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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
Generation DefinitionsAppearance
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 (103 strains)
Phenotype
Phenotype Information
assigned by genotype
Dh/Dh+
B6C3Fe a/a-Dh/J
- skeleton phenotype
- *normal* skeleton phenotype
- lumbar vertebrae are not found to have an abnormal shape on this genetic background (MGI Ref ID J:58793)
- abnormal sternebra morphology
- over 88% of heterozygotes have 5 sternebrae rather than the normal 6 (MGI Ref ID J:58793)
- abnormal tarsal bone morphology
- in heterozygotes in which the tibia is visibly smaller or absent, coalition of the ankle bones and metatarsal synostosis can be found (MGI Ref ID J:58793)
- abnormal tibia morphology
- 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 (MGI Ref ID J:58793)
- bowed fibula
- when there is visible shortening of the tibia the fibula is bowed (MGI Ref ID J:58793)
- decreased lumbar vertebrae number
- over 95% of heterozygotes have only 5 lumbar vertebrae and a few have only 4, whereas wildtype animals have 6 (MGI Ref ID J:58793)
- synostosis
- metatarsal synostosis in more severe expression (MGI Ref ID J:58793)
- limbs/digits/tail phenotype
- abnormal tarsal bone morphology
- in heterozygotes in which the tibia is visibly smaller or absent, coalition of the ankle bones and metatarsal synostosis can be found (MGI Ref ID J:58793)
- abnormal tibia morphology
- 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 (MGI Ref ID J:58793)
- bowed fibula
- when there is visible shortening of the tibia the fibula is bowed (MGI Ref ID J:58793)
- 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
- mortality/aging
- postnatal lethality
- embryogenesis phenotype
- abnormal embryonic tissue morphology
- 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 (MGI Ref ID J:5034)
- skeleton phenotype
- abnormal sternebra morphology
- fewer than normal sternebrae, with homozygotes having an average of 5.0 sternebrae and wild-type having 6.1 (MGI Ref ID J:112)
- absent patella
- patellae are often absent (MGI Ref ID J:112)
- absent tibia
- both tibiae are usually absent (MGI Ref ID J:112)
- decreased presacral vertebrae number
- homozygotes have an average of 1.6 fewer presacral vertebrae because of a tendency for fewer than normal lumbar and thoracic vertebrae (MGI Ref ID J:112)
- decreased rib number
- homozygotes have an average of 12.5 thoracic ribs and wild-type have 13 (MGI Ref ID J:112)
- short femur
- femur is shortened, distorted and often fragmented at birth (MGI Ref ID J:112)
- limbs/digits/tail phenotype
- *normal* limbs/digits/tail phenotype
- forelimbs are normal (MGI Ref ID J:112)
- 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 (MGI Ref ID J:112)
- digestive/alimentary phenotype
- abnormal digestive system morphology
- 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 (MGI Ref ID J:152370)
- absent anus
- 44% of homozygotes examined at birth or within a few days of birth are found to have no anus (MGI Ref ID J:112)
- absent cecum
- 28% of homozygotes examined at birth or within a few days of birth have no caecum (MGI Ref ID J:112)
- anal atresia (MGI Ref ID J:152370)
- small stomach (MGI Ref ID J:152370)
- extreme reduction in stomach size in all homozygotes (MGI Ref ID J:112)
- renal/urinary system phenotype
- abnormal renal/urinary system morphology
- severe hydronepohrosis and hydroureter with the two ureters often joining together and having no bladder and an incompletely formed urethra (MGI Ref ID J:152370)
- abnormal ureter development
- 20% of newborn homozygotes have blind endings to the ureters (MGI Ref ID J:112)
- 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 (MGI Ref ID J:112)
- hydroureter (MGI Ref ID J:152370)
- urethra atresia
- 20% of newborn homozygotes have blind endings to the urethras (MGI Ref ID J:112)
- urinary bladder hypoplasia
- 32% of newborn homozygotes have no bladder or a vestigial bladder (MGI Ref ID J:112)
- 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 (MGI Ref ID J:112)
- reproductive system phenotype
- abnormal vagina development
- 10% of homozygous newborns have a gap in the vagina and 4% have no external genital papilla or opening (MGI Ref ID J:112)
- absent external male genitalia
- in some homozygotes (MGI Ref ID J:152370)
- blind uterine horn
- 10% of newborn homozygotes have blind endings to the uterine horns (MGI Ref ID J:112)
- vagina atresia
- 4% of newborn homozygotes have no vaginal opening (MGI Ref ID J:112)
- cardiovascular system phenotype
- abnormal cardinal vein morphology (MGI Ref ID J:5034)
- abnormal vasculogenesis
- the vitelline vein does not pass around the duodenum and the duodenum is usually displaced medially and caudally from its normal position (MGI Ref ID J:5034)
- 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 (MGI Ref ID J:5034)
- the vitelline vein enters the liver at a more ventral point than normal (MGI Ref ID J:5034)
- 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 (MGI Ref ID J:5034)
- abnormal vena cava morphology (MGI Ref ID J:5034)
Dh/Dh
involves: C3H/He
- limbs/digits/tail phenotype
- abnormal caudal vertebrae morphology
- 1 of 33 homozygous newborns have a curled tail due to distortion of caudal vertebrae (MGI Ref ID J:31339)
- skeleton phenotype
- abnormal caudal vertebrae morphology
- 1 of 33 homozygous newborns have a curled tail due to distortion of caudal vertebrae (MGI Ref ID J:31339)
- abnormal lumbar vertebrae morphology
- the last lumbar vertebra is abnormal in shape and irregularly connected with sacral vertebrae on one side in 7 of 33 homozygous newborns (MGI Ref ID J:31339)
- decreased lumbar vertebrae number
- 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 (MGI Ref ID J:31339)
- abnormal sternum morphology
- 10 of 33 homozygous newborns have a distorted sternum often with bifurcated xiphoid process (MGI Ref ID J:31339)
- decreased rib number
- 32 of 33 homozygous newborns have only 6 true ribs on the right and left, instead of the normal 7 (MGI Ref ID J:31339)
Dh/Dh+
Background Not Specified
- mortality/aging
- partial neonatal lethality
- the neonatal death rate is higher than normal (MGI Ref ID J:152370)
- postnatal lethality
- approximately 27% fewer heterozygotes than wild-type siblings survive to wean age (MGI Ref ID J:112)
- embryogenesis phenotype
- abnormal embryonic tissue morphology
- 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 (MGI Ref ID J:5034)
- limbs/digits/tail phenotype
- abnormal digit morphology
- 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 (MGI Ref ID J:112)
- oligodactyly (MGI Ref ID J:152370)
- preaxial oligodactyly of the hindlimbs (MGI Ref ID J:112)
- polydactyly (MGI Ref ID J:152370)
- 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 (MGI Ref ID J:112)
- polysyndactyly (MGI Ref ID J:112)
- triphalangia (MGI Ref ID J:152370)
- abnormal hindlimb morphology
- luxation and reduction in length of one or both hindlimbs can be found in some heterozygotes accompanied by oligodactyly (MGI Ref ID J:112)
- luxation is found in 40.8% of left hind legs and 49.2% of right hind legs (MGI Ref ID J:112)
- in the more severe cases the patella and trochlea patellaris are reduced or absent (MGI Ref ID J:112)
- abnormal femur morphology
- the femur is reduced in size and in some cases fragmented (MGI Ref ID J:152370)
- abnormal tibia morphology
- tibial hemimelia or absence of the tibia accompanied by fibular distortion (MGI Ref ID J:152370)
- bowed fibula (MGI Ref ID J:152370)
- can result from the reduction or absence of the tibia (MGI Ref ID J:112)
- 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 (MGI Ref ID J:112)
- skeleton phenotype
- abnormal femur morphology
- the femur is reduced in size and in some cases fragmented (MGI Ref ID J:152370)
- abnormal patella morphology (MGI Ref ID J:112)
- absent patella (MGI Ref ID J:112)
- abnormal pubis morphology
- rarely there is a reduction or even loss of the pubic element of the pelvic girdle (MGI Ref ID J:152370)
- abnormal sternebra morphology
- abnormal tibia morphology
- tibial hemimelia or absence of the tibia accompanied by fibular distortion (MGI Ref ID J:152370)
- bowed fibula (MGI Ref ID J:152370)
- can result from the reduction or absence of the tibia (MGI Ref ID J:112)
- decreased presacral vertebrae number
- growth/size phenotype
- decreased body weight
- heterozygotes weigh approximately 15% less than wild-type siblings at 3 to 4 weeks of age (MGI Ref ID J:112)
- hematopoietic system phenotype
- absent spleen
- 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
- 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
- hydronephrosis
- can occur, but is not common (MGI Ref ID J:152370)
- hydroureter
- digestive/alimentary phenotype
- abnormal digestive system morphology
- shorter than normal alimentary canal (MGI Ref ID J:152370)
- cardiovascular system phenotype
- abnormal cardinal vein morphology (MGI Ref ID J:5034)
- abnormal vasculogenesis
- the vitelline vein does not pass around the duodenum and the duodenum is usually displaced medially and caudally from its normal position (MGI Ref ID J:5034)
- 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 (MGI Ref ID J:5034)
- the vitelline vein enters the liver at a more ventral point than normal (MGI Ref ID J:5034)
- 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 (MGI Ref ID J:5034)
- abnormal vena cava morphology (MGI Ref ID J:5034)
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)
- cellular phenotype
- abnormal T cell differentiation (MGI Ref ID J:5834)
Dh/Dh+
involves: C3H/He
- skeleton phenotype
- abnormal caudal vertebrae morphology
- 1 of 109 heterozygous newborns show a curled tail due to distortion of caudal vertebrae (MGI Ref ID J:31339)
- abnormal rib morphology
- the ventral segment of adjacent ribs, both true and false ribs, in newborn heterozygotes is sometimes fused which forms a fork-like structure (MGI Ref ID J:31339)
- decreased rib number
- the majority of newborn heterozygotes have only 6 true ribs on the right and left, instead of the normal 7 (MGI Ref ID J:31339)
- abnormal sternum morphology
- the sternum is often distorted and xiphoid process bifurcated in newborn heterozygotes that have abnormal ribs (MGI Ref ID J:31339)
- split xiphoid process (MGI Ref ID J:31339)
- decreased lumbar vertebrae number
- all newborn heterozygotes are found to have 5, instead of the normal 6, lumbar vertebrae (MGI Ref ID J:31339)
- limbs/digits/tail phenotype
- abnormal caudal vertebrae morphology
- 1 of 109 heterozygous newborns show a curled tail due to distortion of caudal vertebrae (MGI Ref ID J:31339)
This mouse can be used to support research in many areas including:Dh related
Developmental Biology Research
Internal/Organ Defects
spleen: GI
Skeletal Defects
Oligodactyly
Immunology and Inflammation Research
Immunodeficiency Associated with Other Defects
Internal/Organ Research
Gastrointestinal Defects
Spleen Defects
asplenic
Genes & Alleles
Gene & Allele Information provided by MGI
| 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 | ||
| Strain of Origin | old mutant of the mouse fancy | ||
| Gene Symbol and Name | a, nonagouti | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | AGSW; AGTI; AGTIL; ASP; As; SHEP9; agouti; agouti signal protein; agouti suppressor; | ||
| Molecular Note | Characterization of this allele shows an insertion of DNA comprised of a 5.5kb virus-like element, VL30, into the first intron of the agouti gene. The VL30 element itself contains an additional 5.5 kb sequence, flanked by 526 bp of direct repeats. The host integration site is the same as for at-2Gso and Aw-38J and includes a duplication of four nucleotides of host DNA and a deletion of 2 bp from the end of each repeat. Northern analysis of mRNA from skin of homozygotes shows a smaller agouti message and levels 8 fold lower than found in wild-type. [MGI Ref ID J:16984] [MGI Ref ID J:24934] | ||
References
References provided by MGI
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 relateda 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]
Baba K; Sakakibara S; Setsu T; Terashima T. 2007. The superficial layers of the superior colliculus are cytoarchitectually and myeloarchitectually disorganized in the reelin-deficient mouse, reeler. Brain Res 1140:205-15. [PubMed: 17173877] [MGI Ref ID J:120267]
Batchelor AL; Phillips RJ; Searle AG. 1966. A comparison of the mutagenic effectiveness of chronic neutron- and gamma-irradiation of mouse spermatogonia. Mutat Res 3(3):218-29. [PubMed: 5962396] [MGI Ref ID J:5021]
Bjorbaek C; Elmquist JK; Frantz JD; Shoelson SE; Flier JS. 1998. Identification of SOCS-3 as a potential mediator of central leptin resistance. Mol Cell 1(4):619-25. [PubMed: 9660946] [MGI Ref ID J:119803]
Bultman SJ; Klebig ML; Michaud EJ; Sweet HO; Davisson MT; Woychik RP. 1994. Molecular analysis of reverse mutations from nonagouti (a) to black-and-tan (a(t)) and white-bellied agouti (Aw) reveals alternative forms of agouti transcripts. Genes Dev 8(4):481-90. [PubMed: 8125260] [MGI Ref ID J:16984]
Bultman SJ; Michaud EJ; Woychik RP. 1992. Molecular characterization of the mouse agouti locus. Cell 71(7):1195-204. [PubMed: 1473152] [MGI Ref ID J:3523]
Bultman SJ; Russell LB; Gutierrez-Espeleta GA; Woychik RP. 1991. Molecular characterization of a region of DNA associated with mutations at the agouti locus in the mouse. Proc Natl Acad Sci U S A 88(18):8062-6. [PubMed: 1896452] [MGI Ref ID J:16567]
Bundschuh VG; Madry M. 1988. [atwp mutation in an albino mouse substrain (AB/Hum-1)] Z Versuchstierkd 31(6):249-54. [PubMed: 3227730] [MGI Ref ID J:16568]
Butler AE; Janson J; Soeller WC; Butler PC. 2003. Increased beta-cell apoptosis prevents adaptive increase in beta-cell mass in mouse model of type 2 diabetes: evidence for role of islet amyloid formation rather than direct action of amyloid. Diabetes 52(9):2304-14. [PubMed: 12941770] [MGI Ref ID J:132530]
Cattanach BM. 1961. A chemically-induced variegated-type position effect in the mouse. Z Vererbungsl 92:165-82. [PubMed: 13877379] [MGI Ref ID J:160128]
Cropley JE; Suter CM; Beckman KB; Martin DI. 2006. Germ-line epigenetic modification of the murine A vy allele by nutritional supplementation. Proc Natl Acad Sci U S A 103(46):17308-12. [PubMed: 17101998] [MGI Ref ID J:117156]
De Souza J; Butler AA; Cone RD. 2000. Disproportionate inhibition of feeding in A(y) mice by certain stressors: a cautionary note. Neuroendocrinology 72(2):126-32. [PubMed: 10971147] [MGI Ref ID J:102986]
Dickie MM. 1969. Mutations at the agouti locus in the mouse. J Hered 60(1):20-5. [PubMed: 5798139] [MGI Ref ID J:30922]
Duchesnes CE; Naggert JK; Tatnell MA; Beckman N; Marnane RN; Rodrigues JA; Halim A; Pontre B; Stewart AW; Wolff GL; Elliott R; Mountjoy KG. 2009. New Zealand Ginger Mouse: Novel model that associates the tyrp1b pigmentation gene locus with regulation of lean body mass. Physiol Genomics 37(3):164-74. [PubMed: 19293329] [MGI Ref ID J:146052]
Dunn LC. 1928. A Fifth Allelomorph in the Agouti Series of the House Mouse. Proc Natl Acad Sci U S A 14(10):816-9. [PubMed: 16587414] [MGI Ref ID J:15011]
Dunn LC; Macdowell EC; Lebedeff GA. 1937. Studies on Spotting Patterns III. Interaction between Genes Affecting White Spotting and Those Affecting Color in the House Mouse. Genetics 22(2):307-18. [PubMed: 17246842] [MGI Ref ID J:12954]
Enshell-Seijffers D; Lindon C; Morgan BA. 2008. The serine protease Corin is a novel modifier of the Agouti pathway. Development 135(2):217-25. [PubMed: 18057101] [MGI Ref ID J:130426]
Feuerer M; Herrero L; Cipolletta D; Naaz A; Wong J; Nayer A; Lee J; Goldfine AB; Benoist C; Shoelson S; Mathis D. 2009. Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters. Nat Med 15(8):930-9. [PubMed: 19633656] [MGI Ref ID J:152186]
Fujimoto W; Shiuchi T; Miki T; Minokoshi Y; Takahashi Y; Takeuchi A; Kimura K; Saito M; Iwanaga T; Seino S. 2007. Dmbx1 is essential in agouti-related protein action. Proc Natl Acad Sci U S A 104(39):15514-9. [PubMed: 17873059] [MGI Ref ID J:125193]
Gajewska M; Krysiak E; Wirth-Dziecialowska E. 2010. New coat color mutation mapped in distal part MMU10 MGI Direct Data Submission :. [MGI Ref ID J:162146]
Galbraith DB; Arceci RJ. 1974. Melanocyte populations of yellow and black hair bulbs in the mouse. J Hered 65(6):381-2. [PubMed: 4448905] [MGI Ref ID J:5512]
Galbraith DB; Patrignani AM. 1976. Sulfhydryl compounds in melanocytes of yellow (Ay/a), nonagouti (a/a), and agouti (A/A) mice. Genetics 84(3):587-91. [PubMed: 1001879] [MGI Ref ID J:5737]
Galbraith DB; Wolff GL; Brewer NL. 1980. Hair pigment patterns in different integumental environments of the mouse. Influence of the agouti suppressor (A<s>) mutation on expression of agouti locus alleles. J Hered 71:229-234. [MGI Ref ID J:12033]
Galbraith DB; Wolff GL; Brewer NL. 1979. Tissue microenvironment and the genetic control of hair pigment patterns in mice Dev Genet 1(2):167-179. [MGI Ref ID J:156092]
Geschwind II; Huseby RA; Nishioka R. 1972. The effect of melanocyte-stimulating hormone on coat color in the mouse. Recent Prog Horm Res 28:91-130. [PubMed: 4631622] [MGI Ref ID J:5324]
Granholm DE; Reese RN; Granholm NH. 1996. Agouti alleles alter cysteine and glutathione concentrations in hair follicles and serum of mice (A y/a, A wJ/A wJ, and a/a). J Invest Dermatol 106(3):559-63. [PubMed: 8648194] [MGI Ref ID J:32132]
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Heaney JD; Michelson MV; Youngren KK; Lam MY; Nadeau JH. 2009. Deletion of eIF2beta suppresses testicular cancer incidence and causes recessive lethality in agouti-yellow mice. Hum Mol Genet 18(8):1395-404. [PubMed: 19168544] [MGI Ref ID J:146879]
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Kaminen-Ahola N; Ahola A; Maga M; Mallitt KA; Fahey P; Cox TC; Whitelaw E; Chong S. 2010. Maternal ethanol consumption alters the epigenotype and the phenotype of offspring in a mouse model. PLoS Genet 6(1):e1000811. [PubMed: 20084100] [MGI Ref ID J:156866]
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Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, RG10/RG30.
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $1980.00 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.
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Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
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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. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 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).
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2574.00 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.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
- Cryorecovery - Standard.
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. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 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).
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Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
General Supply Notes
- Genomic DNA is available for this strain from the Mouse DNA Resource.
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"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.No Warranty
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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.