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- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
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 B6C3Fe-a/a-Dh (Changed: 15-DEC-04 ) Type Mutant Stock; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation N74p Appearance
black
Related Genotype: a/aDescription
A spontaneous mutation on chromosome 1 of the dominant hemimelia gene, Dh, causes a defect in the embryonic splanchnic mesoderm and induces congenital absence of the spleen and widespread visceral and skeletal abnormalities. Mice homozygous for the Dh mutation die shortly after birth. Heterozygotes may exhibit tibial hemimelia, polydactyly, and extra fused toes. Rear leg(s) may be held at an odd angle with bent rear ankles. Heterozygotes have enlarged lymph nodes and elevated numbers of circulating lymphocytes, granulocytes and thrombocytes. They show reduced serum IgM and IgG2 and impaired humoral antibody response as well as decreased numbers of lymph node mast cells. The Pde6brd1 allele contributed to this strain by C3FeLe.B6-a causes blindness and is segregating in this strain.Development
Dominant hemimelia arose spontaneously in a cross bred translocation stock at the Institute of Animal Genetics in Edinburgh and was received by Dr. Margaret Green at The Jackson Laboratory in 1961 from Mary Lyon of Harwell, England. This HCD stock was carrying white bellied agouti, leaden, brown, and dominant hemimelia. This stock was sibling mated for 2 generations then outcrossed to C57BL/6J twice followed by an outcross to a (C3HeB/FeJ x CBA/J)F1, and then sibling breeding for 6 generations before alternate crosses to C57BL/6J-Aw-J and CBA/J and then continuous backcrossing to B6CBAF1 for 30 generations. It was then outcrossed to B6C3FeF1-a/a/J in approximately 1972 and maintained by continual outcross to this F1. In 1987 embryos were generated for cryopreservation at generation N73 by mating either heterozygous females with wildtype males or wildtype females with heterozygous males.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying a allele
View Strains carrying a (104 strains)
Phenotype
Phenotype Information
assigned by genotype
Dh/Dh+
B6C3Fe a/a-Dh/J
- skeleton phenotype
- *normal* skeleton phenotype (MGI Ref ID J:58793)
- lumbar vertebrae are not found to have an abnormal shape on this genetic background
- abnormal sternebra morphology (MGI Ref ID J:58793)
- over 88% of heterozygotes have 5 sternebrae rather than the normal 6
- abnormal tarsal bone morphology (MGI Ref ID J:58793)
- in heterozygotes in which the tibia is visibly smaller or absent, coalition of the ankle bones and metatarsal synostosis can be found
- abnormal tibia morphology (MGI Ref ID J:58793)
- the tibia is reduced in size to a degree that can be used to classify heterozygotes in one of three discrete categories: imperceptibly shortened, noticably shortened, or entirely absent
- absent tibia (MGI Ref ID J:58793)
- short tibia (MGI Ref ID J:58793)
- the shortened tibia has a tapered appearance and always results from a deficiency of the distal portion
- bowed fibula (MGI Ref ID J:58793)
- when there is visible shortening of the tibia the fibula is bowed
- decreased lumbar vertebrae number (MGI Ref ID J:58793)
- over 95% of heterozygotes have only 5 lumbar vertebrae and a few have only 4, whereas wildtype animals have 6
- synostosis (MGI Ref ID J:58793)
- metatarsal synostosis in more severe expression
- limbs/digits/tail phenotype
- abnormal tarsal bone morphology (MGI Ref ID J:58793)
- in heterozygotes in which the tibia is visibly smaller or absent, coalition of the ankle bones and metatarsal synostosis can be found
- abnormal tibia morphology (MGI Ref ID J:58793)
- the tibia is reduced in size to a degree that can be used to classify heterozygotes in one of three discrete categories: imperceptibly shortened, noticably shortened, or entirely absent
- absent tibia (MGI Ref ID J:58793)
- short tibia (MGI Ref ID J:58793)
- the shortened tibia has a tapered appearance and always results from a deficiency of the distal portion
- bowed fibula (MGI Ref ID J:58793)
- when there is visible shortening of the tibia the fibula is bowed
- hemimelia (MGI Ref ID J:58793)
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Dh/Dh
Background Not Specified
- embryogenesis phenotype
- abnormal embryonic tissue morphology (MGI Ref ID J:5034)
- splanchnic mesodermat embryonic day 9.5 is abnormal in appearance from the stomach to the posterior end of the coelom where there is no epithelial plate, although the anterior end is normal, and aberrant development in the gut follows
- lethality-postnatal
- postnatal lethality (MGI Ref ID J:112)
- homozygotes usually die in the first few days of life and approximately 4% survive to wean age and may breed
- homozygotes die, usually within 4 days of birth
- skeleton phenotype
- abnormal sternebra morphology (MGI Ref ID J:112)
- fewer than normal sternebrae, with homozygotes having an average of 5.0 sternebrae and wild-type having 6.1
- absent patella (MGI Ref ID J:112)
- patellae are often absent
- absent tibia (MGI Ref ID J:112)
- both tibiae are usually absent
- decreased presacral vertebrae number (MGI Ref ID J:112)
- homozygotes have an average of 1.6 fewer presacral vertebrae because of a tendency for fewer than normal lumbar and thoracic vertebrae
- decreased rib number (MGI Ref ID J:112)
- homozygotes have an average of 12.5 thoracic ribs and wild-type have 13
- short femur (MGI Ref ID J:112)
- femur is shortened, distorted and often fragmented at birth
- limbs/digits/tail phenotype
- *normal* limbs/digits/tail phenotype (MGI Ref ID J:112)
- forelimbs are normal
- abnormal hindlimb morphology (MGI Ref ID J:112)
- hind legs are short and twisted and all homozygotes are affected
- the hind leg is always greatly twisted and reduced in size
- absent tibia (MGI Ref ID J:112)
- both tibiae are usually absent
- short femur (MGI Ref ID J:112)
- femur is shortened, distorted and often fragmented at birth
- absent patella (MGI Ref ID J:112)
- patellae are often absent
- oligodactyly (MGI Ref ID J:112)
- absence of 1 to 4 digits in all homozygotes with the left hind feet more affected than the right hind feet
- loss of up to three digits from the pre-axial side of the hind foot
- syndactyly (MGI Ref ID J:112)
- on 5% of feet of homozygotes, usually between digits III and IV
- immune system phenotype
- absent spleen (MGI Ref ID J:152370)
- of 25 homozygotes assessed at birth or within a few days of birth none had a spleen
- digestive/alimentary phenotype
- abnormal digestive system morphology (MGI Ref ID J:152370)
- the anus and external opening of the urethra may be closed, the stomach is always very small, the intestine is half the normal length and ends blindly in the region of the colon
- absent anus (MGI Ref ID J:112)
- 44% of homozygotes examined at birth or within a few days of birth are found to have no anus
- absent cecum (MGI Ref ID J:112)
- 28% of homozygotes examined at birth or within a few days of birth have no caecum
- anal atresia (MGI Ref ID J:152370)
- small stomach (MGI Ref ID J:152370)
- extreme reduction in stomach size in all homozygotes
- renal/urinary system phenotype
- abnormal urinary system morphology (MGI Ref ID J:152370)
- severe hydronepohrosis and hydroureter with the two ureters often joining together and having no bladder and an incompletely formed urethra
- abnormal ureter development (MGI Ref ID J:112)
- 20% of newborn homozygotes have blind endings to the ureters
- absent urinary bladder (MGI Ref ID J:152370)
- hydronephrosis (MGI Ref ID J:152370)
- found as early as embryonic day 15.5 and all homozygotes have hydropic kidneys and ureters
- hydroureter (MGI Ref ID J:152370)
- urethra atresia (MGI Ref ID J:112)
- 20% of newborn homozygotes have blind endings to the urethras
- urinary bladder hypoplasia (MGI Ref ID J:112)
- 32% of newborn homozygotes have no bladder or a vestigial bladder
- hematopoietic system phenotype
- absent spleen (MGI Ref ID J:152370)
- of 25 homozygotes assessed at birth or within a few days of birth none had a spleen
- reproductive system phenotype
- abnormal vagina development (MGI Ref ID J:112)
- 10% of homozygous newborns have a gap in the vagina and 4% have no external genital papilla or opening
- absent external male genitalia (MGI Ref ID J:152370)
- in some homozygotes
- blind uterine horn (MGI Ref ID J:112)
- 10% of newborn homozygotes have blind endings to the uterine horns
- vagina atresia (MGI Ref ID J:112)
- 4% of newborn homozygotes have no vaginal opening
- cardiovascular system phenotype
- abnormal cardinal vein morphology (MGI Ref ID J:5034)
- abnormal vasculogenesis (MGI Ref ID J:5034)
- the vitelline vein does not pass around the duodenum and the duodenum is usually displaced medially and caudally from its normal position
- the posterior vena cava usually develops from the left posterior cardinal vein instead of the right and is positioned on the left side of the aorta, runs anteriorly in the body wall and joins the azygous vein
- the vitelline vein enters the liver at a more ventral point than normal
- the left posterior cardinal vein becomes enlarged and acts as the main drainage for the whole body posterior to the heart and eventually forms the definitive posterior vena cava, and pushes against the left kidney which becomes flattened
- abnormal vena cava morphology (MGI Ref ID J:5034)
Dh/Dh
involves: C3H/He
- limbs/digits/tail phenotype
- abnormal caudal vertebrae morphology (MGI Ref ID J:31339)
- 1 of 33 homozygous newborns have a curled tail due to distortion of caudal vertebrae
- skeleton phenotype
- abnormal caudal vertebrae morphology (MGI Ref ID J:31339)
- 1 of 33 homozygous newborns have a curled tail due to distortion of caudal vertebrae
- abnormal lumbar vertebrae morphology (MGI Ref ID J:31339)
- the last lumbar vertebra is abnormal in shape and irregularly connected with sacral vertebrae on one side in 7 of 33 homozygous newborns
- decreased lumbar vertebrae number (MGI Ref ID J:31339)
- all of 33 homozygous newborns have fewer than the normal 6 lumbar vertebrae, with 32 having 5 lumbar vertebrae and 1 having only 4 lumbar vertebrae
- abnormal sternum morphology (MGI Ref ID J:31339)
- 10 of 33 homozygous newborns have a distorted sternum often with bifurcated xiphoid process
- decreased rib number (MGI Ref ID J:31339)
- 32 of 33 homozygous newborns have only 6 true ribs on the right and left, instead of the normal 7
Dh/Dh+
Background Not Specified
- embryogenesis phenotype
- abnormal embryonic tissue morphology (MGI Ref ID J:5034)
- splanchnic mesoderm at embryonic day 9.5 is abnormal in appearance from the stomach to the posterior end of the coelom, but is normal in the anterior end, and aberrant development in the gut follows
- limbs/digits/tail phenotype
- abnormal digit morphology (MGI Ref ID J:112)
- defects are localized to the preaxial side of the hindlimbs and vary in severity in a range including a slight thickening and lengthening of the hallux, triphalangy of the hallux, addition of a digit or part of a digit on the outside of the hallux, or oligodactyly
- oligodactyly (MGI Ref ID J:152370)
- preaxial oligodactyly of the hindlimbs
- polydactyly (MGI Ref ID J:152370)
- preaxial polydactyly of the hindlimbs
- polydactyly is more common than oligodactyly and triphalangy of the hallux is most common
- polysyndactyly (MGI Ref ID J:112)
- syndactyly (MGI Ref ID J:152370)
- hind-foot syndactyly may occur between digits IV and III, III and II, or II and I
- polysyndactyly (MGI Ref ID J:112)
- triphalangia (MGI Ref ID J:152370)
- abnormal hindlimb morphology (MGI Ref ID J:112)
- luxation and reduction in length of one or both hindlimbs can be found in some heterozygotes accompanied by oligodactyly
- luxation is found in 40.8% of left hind legs and 49.2% of right hind legs
- in the more severe cases the patella and trochlea patellaris are reduced or absent
- abnormal femur morphology (MGI Ref ID J:152370)
- the femur is reduced in size and in some cases fragmented
- abnormal tibia morphology (MGI Ref ID J:152370)
- tibial hemimelia or absence of the tibia accompanied by fibular distortion
- bowed fibula (MGI Ref ID J:152370)
- can result from the reduction or absence of the tibia
- abnormal patella morphology (MGI Ref ID J:112)
- absent patella (MGI Ref ID J:112)
- hemimelia (MGI Ref ID J:152370)
- tibial hemimelia with luxation of the hind legs
- skeleton phenotype
- abnormal femur morphology (MGI Ref ID J:152370)
- the femur is reduced in size and in some cases fragmented
- abnormal patella morphology (MGI Ref ID J:112)
- absent patella (MGI Ref ID J:112)
- abnormal pubis morphology (MGI Ref ID J:152370)
- rarely there is a reduction or even loss of the pubic element of the pelvic girdle
- abnormal sternebra morphology (MGI Ref ID J:112)
- fewer than average sternebrae, with heterozygotes having an average of 5.5 sternabrae and wild-type having 6.1
- the number of sternebrae and presacral vertebrae tends to be reduced
- abnormal tibia morphology (MGI Ref ID J:152370)
- tibial hemimelia or absence of the tibia accompanied by fibular distortion
- bowed fibula (MGI Ref ID J:152370)
- can result from the reduction or absence of the tibia
- decreased presacral vertebrae number (MGI Ref ID J:112)
- heterozygotes have an average of 0.8 fewer presacral vertebrae because of a tendency for fewer than normal lumbar and thoracic vertebrae
- the number of sternebrae and presacral vertebrae tends to be reduced
- lethality-postnatal
- postnatal lethality (MGI Ref ID J:112)
- approximately 27% fewer heterozygotes than wild-type siblings survive to wean age
- growth/size phenotype
- decreased body weight (MGI Ref ID J:112)
- heterozygotes weigh approximately 15% less than wild-type siblings at 3 to 4 weeks of age
- hematopoietic system phenotype
- absent spleen (MGI Ref ID J:112)
- 25 of 25 heterozygotes completely lack the spleen and the splenic artery supplies the posterior branches of the pancreas
- the entire absence of the spleen in all carriers is detectable in newborns by visible assessment of viscera through the body wall
- increased granulocyte number (MGI Ref ID J:30753)
- increased lymphocyte cell number (MGI Ref ID J:30753)
- increased platelet cell number (MGI Ref ID J:30753)
- immune system phenotype
- absent spleen (MGI Ref ID J:112)
- 25 of 25 heterozygotes completely lack the spleen and the splenic artery supplies the posterior branches of the pancreas
- the entire absence of the spleen in all carriers is detectable in newborns by visible assessment of viscera through the body wall
- enlarged lymph nodes (MGI Ref ID J:30753)
- increased granulocyte number (MGI Ref ID J:30753)
- increased lymphocyte cell number (MGI Ref ID J:30753)
- renal/urinary system phenotype
- abnormal kidney morphology (MGI Ref ID J:112)
- most heterozygotes have an abnormal flattening of the left kidney where it abuts the stomach, and the remainder have a hyudropic left kidney and associated hydroureter
- marked flattening of the antero-ventral part of the left kidney
- hydronephrosis (MGI Ref ID J:152370)
- can occur, but is not common
- hydroureter (MGI Ref ID J:112)
- found only in a minority of the left kidneys
- can occur, but is not common
- digestive/alimentary phenotype
- abnormal digestive system morphology (MGI Ref ID J:152370)
- shorter than normal alimentary canal
- small stomach (MGI Ref ID J:112)
- small stomach, primarily due to shortening of the cardiac end, in 17 of 25 heterozygotes
- smaller than normal stomach
- cardiovascular system phenotype
- abnormal cardinal vein morphology (MGI Ref ID J:5034)
- abnormal vasculogenesis (MGI Ref ID J:5034)
- the vitelline vein does not pass around the duodenum and the duodenum is usually displaced medially and caudally from its normal position
- the posterior vena cava usually develops from the left posterior cardinal vein instead of the right and is positioned on the left side of the aorta, runs anteriorly in the body wall and joins the azygous vein
- the vitelline vein enters the liver at a more ventral point than normal
- the left posterior cardinal vein becomes enlarged and acts as the main drainage for the whole body posterior to the heart and eventually forms the definitive posterior vena cava, and pushes against the left kidney which becomes flattened
- abnormal vena cava morphology (MGI Ref ID J:5034)
- lethality-prenatal/perinatal
- neonatal lethality (MGI Ref ID J:152370)
- the neonatal death rate is higher than normal
Dh/Dh+
B6.CBA-Dh
- immune system phenotype
- abnormal T cell differentiation (MGI Ref ID J:5834)
- absent spleen (MGI Ref ID J:5834)
- decreased immunoglobulin level (MGI Ref ID J:5834)
- hematopoietic system phenotype
- abnormal T cell differentiation (MGI Ref ID J:5834)
- absent spleen (MGI Ref ID J:5834)
Dh/Dh+
involves: C3H/He
- skeleton phenotype
- abnormal caudal vertebrae morphology (MGI Ref ID J:31339)
- 1 of 109 heterozygous newborns show a curled tail due to distortion of caudal vertebrae
- abnormal rib morphology (MGI Ref ID J:31339)
- the ventral segment of adjacent ribs, both true and false ribs, in newborn heterozygotes is sometimes fused which forms a fork-like structure
- decreased rib number (MGI Ref ID J:31339)
- the majority of newborn heterozygotes have only 6 true ribs on the right and left, instead of the normal 7
- abnormal sternum morphology (MGI Ref ID J:31339)
- the sternum is often distorted and xiphoid process bifurcated in newborn heterozygotes that have abnormal ribs
- split xiphoid process (MGI Ref ID J:31339)
- decreased lumbar vertebrae number (MGI Ref ID J:31339)
- all newborn heterozygotes are found to have 5, instead of the normal 6, lumbar vertebrae
- limbs/digits/tail phenotype
- abnormal caudal vertebrae morphology (MGI Ref ID J:31339)
- 1 of 109 heterozygous newborns show a curled tail due to distortion of caudal vertebrae
This mouse can be used to support research in many areas including:Dh related
Developmental Biology Research
Internal/Organ Defects
spleen: GI
Skeletal Defects
Immunology and Inflammation Research
Immunodeficiency Associated with Other Defects
Internal/Organ Research
Gastrointestinal Defects
Spleen Defects
asplenic
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Dh | ||
|---|---|---|---|
| Allele Name | dominant hemimelia | ||
| Allele Type | Spontaneous | ||
| Strain of Origin | crossbred stock carrying a translocation | ||
| Gene Symbol and Name | Dh, dominant hemimelia | ||
| Chromosome | 1 | ||
| Allele Symbol | a | ||
| Allele Name | nonagouti | ||
| Allele Type | Spontaneous | ||
Genotyping
Genotyping Information
This strain will not have a genotyping protocol or one is not currently available.
Helpful Links
Genotyping resources and troubleshooting
References
References
Selected Reference(s)
Searle AG. 1964. The genetics and morphology of two 'luxoid' mutants in the house mouse Genet Res 5:171-197. [MGI Ref ID J:112]
Additional References
Dh relatedBattisto JR; Cantor LC; Borek F; Goldstein AL; Cabrerra E. 1969. Immunoglobulin synthesis in hereditarily spleenless mice. Nature 222(199):1196-8. [PubMed: 5788994] [MGI Ref ID J:5116]
Carter TC. 1954. Dominant hemimelia, Dh Mouse News Lett 11:16. [MGI Ref ID J:13384]
Fletcher MP; Ikeda RM; Gershwin ME. 1977. Splenic influence of T cell function: the immunobiology of the inbred hereditarily asplenic mouse. J Immunol 119(1):110-7. [PubMed: 194980] [MGI Ref ID J:5834]
Gershwin ME; Ahmed A; Ikeda RM; Shifrine M; Wilson F. 1978. Immunobiology of congenitally athymic-asplenic mice. Immunology 34(4):631-42. [PubMed: 721133] [MGI Ref ID J:6062]
Gershwin ME; Castles JJ; Ikeda RM; Erickson K; Montero J. 1979. Studies of congenitally immunologic mutant New Zealand mice. I. Autoimmune features of hereditarily asplenic (Dh/+) NZB mice; reduction of naturally occurring thymocytotoxic antibody and normal suppressor function. J Immunol 122(2):710-7. [PubMed: 310848] [MGI Ref ID J:12036]
Green MC. 1967. A defect of the splanchnic mesoderm caused by the mutant gene dominant hemimelia in the mouse. Dev Biol 15(1):62-89. [PubMed: 6067803] [MGI Ref ID J:5034]
Hecksher-Sorensen J; Watson RP; Lettice LA; Serup P; Eley L; De Angelis C; Ahlgren U; Hill RE. 2004. The splanchnic mesodermal plate directs spleen and pancreatic laterality, and is regulated by Bapx1/Nkx3.2. Development 131(19):4665-75. [PubMed: 15329346] [MGI Ref ID J:93234]
Higgins M; Hill RE; West JD. 1992. Dominant hemimelia and En-1 on mouse chromosome 1 are not allelic. Genet Res 60(1):53-60. [PubMed: 1360439] [MGI Ref ID J:2793]
Holmes LB. 1986. Identification of Dh/+ and Dh/Dh embryos through close linkage of Dh and peptidase-3. Teratology 34(3):353-7. [PubMed: 3541275] [MGI Ref ID J:8552]
Lettice L; Hecksher-Sorensen J; Hill RE. 1999. The dominant hemimelia mutation uncouples epithelial-mesenchymal interactions and disrupts anterior mesenchyme formation in mouse hindlimbs. Development 126(21):4729-36. [PubMed: 10518490] [MGI Ref ID J:58081]
Lozzio BB; Wargon LB. 1974. Immune competence of hereditarily asplenic mice. Immunology 27(2):167-78. [PubMed: 4214128] [MGI Ref ID J:5492]
Machado EA; Lozzio BB. 1976. Animal model of human disease: hyposplenia, asplenia, and immunodeficiency. Am J Pathol 85(2):515-8. [PubMed: 998728] [MGI Ref ID J:5729]
Morin BJ; Owen MH; Ramamurthy GV; Holmes LB. 1999. Pattern of skeletal malformations produced by Dominant hemimelia (Dh). Teratology 60(6):348-55. [PubMed: 10590396] [MGI Ref ID J:58793]
SEARLE AG. 1959. Hereditary absence of spleen in the mouse. Nature 184(Suppl 18):1419-20. [PubMed: 14444358] [MGI Ref ID J:152370]
Suto J; Wakayama T; Imamura K; Goto S; Fukuta K. 1996. High lethality of F1 (Dh/+) male mice from the cross between DDD female and DH (Dh/+) male. Exp Anim 45(1):99-101. [PubMed: 8689589] [MGI Ref ID J:31338]
Suto J; Wakayama T; Imamura K; Goto S; Fukuta K. 1996. Skeletal malformations caused by the Dh (Dominant hemimelia) gene in mice. Exp Anim 45(1):95-8. [PubMed: 8689588] [MGI Ref ID J:31339]
Suto Ji J; Sekikawa K. 2002. Y-chromosomal factor is involved in neonatal lethality in (female symbolDDD x male symbolDH- Dh/+) F(1)- Dh/+ male mice. Mamm Genome 13(3):149-52. [PubMed: 11919685] [MGI Ref ID J:75618]
Welles WL; Battisto JR. 1981. The significance of hereditary asplenia for immunologic competence. In: Immunologic Defects in Laboratory Animals. Plenum Press, New York. [MGI Ref ID J:30753]
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 |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $1900.00 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.
Additional Supply Details
| Pricing for International shipping destinations |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $2470.00 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.
Additional Supply Details
|
|
|
Supply Details
| Standard Supply | Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information. |
|---|---|
| Supply Notes |
|
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. | ||
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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 and Purchasing Information
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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.