mol Brain Res 47(1-2):275-85. [PubMed: 9221926]  [MGI Ref ID J:41519]

Shiromani PJ; Basheer R; Thakkar J; Wagner D; Greco MA; Charness ME. 2000. Sleep and wakefulness in c-fos and fos B gene knockout mice Brain Res Mol Brain Res 80(1):75-87. [PubMed: 11039731]  [MGI Ref ID J:64368]

Silvestre DC; Gil GA; Tomasini N; Bussolino DF; Caputto BL. 2010. Growth of peripheral and central nervous system tumors is supported by cytoplasmic c-Fos in humans and mice. PLoS One 5(3):e9544. [PubMed: 20209053]  [MGI Ref ID J:158701]

Watanabe Y; Johnson RS; Butler LS; Binder DK; Spiegelman BM; Papaioannou VE; McNamara JO. 1996. Null mutation of c-fos impairs structural and functional plasticities in the kindling model of epilepsy. J Neurosci 16(12):3827-36. [PubMed: 8656277]  [MGI Ref ID J:33418]

Wenzel A; Grimm C; Marti A; Kueng-Hitz N; Hafezi F; Niemeyer G; Reme CE. 2000. c-fos controls the 'private pathway' of light-induced apoptosis of retinal photoreceptors. J Neurosci 20(1):81-8. [PubMed: 10627584]  [MGI Ref ID J:59143]

Wenzel A; Grimm C; Samardzija M; Reme CE. 2003. The genetic modifier Rpe65Leu(450): effect on light damage susceptibility in c-Fos-deficient mice. Invest Ophthalmol Vis Sci 44(6):2798-802. [PubMed: 12766089]  [MGI Ref ID J:119424]

Wilkinson J 4th; Radjendirane V; Pfeiffer GR; Jaiswal AK; Clapper ML. 1998. Disruption of c-Fos leads to increased expression of NAD(P)H:quinone oxidoreductase1 and glutathione S-transferase. Biochem Biophys Res Commun 253(3):855-8. [PubMed: 9918819]  [MGI Ref ID J:114196]

Yang DH; Smith ER; Cai KQ; Xu XX. 2009. c-fos elimination compensates for disabled-2 requirement in mouse extraembryonic endoderm development. Dev Dyn 238(3):514-23. [PubMed: 19191218]  [MGI Ref ID J:146504]

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 Fostm1Pa strain is maintained by mating heterozygous mice to normal wildtype siblings. Heterozygous mice and normal wildtype siblings may be ordered. Recovery of homozygotes from het x het matings is ~10%.
Diet Information LabDiet® 5K52/5K67

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* $2250.00
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* $2925.00
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).

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

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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