Strain Name:

B6 x BALB/cByJ-Lpin1fld/J

Stock Number:

002533

Availability:

Repository-Cryopreserved

Description

Strain Information

Type Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered Mutant Mice.
Specieslaboratory mouse
GenerationF34N1p

Related Strains

Strains carrying   Lpin1fld allele
001592   BALB/cByJ-Lpin1fld/J
View Strains carrying   Lpin1fld     (1 strain)

Strains carrying other alleles of Lpin1
003401   C3H/HeJ-Lpin1fld-2J/J
View Strains carrying other alleles of Lpin1     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      assigned by genotype

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

Lpin1fld/Lpin1fld

        BALB/cByJ-Lpin1fld/J
  • homeostasis/metabolism phenotype
  • abnormal enzyme/ coenzyme level (MGI Ref ID J:121022)
    • mRNA levels of phophoenolpyruvate carboxykinase (PEPCK) and pyruvate carboxylase are significantly lower relative to wild-type; PEPCK expression is downregulated in response to feeding similar to wild-type, but pyruvate carboxylase levels do not change in mutants after feeding, indicating fatty acid synthesis is favored upon refeeding in mutants
  • abnormal glucose homeostasis (MGI Ref ID J:121022)
    • abnormal gluconeogenesis (MGI Ref ID J:121022)
      • fasting hepatic glucose production (HGP) is reduced by 43% relative to wild-type, indicating significant reduction in peripheral glucose uptake
    • increased circulating glucose level (MGI Ref ID J:121022)
      • fasting plasma glucose levels are elevated (150 mg/dl) relative to wild-type (106 mg/dl)
    • increased glycogen level (MGI Ref ID J:121022)
      • mutants have ~2-fold higher glycogen in liver and skeletal muscle as wild-type at 5 hours of re-feeding with normal chow after an 18 hour overnight fast
      • this increase in glycogen content is not due to differences in food intake
      • after 18 hour fast, liver glycogen content is reduced to ~4.5 mg/gram tissue in both wild-type and mutant, showing no significant difference
  • abnormal metabolism (MGI Ref ID J:121022)
    • mutants display altered Cori cycle activity, as shown by significantly lower lactate production in response to 5 hours of refeeding; this contributes to the observed hepatic gluconeogenesis
    • mutants have an overall reduction in flux through the Cori cycle
  • abnormal respiratory quotient (MGI Ref ID J:121022)
    • during a 12 hour fast, the respiratory quotient (RQ) in wild-type mice drops from ~0.9 to 0.7, as shift from carbohydrate to primarily fatty acid metabolism by the end of the fast occurs, whereas in mutants, a decrease in RQ occurs but is considerably blunted
    • homozygotes maintain significantly higher RQ than wild-type during the final 5 hours of the fast, indicating failure to rely on fatty acid fuels exclusively
    • in contrast to wild-type, mutant RQ reaches its maximum value (0.85-0.89) at beginning of fasting and is only 0.83 at 5 hours of feeding; wild-type RQ increases to ~0.9 immediately upon feeding and remains relatively high until fasting begins
  • increased fatty acid level (MGI Ref ID J:121022)
    • mutants show increased hepatic fatty acid synthesis compared to wild-type mice
    • fatty acid synthesis rate for mutants is 0.27 vs 0.063 in wild-type
  • nervous system phenotype
  • abnormal action potential (MGI Ref ID J:137213)
    • reduced motor nerve conduction velocity is accompanied by temporal dispersion and reduction of compound muscle action potentials
  • abnormal myelination (MGI Ref ID J:137213)
    • delay in myelination apparent in the sciatic nerve by P10
    • at P56 no normally myelinated axons are present in the sciatic nerve
  • abnormal sciatic nerve (MGI Ref ID J:137213)
    • dramatic reduction in the number of adipocytes in the epineurium
    • massive accumulation of lipid droplets in the perineurial and endoneurial compartments
  • reduced nerve conduction velocity (MGI Ref ID J:137213)
    • strong reduction in motor nerve conduction velocity of the sciatic nerve at P56
  • behavior/neurological phenotype
  • limb grasping (MGI Ref ID J:137213)
    • clench toes of the hind feet when lifted by the tail

Lpin1fld/Lpin1fld

        BALB/cByJ-Lpin1fld
  • lethality-postnatal
  • postnatal lethality (MGI Ref ID J:82882)
    • some mice die before weaning
  • life span-post-weaning/aging
  • premature death (MGI Ref ID J:82882)
    • many mice die between 19 and 35 days after birth
  • growth/size phenotype
  • decreased body weight (MGI Ref ID J:63448)
    • by third day after birth, mice display significantly reduced weigh gain, and remain 25-30% underweight throughout their lifetime
  • decreased lean body mass (MGI Ref ID J:63448)
    • may be reduced, as body weight is reduced 25-30% and adipose tissue is ~15% of body weight
  • distended abdomen (MGI Ref ID J:82882)
    • by P3, mutants can be identified by their distended abdomens
  • behavior/neurological phenotype
  • abnormal gait (MGI Ref ID J:82882)
    • homoyzgotes develop an unsteady gait starting at ~P10, and this persists throughout life
  • limb grasping (MGI Ref ID J:82882)
    • when lifted by the tail, mice clench toes of the hind feet and clasp hind limbs together
  • tremors (MGI Ref ID J:82882)
    • mice display generalized tremors starting ~P10
  • nervous system phenotype
  • abnormal PNS glial cell morphology (MGI Ref ID J:82882)
    • abnormal Schwann cell morphology (MGI Ref ID J:82882)
      • numerous hypertrophic cells with increased nuclear size, abnormally large mitochondria and copius cytoplasm are observed, and some cells contain myelin degradation debris; this becomes more widely distributed by 30 days and persist through 1 year
      • abnormal cells are more common in older mice
      • in adults, free cell processes and basal lamina are frequently found, but onion bulb formation is rare
  • abnormal axon morphology (MGI Ref ID J:82882)
    • abnormal myelin sheath morphology (MGI Ref ID J:82882)
      • sheaths around axons of the sciatic nerve at postnatal day 4 are markedly thin compared to controls; this persists through 1 year of age
  • abnormal sciatic nerve (MGI Ref ID J:82882)
    • axonal myelin sheaths are thin, hypertrophic Schwann cells are observed, sometimes accumulating myelin debris with age
  • axon degeneration (MGI Ref ID J:82882)
    • in adult sciatic nerves, some degenerating axons are observed, along with bands of Bugner, and regenerative clusters occasionally
  • reproductive system phenotype
  • delayed female fertility (MGI Ref ID J:82882)
    • females do not generally produce their first litter until ~90 days of age
  • female infertility (MGI Ref ID J:82882)
    • ~50% of females are infertile
  • male infertility (MGI Ref ID J:82882)
    • all males appear to be infertile, possibly due to behavior impairment
  • adipose tissue phenotype
  • abnormal adipocyte morphology (MGI Ref ID J:63448)
    • at 1 and 6 months of age, adipocytes are found to be severely depleted of lipid
    • by 6 months, white adipocytes have accumulated more lipid than at 1 month, but cells remain reduced in size and contain a heterogeneous population of lipid droplets characteristic of incompletely differentiated adipocytes
    • in some regions of brown adipose tissue sections at 1 and 6 months of age, tissue consists largely of muscle with small masses of lipid-poor adipocytes
  • abnormal adipose tissue physiology (MGI Ref ID J:63448)
    • brown adipose tissue levels of uncoupling protein 1 mRNA are reduced
    • PPARgamma and adipocyte fatty acid-binding protein aP2 mRNA levels are markedly elevated in mutants, most evident at 2 weeks of age and less pronounced in older mice
    • abnormal white adipose tissue physiology (MGI Ref ID J:63448)
      • white adipose tissue expresses reduced mRNA levels of lipoprotein lipase, as well as adipsin and uncoupling protein 1
      • after weaning, expression of fatty acid synthase and acetyl-CoA carboxylase is relatively unchanged compared to wild-type where expression is highly induced
  • abnormal brown adipose tissue morphology (MGI Ref ID J:63448)
    • in adults and neonates, tissue appears abnormal
    • brown adipose tissue sections at 1 and 6 months of age exhibit dramatically reduced lipid content relative to controls; in some regions, tissue consists largely of muscle with small masses of lipid-poor adipocytes
    • decreased brown adipose tissue amount (MGI Ref ID J:63448)
      • mice exhibit reduced fat mass in brown adipose tissue depots
      • interscapular brown adipose tissue mass is reduced 80% in adults, but not in neonates
  • abnormal epididymal fat pad morphology (MGI Ref ID J:63448)
    • epididymal fat pad mass is reduced ~80% in neonates and adults
    • epididymal fat pads from 1-month old mice have immature cells containing mostly small, sparse lipid droplets
  • abnormal inguinal fat pad morphology (MGI Ref ID J:63448)
    • fat pad mass is reduced ~80% in neonates and adults
  • abnormal interscapular fat pad morphology (MGI Ref ID J:63448)
    • interscapular brown adipose tissue mass is reduced 80% in adults, but not in neonates
  • decreased white adipose tissue amount (MGI Ref ID J:63448)
    • mice exhibit reduced fat mass in white adipose tissue depots
  • cardiovascular system phenotype
  • abnormal aorta morphology (MGI Ref ID J:63448)
    • after 16 weeks of an atherogenic diet, mutants display 2-fold greater lesion area relative to wild-type littermates; lesions are qualitatively more advanced than in wild-type
    • lesions extend beyond aortic valve attachment points to form raised lesions in the free aortic wall
    • raised lesions are detected in 92% of homozygotes vs only 44% of wild-type mice
  • homeostasis/metabolism phenotype
  • abnormal enzyme/coenzyme activity (MGI Ref ID J:82882)
    • during the suckling period, lipoprotein lipase activity is reduced by ~16-fold in white adipose tissue and by <2-fold in the heart of mutants
    • hepatic lipase activity and mRNA levels are reduced ~6-fold and 2-fold respectively compared to wild-type: abnormalities resolve between 14 and 28 days postnatal
    • in 3-week old mice, hormone-sensitive lipase activity is reduced ~50% compared to wild-type tissue (29 vs 60 mU/mg)
  • abnormal lipid homeostasis (MGI Ref ID J:82882)
    • sphingomyelin and galactosphingolipids and sulfatides exhibit age-dependent decreases in levels relative to phosphotidylcholine in mutants but not in wild-type
    • abnormal cholesterol homeostasis (MGI Ref ID J:82882)
      • mice have increased cholesterol ester levels in sciatic nerve extracts at 1-2 and 3+ months of age relative to wild-type
      • decreased circulating LDL cholesterol level (MGI Ref ID J:63448)
        • on an atherogenic diet, the LDL/VLDL fraction (60%) makes up less of the total cholesterol compared to wild-type (76%)
      • decreased circulating VLDL cholesterol level (MGI Ref ID J:63448)
        • on an atherogenic diet for 16 weeks, the LDL/VLDL fraction (60%) makes up less of the total cholesterol compared to wild-type (76%)
      • increased cholesterol level (MGI Ref ID J:82882)
        • levels are significantly less in sciatic nerve lipids (552, 226 ng/ug) vs wild-type (896, 526 ng/ug) at 1-2 months and 3+ months respectively
        • increased circulating HDL cholesterol level (MGI Ref ID J:63448)
          • on an atherogenic diet for 16 weeks, the HDL fraction (40% of total) accounts for more cholesterol than in wild-type (24%)
    • abnormal lipid level (MGI Ref ID J:82882)
      • within several days of birth, hepatic levels of apolipoprotein ApoA-IV mRNA are increased 100-fold and ApoC-II mRNA levels are 6-fold increased relative to wild-type
      • abnormal phospholipid level (MGI Ref ID J:82882)
        • at 3 months of age, sciatic nerve lipids show an elevation of neutral lipid species and alteration of relative amounts of phosphatidylserine, phophatidyl- or phophatidalethanolamine, phophatidylcholine, and sphingomyelin compared to control levels
        • phosphotidylinositol:phosphotidylcholine ratio is slightly increased in mutant nerves relative to wild-type
        • lipid profile resembles that of an immature nerve or one undergoing repair
        • at 3+ months of age, phosphatidylcholine levels in sciatic nerve extracts are 3.3 times the level in wild-type, while levels of phosphatidal- and phosphotidylethanolamines and phosphotidalserine are lower than controls at all ages, and difference from wild type increases with age
      • abnormal triglyceride level (MGI Ref ID J:82882)
        • decreased triglyceride level (MGI Ref ID J:82882)
          • at 3+ months, ratio of triglycerides to cholesterol in sciatic nerves is slightly lower than wild-type
        • increased triglyceride level (MGI Ref ID J:82882)
          • within a few days after birth, hepatic and serum triglyceride levels are elevated by several fold relative to controls
      • decreased circulating LDL cholesterol level (MGI Ref ID J:63448)
        • on an atherogenic diet, the LDL/VLDL fraction (60%) makes up less of the total cholesterol compared to wild-type (76%)
      • decreased circulating VLDL cholesterol level (MGI Ref ID J:63448)
        • on an atherogenic diet for 16 weeks, the LDL/VLDL fraction (60%) makes up less of the total cholesterol compared to wild-type (76%)
      • decreased fatty acid level (MGI Ref ID J:63448)
        • in response to atherogenic diet, mutants have slightly lower fatty acid levels than wild-type
      • increased cholesterol level (MGI Ref ID J:82882)
        • levels are significantly less in sciatic nerve lipids (552, 226 ng/ug) vs wild-type (896, 526 ng/ug) at 1-2 months and 3+ months respectively
        • increased circulating HDL cholesterol level (MGI Ref ID J:63448)
          • on an atherogenic diet for 16 weeks, the HDL fraction (40% of total) accounts for more cholesterol than in wild-type (24%)
      • increased fatty acid level (MGI Ref ID J:82882)
        • levels in sciatic nerve extracts are 2-fold higher than wild-type at 3+ months of age
  • impaired glucose tolerance (MGI Ref ID J:63448)
    • mice have impaired clearance of a glucose dose with levels remaining >400 mg/dl for 2 hours after glucose administration, in contrast to levels in wild-type mice which return to baseline after 1 hour
  • increased circulating insulin level (MGI Ref ID J:63448)
    • nonfasting insulin levels are elevated 2.5-fold in mutants on a regular chow diet
    • on an atherogenic diet for 16 weeks, insulin levels in plasma are reduced in mutants and wild-type, but levels in mutant mice are 4-fold higher than in wild-type
  • insulin resistance (MGI Ref ID J:63448)
    • administration of exogenous insulin with glucose injection does not produce the typical hypoglycemic response seen in wild-type
  • liver/biliary system phenotype
  • enlarged liver (MGI Ref ID J:82882)
    • homozygotes can be recognized as early as P3 by their large livers
    • liver is 2-fold larger than wild-type in neonates, and 20% larger in adults
  • pale liver (MGI Ref ID J:82882)
    • homozygotes can be recognized as early as P3 by their pale livers
  • skin/coat/nails phenotype
  • abnormal hair growth (MGI Ref ID J:82882)
    • ruffled coat appearance is due to reduced hair growth
  • disheveled coat (MGI Ref ID J:82882)
    • mice have unkempt coat appearance
  • ruffled hair (MGI Ref ID J:82882)
    • mice have coats with ruffled appearance
  • digestive/alimentary phenotype
  • decreased insulin secretion (MGI Ref ID J:63448)
    • 60 minutes following glucose injection, mutant insulin levels are slightly higher than in wild-type but lower than that measured in non-glucose-challenged mutants indicating impaired secretion
  • endocrine/exocrine gland phenotype
  • decreased insulin secretion (MGI Ref ID J:63448)
    • 60 minutes following glucose injection, mutant insulin levels are slightly higher than in wild-type but lower than that measured in non-glucose-challenged mutants indicating impaired secretion
View Research Applications

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

Lpin1fld related

Developmental Biology Research
Internal/Organ Defects (liver)

Internal/Organ Research
Liver Defects

Metabolism Research

Neurobiology Research
Ataxia (Movement) Defects
Metabolic Defects
Myelination Defects (peripheral neuropathy)
Tremor Defects

Genes & Alleles

Gene & Allele Information

Allele Symbol Lpin1fld
Allele Name fatty liver dystrophy
Allele Type Spontaneous
Common Name(s) fld;
Strain of OriginBALB/cByJ
Gene Symbol and Name Lpin1, lipin 1
Chromosome 12
Gene Common Name(s) DKFZp781P1796; KIAA0188; PAP1; fatty liver dystrophy; fld; mKIAA0188;
General Note This mutation arose at The Jackson Laboratory in 1981. The mutant phenotype can be identified soon after birth by an enlarged and pale liver. These features disappear by about 28 days of age or following the transition from suckling to weaning. Mutant mice are smaller than their normal littermates by three days of age and remain smaller throughout life. Hair growth is retarded and abnormal. These mice develop a progressive tremor and unsteady gait by 14 days of age and adults lack hind limb coordination.Many homozygous mutant mice die within the first one to two months after birth. Surviving females will breed, although they do not usually produce a first litter before 3 months of age. Only one male has bred. Homozygous mutant mice have abnormalities inseveral messenger RNAs and proteins related to fat metabolism. Suckling mutant mice have elevated serum and hepatic triglycerides, a liver-specific increase in mRNAs for apolipoproteins (APO) A-IV and C-II, reduced apolipoprotein lipase (LPL) activity inwhite adipose tissue, and reduced hepatic lipase (HL) mRNA and activity. All these return to normal after the suckling-weaning transition (J:9801).
Molecular Note Three genetic abnormalities have been identified in this allele. A 2 kb deletion encompasses exons 2 and 3 including the translation initiation sequence. An inversion exceeding 40 kb encompasses much of the coding region. An additional 0.5 kb sequence downstream of the inverted 40 kb has been duplicated and inserted in reverse orientation just upstream of this 40 kb inversion. Northern blots of adipose tissue extracts failed to detect mRNA from mice homozygous for this allele. [MGI Ref ID J:66739]

Genotyping

Genotyping Information

This strain will not have a genotyping protocol or one is not currently available.

Helpful Links

Optimizing PCR Protocols

References

References

Additional References

Lpin1fld related

Donkor J; Sariahmetoglu M; Dewald J; Brindley DN; Reue K. 2007. Three mammalian lipins act as phosphatidate phosphatases with distinct tissue expression patterns. J Biol Chem 282(6):3450-7. [PubMed: 17158099]  [MGI Ref ID J:120935]

Finck BN; Gropler MC; Chen Z; Leone TC; Croce MA; Harris TE; Lawrence JC Jr; Kelly DP. 2006. Lipin 1 is an inducible amplifier of the hepatic PGC-1alpha/PPARalpha regulatory pathway. Cell Metab 4(3):199-210. [PubMed: 16950137]  [MGI Ref ID J:129744]

Klingenspor M; Xu P; Cohen RD; Welch C; Reue K. 1999. Altered gene expression pattern in the fatty liver dystrophy mouse reveals impaired insulin-mediated cytoskeleton dynamics. J Biol Chem 274(33):23078-84. [PubMed: 10438476]  [MGI Ref ID J:42314]

Langner CA; Birkenmeier EH; Ben-Zeev O; Schotz MC; Sweet HO; Davisson MT; Gordon JI. 1989. The fatty liver dystrophy (fld) mutation. A new mutant mouse with a developmental abnormality in triglyceride metabolism and associated tissue-specific defects in lipoprotein lipase and hepatic lipase activities. J Biol Chem 264(14):7994-8003. [PubMed: 2722772]  [MGI Ref ID J:9801]

Langner CA; Birkenmeier EH; Roth KA; Bronson RT; Gordon JI. 1991. Characterization of the peripheral neuropathy in neonatal and adult mice that are homozygous for the fatty liver dystrophy (fld) mutation. J Biol Chem 266(18):11955-64. [PubMed: 2050689]  [MGI Ref ID J:82882]

Nadra K; Charles AS; Medard JJ; Hendriks WT; Han GS; Gres S; Carman GM; Saulnier-Blache JS; Verheijen MH; Chrast R. 2008. Phosphatidic acid mediates demyelination in Lpin1 mutant mice. Genes Dev 22(12):1647-61. [PubMed: 18559480]  [MGI Ref ID J:137213]

Peterfy M; Phan J; Xu P; Reue K. 2001. Lipodystrophy in the fld mouse results from mutation of a new gene encoding a nuclear protein, lipin Nat Genet 27(1):121-4. [PubMed: 11138012]  [MGI Ref ID J:66739]

Phan J; Peterfy M; Reue K. 2004. Lipin expression preceding peroxisome proliferator-activated receptor-gamma is critical for adipogenesis in vivo and in vitro. J Biol Chem 279(28):29558-64. [PubMed: 15123608]  [MGI Ref ID J:91675]

Phan J; Reue K. 2005. Lipin, a lipodystrophy and obesity gene. Cell Metab 1(1):73-83. [PubMed: 16054046]  [MGI Ref ID J:129850]

Rehnmark S; Giometti CS; Slavin BG; Doolittle MH; Reue K. 1998. The fatty liver dystrophy mutant mouse: microvesicular steatosis associated with altered expression levels of peroxisome proliferator-regulated proteins. J Lipid Res 39(11):2209-17. [PubMed: 9799807]  [MGI Ref ID J:50756]

Reue K; Doolittle MH. 1996. Naturally occurring mutations in mice affecting lipid transport and metabolism. J Lipid Res 37(7):1387-405. [PubMed: 8827513]  [MGI Ref ID J:34179]

Reue K; Xu P; Wang XP; Slavin BG. 2000. Adipose tissue deficiency, glucose intolerance, and increased atherosclerosis result from mutation in the mouse fatty liver dystrophy (fld) gene J Lipid Res 41(7):1067-76. [PubMed: 10884287]  [MGI Ref ID J:63448]

Sweet HO; Birkenmeier E; Davisson MT. 1988. fld - fatty liver dystrophy Mouse News Lett 81:69.  [MGI Ref ID J:64452]

Verheijen MH; Chrast R; Burrola P; Lemke G. 2003. Local regulation of fat metabolism in peripheral nerves. Genes Dev 17(19):2450-64. [PubMed: 14522948]  [MGI Ref ID J:90859]

Xu J; Lee WN; Phan J; Saad MF; Reue K; Kurland IJ. 2006. Lipin deficiency impairs diurnal metabolic fuel switching. Diabetes 55(12):3429-38. [PubMed: 17130489]  [MGI Ref ID J:121022]

Health & husbandry

Health & Colony Maintenance Information

Currently there no information available for this strain. This may be due to the supply level of this strain.

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Pricing for USA, Canada and Mexico shipping destinations View International pricing
Weeks of AgePrice*Gender
Cryorecovery Fee $1900.00
*Price(s) in US dollars ($)

Additional Supply Details

Pricing for International shipping destinations View USA Canada and Mexico pricing
Weeks of AgePrice*Gender
Cryorecovery Fee $2470.00
*Price(s) in US dollars ($)

Additional Supply Details

Supply Details

Standard SupplyRepository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information.
Supply Notes
  • Cryorecovery - Standard.
    The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
    One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 or 1-207-288-5845.

General Terms and Conditions


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