Description

Strain Information

Type Congenic; Mutant Strain; Additional information on Genetically Engineered Mutant Mice. Mating System Heterozygote x Inbred         (Female x Male) TJL Breeding Summary: heterozygote x C57BL/6JEi Species laboratory mouse Background Strain C57BL/6JEiJ Donor Strain Oak Ridge stock Generation N92F1 (20-NOV-08)

Appearance
tan mosaic
Related Genotype: a/a Atp7a^Mo-blo/+ (female)

black
Related Genotype: a/a +/+ or a/a +/Y

Description
Female mice heterozygous for the blotchy alleles (Atp7a^Mo-blo) are viable and fertile. They have irregular patches of light-colored fur. Hemizygous males and homozygous females have reduced viability and many are infertile. Hemizygotes and homozygotes are light all over with no blotching, are usually small, and occasionally have deformed hindlegs.. Most hemizygotes and homozygotes have defective elastin in the aorta and usually die with aortic aneurysm. Hemizygous males have enlarged air spaces in the lung (emphysema), probably because of defective elastin and collagen. Skin collagen and aortic elastin have defective crosslinking at the step at which lysine residues are converted to aldehydes. Hemizygous males have a deficiency of noradrenalin in the brain, probably because a deficiency of copper shown to exist in the brain causes defective activity of the enzyme dopamine-beta-hydroxylase. Copper absorption from the gut and hepatic copper concentration are reduced to 64% and 56% of normal, respectively.

Control Information

	Control
	Wild-type from the colony
Considerations for Choosing Controls

Related Strains

Strains carrying   Atp7a^Mo-blo allele

000535

B6.Cg-Atp7aMo-blo/J

View Strains carrying   Atp7a^Mo-blo     (1 strain)

Strains carrying other alleles of Atp7a

001381	B6.Cg-Atp7aMo-pew2J/J
000053	B6.Cg-Atp7aMo-to/J
002062	B6C3Fe a/a-Atp7aMo-8J/J
002566	C57BL/6-Atp7aMo-br/J
000813	CBA/J-Atp7aMo-pew/J
000623	TR/DiEiJ

View Strains carrying other alleles of Atp7a     (6 strains)

Additional Web Information

Congenic Nomenclature

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

Atp7a^Mo-blo/Y

        B6.Cg-Atp7a^Mo-blo/J

• skeleton phenotype
• abnormal cartilage morphology (MGI Ref ID J:36378)
  • 2 month-old mice show decreased collagen crosslinks in cartilage compared to wild-type
  • lesions such as defects in cartilage integrity are observed in joints at 10 months of age
• osteoarthritis (MGI Ref ID J:36378)
  • at 2-4 months of age, femoral-tibial joints show structural and cellular changes correlating with mild to moderate osteoarthritis; changes increase in severity with age
  • at 10 months, loss of integrity of weight bearing regions of the joints is detected, with cellular changes including cloning and cell loss
• immune system phenotype
• osteoarthritis (MGI Ref ID J:36378)
  • at 2-4 months of age, femoral-tibial joints show structural and cellular changes correlating with mild to moderate osteoarthritis; changes increase in severity with age
  • at 10 months, loss of integrity of weight bearing regions of the joints is detected, with cellular changes including cloning and cell loss
• cellular phenotype
• oxidative stress (MGI Ref ID J:105736)
  • vascular superoxide anion production is increased in all layers of aortas in mutants compared to controls

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

Atp7a^Mo-blo/Atp7a⁺

        Background Not Specified

• growth/size phenotype
• decreased body size (MGI Ref ID J:13383)
  • usually smaller than wild-type
• cachexia (MGI Ref ID J:5516)
  • prior to death
• pigmentation phenotype
• diluted coat color (MGI Ref ID J:13383)
  • females have irregular patches of dilute-color (pale) fur; expression of dilution is poor in some up to weaning age, but is complete in adults
• skin/coat/nails phenotype
• coarse hair (MGI Ref ID J:5516)
  • mutants have thin rough coats
• diluted coat color (MGI Ref ID J:13383)
  • females have irregular patches of dilute-color (pale) fur; expression of dilution is poor in some up to weaning age, but is complete in adults
• touch/vibrissae phenotype
• curly vibrissae (MGI Ref ID J:13383)
  • whiskers are curly at birth but straighten by weaning age
• limbs/digits/tail phenotype
• abnormal hindlimb morphology (MGI Ref ID J:13383)
  • occasionally hindlimbs are deformed
• reproductive system phenotype
• *normal* reproductive system phenotype (MGI Ref ID J:13383)
  • viability and fertility are normal
• behavior/neurological phenotype
• hunched posture (MGI Ref ID J:5516)
• lethargy (MGI Ref ID J:5516)
  • prior to death
• cardiovascular system phenotype
• abnormal aorta morphology (MGI Ref ID J:5516)
  • uniform dilatation of aorta to level of superior mesenteric artery is frequently observed
  • kink in distal part of descending aorta is commonly observed; in some animals, seen at 15 days of age
  • at 21 days of age, degenerative changes are seen in elastic fibers of tunica media; lesions include irregular fiber thickness, vacuolation, and fragmentation (grade II lesions)
• abnormal aorta elastic fiber morphology (MGI Ref ID J:5516)
  • at 21 days of age, degenerative changes are seen in elastic fibers of tunica media; lesions include irregular fiber thickness, vacuolation, and fragmentation (grade II lesions)
• decreased aorta elastin content (MGI Ref ID J:5516)
  • in grades II-IV lesions, aorta elastic fiber fibers show increasing vacuolation and fragmentation; in grade V lesions elastic fibers are absent
• aortic aneurysm (MGI Ref ID J:5516)
  • one or more spontaneous aneurysms can be identified; majority are fusiform or saccular, most commonly on the aortic arch or proximal part of descending aorta
  • 32% of mutants display aortic aneurysms and 5% show S-shaped lesions (lesions/aneurysms involve the thoracic and abdominal aorta and its branches)
• aneurysm (MGI Ref ID J:5516)
  • aneurysms may also occur at level of diaphragmatic hiatus
• aortic aneurysm (MGI Ref ID J:5516)
  • one or more spontaneous aneurysms can be identified; majority are fusiform or saccular, most commonly on the aortic arch or proximal part of descending aorta
  • 32% of mutants display aortic aneurysms and 5% show S-shaped lesions (lesions/aneurysms involve the thoracic and abdominal aorta and its branches)
• hemoperitoneum (MGI Ref ID J:5516)
  • seen in several pregnant females
• hemothorax (MGI Ref ID J:5516)
  • at time of death, many animals exhibit bilateral hemothorax
• respiratory system phenotype
• hemothorax (MGI Ref ID J:5516)
  • at time of death, many animals exhibit bilateral hemothorax

Atp7a^Mo-blo/Atp7a^Mo-blo

        Background Not Specified

• life span-post-weaning/aging
• premature death (MGI Ref ID J:13383)
  • mice have reduced viability
• growth/size phenotype
• decreased body size (MGI Ref ID J:13383)
  • usually smaller than wild-type
• cardiovascular system phenotype
• aortic aneurysm (MGI Ref ID J:5397)
  • 85% of mutants display aortic aneurysms (S-shaped or saccular involving the thoracic and abdominal aorta and its branches)
• pigmentation phenotype
• diluted coat color (MGI Ref ID J:13383)
  • homozygous mice are light-colored all over
• skin/coat/nails phenotype
• diluted coat color (MGI Ref ID J:13383)
  • homozygous mice are light-colored all over
• touch/vibrissae phenotype
• curly vibrissae (MGI Ref ID J:13383)
  • whiskers are curly at birth but straighten by weaning age
• reproductive system phenotype
• female infertility (MGI Ref ID J:13383)
  • many homozygotes are sterile
• limbs/digits/tail phenotype
• abnormal hindlimb morphology (MGI Ref ID J:13383)
  • occasionally hindlimbs are deformed

Atp7a^Mo-blo/Y

        Background Not Specified

• life span-post-weaning/aging
• *normal* life span-post-weaning/aging (MGI Ref ID J:38977)
  • hemizygous males are viable at birth
• premature death (MGI Ref ID J:13383)
  • mice have reduced viability after birth
• cardiovascular system phenotype
• abnormal aorta morphology (MGI Ref ID J:15796)
  • at 18-19 weeks, external diameter of ascending aorta is twice that of wild-type male littermates
  • histologic changes are detected by 21 days of age in some males, prior to visible aneurysm
  • histologically, disrupted and wavy lamellae are observed and these structures have irregular surfaces; interlamellar spaces are thickened
  • smooth muscle cells are large and pleomorphic
  • uniform dilatation of aorta to level of superior mesenteric artery is frequently observed
  • kink in distal part of descending aorta is commonly observed; in some animals, seen at 15 days of age
  • at 21 days of age, degenerative changes are seen in elastic fibers of tunica media; lesions include irregular fiber thickness, vacuolation, and fragmentation (grade II lesions)
  • without obvious aneurysm, aorta dry weight is significantly greater than control; in aneurismal aortas, dry weight is >3-fold greater than controls
  • in areas of aneurysm, tissue is largely made up of collagen, whereas normal tissue is mainly collagen and elastin
• abnormal aorta elastic fiber morphology (MGI Ref ID J:5516)
  • at 21 days of age, degenerative changes are seen in elastic fibers of tunica media; lesions include irregular fiber thickness, vacuolation, and fragmentation (grade II lesions)
• decreased aorta elastin content (MGI Ref ID J:5516)
  • in grades II-IV lesions, aorta elastic fiber fibers show increasing vacuolation and fragmentation; in grade V lesions elastic fibers are absent
• aortic aneurysm (MGI Ref ID J:15796)
  • by 6 months of age, all male hemizygotes display aortic aneurysms; aneurysms occur mainly in ascending thoracic aorta with some found in the descending or abdominal aorta
  • one or more spontaneous aneurysms can be identified; majority are fusiform or saccular, most commonly on the aortic arch or proximal part of descending aorta
  • 93% of males display aortic aneurysms
• aneurysm (MGI Ref ID J:5516)
  • aneurysms may also occur at level of diaphragmatic hiatus
• aortic aneurysm (MGI Ref ID J:15796)
  • by 6 months of age, all male hemizygotes display aortic aneurysms; aneurysms occur mainly in ascending thoracic aorta with some found in the descending or abdominal aorta
  • one or more spontaneous aneurysms can be identified; majority are fusiform or saccular, most commonly on the aortic arch or proximal part of descending aorta
  • 93% of males display aortic aneurysms
• hemothorax (MGI Ref ID J:5516)
  • at time of death, many animals exhibit bilateral hemothorax
• pigmentation phenotype
• diluted coat color (MGI Ref ID J:15796)
  • male hemizygotes are distinguished based on pale coat color in contrast to normal black-colored littermates
  • hemizygotes surviving beyond birth have severe dilution in hair pigment
  • hemizygous males are light-colored all over
• skin/coat/nails phenotype
• coarse hair (MGI Ref ID J:5516)
  • mutants have thin rough coats
• diluted coat color (MGI Ref ID J:15796)
  • male hemizygotes are distinguished based on pale coat color in contrast to normal black-colored littermates
  • hemizygotes surviving beyond birth have severe dilution in hair pigment
  • hemizygous males are light-colored all over
• behavior/neurological phenotype
• hunched posture (MGI Ref ID J:5516)
• hypoactivity (MGI Ref ID J:5462)
  • males display general inactivity
• lethargy (MGI Ref ID J:5516)
  • prior to death
• tremors (MGI Ref ID J:5462)
  • mild sustained tremor is observed in mutants
• homeostasis/metabolism phenotype
• abnormal noradrenaline level (MGI Ref ID J:5462)
  • brain levels are reduced by 30% compared to wild-type males
• reproductive system phenotype
• male infertility (MGI Ref ID J:13383)
  • many males are sterile
• priapism (MGI Ref ID J:5516)
  • occasional males display priapism with balanoposthitis
• growth/size phenotype
• decreased body size (MGI Ref ID J:13383)
  • usually smaller than wild-type
• cachexia (MGI Ref ID J:5516)
  • prior to death
• limbs/digits/tail phenotype
• abnormal hindlimb morphology (MGI Ref ID J:13383)
  • occasionally hindlimbs are deformed
• touch/vibrissae phenotype
• curly vibrissae (MGI Ref ID J:13383)
  • whiskers are curly at birth but straighten by weaning age
• respiratory system phenotype
• hemothorax (MGI Ref ID J:5516)
  • at time of death, many animals exhibit bilateral hemothorax

Atp7a^Mo-blo/Y

        Background Not Specified

• homeostasis/metabolism phenotype
• abnormal enzyme/coenzyme activity (MGI Ref ID J:5880)
  • lysyl oxidase activity in lungs is significantly decreased compared to wild-type; levels are nearly undetectable in some lungs
  • lysyl oxidase activity in lung fibroblasts in culture is reduced to about 42% of that in wild-type cells
• cellular phenotype
• abnormal cell content/ morphology (MGI Ref ID J:5880)
  • initially in culture, cells are less ordered than wild-type and exhibit large empty areas between cells; after prolonged culture, cells display similar morphology to wild-type

Atp7a^Mo-blo/Y

        involves: C57BL/10

• respiratory system phenotype
• abnormal lung morphology (MGI Ref ID J:5664)
  • lungs show generalized enlargement of airspaces
  • internal surface area of inflated lungs is lower than controls in adult males
• abnormal respiratory alveolar duct morphology (MGI Ref ID J:5664)
  • alveolar ducts show generalized dilatation at birth
• abnormal respiratory alveoli morphology (MGI Ref ID J:5664)
  • alveoli are shallow with shortened (or absent) alveolar septa in some regions, surrounding regions of relatively normal architecture
• enlarged lung (MGI Ref ID J:5664)
  • at 12 hours after birth, newborn lungs are grossly larger than wild-type littermates, with enlarged airspaces; lung volumes are significantly larger than controls
• abnormal respiratory system physiology (MGI Ref ID J:5664)
  • lungs show reduced specific static recoil pressures at various lung volumes during deflation compared to controls lungs; with air inflation, elastic recoil pressures are significantly lower over th 50-90% total lung compliance range
• abnormal breathing (MGI Ref ID J:5664)
  • at rest, adults breathe as if the airways are obstructed, with prolonged expiratory phase and prominent chest wall effort
• abnormal lung compliance (MGI Ref ID J:5664)
  • adult mutants have increased lung compliance (30-70% higher) and increased specific compliance
• abnormal total lung capacity (MGI Ref ID J:5664)
  • adult mutants have increased total lung capacity relative to controls

View Research Applications

Research Applications

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

Atp7a^Mo-blo related

Cardiovascular Research
Heart Abnormalities (aortic aneurysms)

Dermatology Research
Color and White Spotting Defects

Developmental Biology Research
Defects in Extracellular Matrix Molecules

Internal/Organ Research
Heart Abnormalities (aortic aneurysms)

Metabolism Research

Mouse/Human Gene Homologs
Menkes syndrome

Neurobiology Research
Ataxia (Movement) Defects
Metabolic Defects
Tremor Defects

Genes & Alleles

Gene & Allele Information

Allele Symbol		Atp7aMo-blo
Allele Name		blotchy
Allele Type		Spontaneous
Common Name(s)		Blo; Moblo;
Gene Symbol and Name		Atp7a, ATPase, Cu++ transporting, alpha polypeptide
Chromosome		X
Gene Common Name(s)		Blo; FLJ17790; MK; MNK; Menkes protein; Mo; blotchy; br; mottled;
Molecular Note		The mutation is an A-to-C transversion in postition +3 of the intron 11 splice donor. Trancripts derived from this allele are often misspliced and either skip exon 11 or use a cryptic splice site further downstream from the correct splice site. Some normal transcript is also expressed. Western blot and activity analysis demonstrated that only greatly reduced levels of normal sized, but nonfunctional, protein was made. [MGI Ref ID J:17492] [MGI Ref ID J:17493] [MGI Ref ID J:23118] [MGI Ref ID J:38977]

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

Mercer JF; Grimes A; Ambrosini L; Lockhart P; Paynter JA; Dierick H; Glover TW. 1994. Mutations in the murine homologue of the Menkes gene in dappled and blotchy mice [see comments] Nat Genet 6(4):374-8. [PubMed: 8054977]  [MGI Ref ID J:17493]

Starcher B; Madaras JA; Fisk D; Perry EF; Hill CH. 1978. Abnormal cellular copper metabolism in the blotchy mouse. J Nutr 108(8):1229-33. [PubMed: 27591]  [MGI Ref ID J:6013]

Atp7a^Mo-blo related

Andrews EJ; White WJ; Bullock LP. 1975. Spontaneous aortic aneurysms in blotchy mice. Am J Pathol 78(2):199-210. [PubMed: 1115218]  [MGI Ref ID J:5516]

Brophy CM; Tilson JE; Braverman IM; Tilson MD. 1988. Age of onset, pattern of distribution, and histology of aneurysm development in a genetically predisposed mouse model. J Vasc Surg 8(1):45-8. [PubMed: 3385878]  [MGI Ref ID J:15796]

Cecchi C; Biasotto M; Tosi M; Avner P. 1997. The mottled mouse as a model for human Menkes disease: identification of mutations in the Atp7a gene. (Correction: vol. 6(5):829) Hum Mol Genet 6(3):425-33. [PubMed: 9147646]  [MGI Ref ID J:38977]

Coutard M. 1999. Experimental cerebral aneurysms in the female heterozygous Blotchy mouse. Int J Exp Pathol 80(6):357-67. [PubMed: 10632785]  [MGI Ref ID J:59415]

Das S; Levinson B; Vulpe C; Whitney S; Gitschier J; Packman S. 1995. Similar splicing mutations of the Menkes/mottled copper-transporting ATPase gene in occipital horn syndrome and the blotchy mouse. Am J Hum Genet 56(3):570-6. [PubMed: 7887410]  [MGI Ref ID J:23118]

Fisk DE; Kuhn C. 1976. Emphysema-like changes in the lungs of the blotchy mouse. Am Rev Respir Dis 113(6):787-97. [PubMed: 937819]  [MGI Ref ID J:5664]

Glasson SS; Trubetskoy OV; Harlan PM; Chavarria AE; Haimes HB; Jimenez PA. 1996. Blotchy mice: a model of osteoarthritis associated with a metabolic defect. Osteoarthritis Cartilage 4(3):209-12. [PubMed: 8895222]  [MGI Ref ID J:36378]

Grahn D. 1972. Linkage of Mo and GS Mouse News Lett 47:20.  [MGI Ref ID J:13529]

Grahn D; Fry RJM; Hamilton KF. 1969. Genetic and pathological analysis of the sex-linked allelic series, mottled, in the mouse. Genetics 61:s22-s23.  [MGI Ref ID J:12963]

Hunt DM. 1976. A study of copper treatment and tissue copper levels in the murine congenital copper deficiency, mottled. Life Sci 19(12):1913-9. [PubMed: 187892]  [MGI Ref ID J:5747]

Hunt DM. 1974. Primary defect in copper transport underlies mottled mutants in the mouse. Nature 249(460):852-4. [PubMed: 4858102]  [MGI Ref ID J:5462]

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

La Fontaine S; Firth SD; Lockhart PJ; Brooks H; Camakaris J; Mercer JF. 1999. Intracellular localization and loss of copper responsiveness of Mnk, the murine homologue of the Menkes protein, in cells from blotchy (Mo blo) and brindled (Mo br) mouse mutants. Hum Mol Genet 8(6):1069-75. [PubMed: 10332039]  [MGI Ref ID J:55409]

Levinson B; Vulpe C; Elder B; Martin C; Verley F; Packman S; Gitschier J. 1994. The mottled gene is the mouse homologue of the Menkes disease gene [see comments] Nat Genet 6(4):369-73. [PubMed: 8054976]  [MGI Ref ID J:17492]

Lyon MF. 1970. Genetic activity of sex chromosomes in somatic cells of mammals. Philos Trans R Soc Lond B Biol Sci 259(828):41-52. [PubMed: 4399067]  [MGI Ref ID J:5238]

Mann JR; Camakaris J; Francis N; Danks DM. 1981. Copper metabolism in mottled mouse (Mus musculus) mutants. Studies of blotchy (Moblo) mice and a comparison with brindled (Mobr) mice. Biochem J 196(1):81-8. [PubMed: 7197928]  [MGI Ref ID J:82681]

Mercer JF; Grimes A; Ambrosini L; Lockhart P; Paynter JA; Dierick H; Glover TW. 1994. Mutations in the murine homologue of the Menkes gene in dappled and blotchy mice [see comments] Nat Genet 6(4):374-8. [PubMed: 8054977]  [MGI Ref ID J:17493]

Moursi MM; Beebe HG; Messina LM; Welling TH; Stanley JC. 1995. Inhibition of aortic aneurysm development in blotchy mice by beta adrenergic blockade independent of altered lysyl oxidase activity. J Vasc Surg 21(5):792-9. [PubMed: 7769737]  [MGI Ref ID J:26617]

Packman S. 1987. Regulation of copper metabolism in the mottled mouse. Arch Dermatol 123(11):1545-1547a. [PubMed: 3674914]  [MGI Ref ID J:36271]

Packman S; Chin P; O'Toole C. 1984. Copper utilization in cultured skin fibroblasts of the mottled mouse, an animal model for Menkes' kinky hair syndrome. J Inherit Metab Dis 7(4):168-70. [PubMed: 6441865]  [MGI Ref ID J:36270]

Packman S; O'Toole C; Price DC; Thaler MM. 1983. Cadmium, zinc, and copper metabolism in the mottled mouse, an animal model for Menkes' kinky hair syndrome. J Inorg Biochem 19(3):203-11. [PubMed: 6685755]  [MGI Ref ID J:36268]

Packman S; Palmiter RD; Karin M; O'Toole C. 1987. Metallothionein messenger RNA regulation in the mottled mouse and Menkes kinky hair syndrome. J Clin Invest 79(5):1338-42. [PubMed: 3571489]  [MGI Ref ID J:36267]

Paynter JA; Grimes A; Lockhart P; Mercer JF. 1994. Expression of the Menkes gene homologue in mouse tissues lack of effect of copper on the mRNA levels. FEBS Lett 351(2):186-90. [PubMed: 8082762]  [MGI Ref ID J:20585]

Qin Z; Itoh S; Jeney V; Ushio-Fukai M; Fukai T. 2006. Essential role for the Menkes ATPase in activation of extracellular superoxide dismutase: implication for vascular oxidative stress. FASEB J 20(2):334-6. [PubMed: 16371425]  [MGI Ref ID J:105736]

Reed V; Boyd Y. 1997. Mutation analysis provides additional proof that mottled is the mouse homologue of Menkes' disease. Hum Mol Genet 6(3):417-23. [PubMed: 9147645]  [MGI Ref ID J:38978]

Rowe DW; McGoodwin EB; Martin GR; Grahn D. 1977. Decreased lysyl oxidase activity in the aneurysm-prone, mottled mouse. J Biol Chem 252(3):939-42. [PubMed: 14140]  [MGI Ref ID J:5777]

Rowe DW; McGoodwin EB; Martin GR; Sussman MD; Grahn D; Faris B; Franzblau C. 1974. A sex-linked defect in the cross-linking of collagen and elastin associated with the mottled locus in mice. J Exp Med 139(1):180-92. [PubMed: 4808708]  [MGI Ref ID J:5397]

Russell LB. 1960. Recombination, Blo-Ta. Mouse News Lett 23:58.  [MGI Ref ID J:189]

Russell LB. 1960. Sex-linked dominant mottling Mouse News Lett 23:58.  [MGI Ref ID J:13383]

Starcher B; Madaras JA; Fisk D; Perry EF; Hill CH. 1978. Abnormal cellular copper metabolism in the blotchy mouse. J Nutr 108(8):1229-33. [PubMed: 27591]  [MGI Ref ID J:6013]

Starcher BC; Madaras JA; Tepper AS. 1977. Lysyl oxidase deficiency in lung and fibroblasts from mice with hereditary emphysema. Biochem Biophys Res Commun 78(2):706-12. [PubMed: 20889]  [MGI Ref ID J:5880]

Sundberg JP (ed.). 1994. . In: Handbook of Mouse Mutations with Skin and Hair Abnormalities: Animal Models and Biomedical Tools. CRC Press, Boca Raton.  [MGI Ref ID J:30359]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           FGB29

Colony Maintenance

Mating System	Heterozygote x Inbred         (Female x Male)
	TJL Breeding Summary: heterozygote x C57BL/6JEi
Diet Information	LabDiet® 5K52/5K67

Purchasing information

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

Pricing

Supply Details

Standard Supply

Repository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement.

Supply Notes

Usually shipped between four and eight weeks of age. This strain is included in the Mouse Mutant Resource collection. Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	Wild-type from the colony
Considerations for Choosing Controls
USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
International - Control Pricing Information for Genetically Engineered Mutant Strains.

General Terms and Conditions

See Terms of Use

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.

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Ordering and Purchasing Information

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Contact Information
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Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
Technical Support Email Form

Terms of Use

Terms of Use

General Terms and Conditions

Contact information

General inquiries

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phone:	207-288-6470
fax:	207-288-6655

JAX^® Mice & Services Conditions of Use

“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (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 with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”

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, The Jackson Laboratory will, at its option, provide credit or replacement for the MICE or product received or the services provided.

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MICE and biological materials 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 The Jackson Laboratory’s MICE, products and services. In addition, special terms and conditions of sale of certain MICE, products and services may be set forth separately in The Jackson Laboratory 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 The Jackson Laboratory, 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 The Jackson Laboratory, 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 services by The Jackson Laboratory.