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- Description
- Phenotype
- Genes & alleles
- Genotyping
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- References
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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 C3FeB6 A/Aw-J-ank/J (Changed: 15-DEC-04 ) Type Mutant Stock; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Background Strain C3FeB6 Donor Strain JGBF F15 Generation N32 F2p Appearance
agouti with stiff feet
Related Genotype: A/A Ankank/Ankank
white-bellied agouti with stiff feet
Related Genotype: A/Aw-J Ankank/Ankank
agouti, unaffected
Related Genotype: A/A +/?
white-bellied agouti, unaffected
Related Genotype: A/Aw-J +/? or Aw-J/Aw-J +/?Description
The progressive ankylosis allele (ank) is a spontaneous recessive mutation that causes a severe phenotype of joint calcification and degeneration. Few homozygotes survive beyond 5 months of age, although the adults can breed. Generally no more than 2 litters are produced by homozygotes of either sex. At 4 or 5 weeks of age, homozygotes can be identified by their inability to grasp a wire cage lid with their front paws when suspended above it. The joints swell with a milky fluid, and undergo a process proceeding through mononuclear inflammatory infiltration, hydroxyapatite deposition and increased calcification, hyperplasia, and fibrous and bony ankylosis. (for details see Mahowald et al., 1989; Hakim et al., 1984; Sweet and Green, 1981.) The front feet are affected before the hind feet and the phenotype is more severe in the most distal joints of the limbs. Hyperplasia and degeneration of the joint tissues, and ankylosis occur progressively, decreasing mobility and resulting in a rigid, crouched posture in the adult. Their gate becomes slow, halting, and flatfooted. The morphological changes underlying the stiffening of the vertebral column and resulting thoracic kyphosis are detailed by Sampson, 1988a and 1988b, and Sampson et al., 1991.There is an immune cell involvement in the joints secondary to the central defect. Treatment of ank/ank mice with hydrocortisone beginning at 5 weeks of age resulted in reduced synovial and subsynovial hyperplasia, reduced growth of cartilaginous and bony bridges, and increased accumulation of intra-articular apatite possibly due to the reduction in macrophage activity (Hakim et al., 1986.). Reconstitution of wild type mice with bone marrow or spleen cells from ank/ank mice does not transfer disease and reconstitution of ank/ank mice with wild type bone marrow or spleen cells does not prevent disease (Krug et al., 1997). Additionally, there is an immune cell defect. There is a reduction in the response of spleen cells to phytohaemagglutinin or concanavalin A although the response to LPS appears normal. Spleen cells or macrophages from ank/ank mice do not suppress normal spleen cell responses to phytohaemagglutinin and wild type spleen cells or macrophages do not restore phytohaemagglutinin responsiveness to spleen cells from ank/ank mice (Krug et al., 1989). Fibroblasts from ank/ank mice are Hyperproliferative in response to transforming growth factor beta 1 (Krug, 1998). No impact was found on the phenotype of ank/+ or ank/ank mice when transgenic HLA-B27 was co-expressed (Krug and Taurog, 2000).
In addition to progressive ankylosis and calcification of the peripheral joints and axial skeleton, homozygotes have a smaller overall body size, and some develop balanitis, priapism, and scaling skin lesions on the plantar surface of the paws. The hypermineralization phenotype is associated with abnormal inorganic pyrophophate levels and the downregulation of osteopontin (Harmey et al., 2004).
Development
The progressive ankylosis mutation arose spontaneously in the strain JGBF/Le (Stock No. 000260), a balanced stock for jagged tail (jg) and buff (bf). An affected female displaying a flat-footed gait with rigid toes was the founder for the ank strain. This female's progeny were bred onto a C3FeB6 background via an outcross-intercross breeding scheme. Thus homozygotes were bred to C3FeB6F1 then their obligate heterozygous offspring were sibling mated to produce homozygous breeders for the next generation. The initial characterization was done on N5F1 mice. In June 1976 this strain was at N6, in early 1979 it was at N11, and in November 1983 it reached N24. Neither jg nor bf have been found in this strain since N2. C3FeB6-A/Aw-J-ank was frozen in 1987 by breeding N32 homozygotes to C3FeB6-A/Aw-J to get heterozygous N33 embryos.
Control Information
| Control | ||
|---|---|---|
| +/? sibling | ||
| 001203 C3FeB6F1/J A/Aw-J | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying A allele
003301 (C57BL/6J x C3H-Eya1bor)F1/J 002083 B6 x B6EiC3 a/A-T(7;16)235Dn/J 000507 B6 x B6EiC3 a/A-Otcspf/J 000628 B6.CE-A Amy1b Amy2a5b/J 004200 B6;CBACa Aw-J/A-Npr2cn-2J/GrsrJ 000604 B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J 001752 B6CBCa Aw-J/A-T(7;15)9H/J 006450 B6EiC3 a/A-Vss/GrsrJ 000557 B6EiC3-+ a/LnpUl A/J 000504 B6EiC3Sn a/A-Cacnb4lh/J 000553 B6EiC3Sn a/A-Egfrwa2 Wnt3avt/J 001811 B6EiC3Sn a/A-Otcspf-ash/J 002343 B6EiC3Sn a/A-Otcspf/J 001923 B6EiC3Sn a/A-Ts(417)2Lws TimT(4;17)3Lws/J 000638 C3FeB6 A/Aw-J-Spnb4qv-J/J 000283 LT.CAST-A/J 001759 STOCK A Tyrc Sha/J View Strains carrying A (17 strains)
Phenotype
Phenotype Information
assigned by genotype
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Ankank/Ankank
involves: C3HeB/FeJ * C57BL/6J * JGBF/Le
- life span-post-weaning/aging
- premature death (MGI Ref ID J:6580)
- few mutants survive beyond 5 months of age
- growth/size phenotype
- decreased body weight (MGI Ref ID J:6580)
- lower body weight, first noticeable between 10 and 20 days of age
- reproductive system phenotype
- reduced female fertility (MGI Ref ID J:6580)
- do not produce more than two litters
- reduced male fertility (MGI Ref ID J:6580)
- do not produce more than two litters
- skeleton phenotype
- abnormal joint mobility (MGI Ref ID J:122727)
- joint mobility is decreased at 6 weeks and is more severe at 12 weeks similar to in Anktm1.1Kng homozygotes
- reduction in joint mobility in the forelimb joints are more severe than in the hindlimbs and distal joint in the hindlimbs are more severely affected than proximal joints
- progressive loss of mobility of the joints occurs with age; stiffening of the joints is first apparent at 4-5 weeks of age in the forefeet and eventually involves all the joints of the limbs and vertebral column
- when lifted by the tail from a wire grid, 4.5-5 week old mutants are unable to cling to the grid as the toes are very rigid
- abnormal skeleton morphology (MGI Ref ID J:6580)
- progressive ankylosis
- abnormal cartilage morphology (MGI Ref ID J:6580)
- degeneration and increase in calcification in the cartilage
- abnormal joint morphology (MGI Ref ID J:6580)
- mutants develop a noninflammatory degenerative joint disease, with stiffness of joints starting in forefeet and toes, quickly spreading to other joints
- bone volume in joints is significantly increased and increases in severity with time
- mutants show increased numbers of osteoblast-like cells in the synovial membrane of joints and excessive amount of fibrous tissue, cartilage, and bone in joints at later stages, with many areas of cystic necrosis
- synovial lining in most places, except over articular cartilage or ligament, has a thickened surface layer
- abnormal joint capsule morphology (MGI Ref ID J:6580)
- reduction in the size of the joint cavities in the forefoot at 33 days of age, with excessive osteoblasts
- the joint cavity of the shoulder appears shrunken and opaque, with some calcification in the tendons around the joint at 11 weeks of age
- fused joints (MGI Ref ID J:6580)
- progressive akylosis, such that by 17 weeks of age, the joints of the foot, including the wrist, and of the ribs with adjacent sternebrae are completely ankylosed
- fore and hind feet at 31 weeks of age have toe bones that show bony and cartilaginous fusions across the joints, usually including the sesamoid bones
- abnormal ligament morphology (MGI Ref ID J:6580)
- degeneration in many, although not all, ligaments associated with affected joints
- calcification of the transverse acetabular ligament, which bridges the acetabular notch of the hip, is seen at 17 weeks of age
- abnormal sesamoid bone of gastrocnemius morphology (MGI Ref ID J:6580)
- some of the sesamoid bones are enlarged and appear to be fused with the nearest long bone
- abnormal tendon morphology (MGI Ref ID J:6580)
- degeneration in many, although not all, tendons associated with affected joints
- kyphosis (MGI Ref ID J:6580)
- adults exhibit thoracic kyphosis and prominent haunches
- joint calcification (MGI Ref ID J:6580)
- abnormal and increased calcification within some of the joints (knee, elbow, vertebral column) and joint cavities, resulting in calcified masses at various places near joints
- muscle phenotype
- abnormal tendon morphology (MGI Ref ID J:6580)
- degeneration in many, although not all, tendons associated with affected joints
- craniofacial phenotype
- abnormal tooth hard tissue morphology (MGI Ref ID J:122727)
- the calcified materials surrounding the neck and tooth of all 12 molars is increased
- the neck thickness relative to the enamel cap width is increased
- abnormal cementum morphology (MGI Ref ID J:122727)
- at 12 weeks, enlargement of the cementum
- behavior/neurological phenotype
- abnormal gait (MGI Ref ID J:6580)
- slow halting gait, with all feet flat against the surface
- abnormal posture (MGI Ref ID J:6580)
- adults exhibit a rigid posture
- limbs/digits/tail phenotype
- abnormal limb morphology (MGI Ref ID J:6580)
- in the limbs, abnormalities are more severe in the distal than proximal joints and in the forelimbs than in the hindlimbs
- abnormal digit morphology (MGI Ref ID J:6580)
- toes of the forefeet are stiff and flattened at 33 and 35 days of age, while these abnormalities occur later in the hindfeet (11-17 weeks of age)
- abnormal sesamoid bone of gastrocnemius morphology (MGI Ref ID J:6580)
- some of the sesamoid bones are enlarged and appear to be fused with the nearest long bone
- cellular phenotype
- necrosis (MGI Ref ID J:6580)
- necrosis in the fibrous tissue of the joints, including the ligamets and cartilage
Ankank/Ankank
involves: C3HeB/FeJ * C57BL/6J * JGBF/LeJ
- homeostasis/metabolism phenotype
- abnormal ion homeostasis (MGI Ref ID J:63420)
- primary skin fibroblast cultures show an increase in intracellular and a decrease in extracellular pyrophosphate indicative of defective phosphate homeostatis, and this defect is corrected by transfection with wildtype Ank
- immune system phenotype
- arthritis (MGI Ref ID J:63420)
- histology of the digit joints shows narrowing of the joint spaces, erosion of cartilage, accumulation of debris, and ectopic calcification
- skeleton phenotype
- abnormal cartilage morphology (MGI Ref ID J:63420)
- cartilage erosion
- abnormal joint mobility (MGI Ref ID J:63420)
- wean age homozygotes are unable to grasp a wire cage tope due to stiffness in the digits
- abnormal joint morphology (MGI Ref ID J:63420)
- joint space narrowing, accumulation of debris in the joint space, and ectopic calcification in and around the affected joints
- arthritis (MGI Ref ID J:63420)
- histology of the digit joints shows narrowing of the joint spaces, erosion of cartilage, accumulation of debris, and ectopic calcification
- joint calcification (MGI Ref ID J:63420)
- ectopic calcification in and around the affected joints
Ankank/Ankank
involves: BALB/c * C3H * C57BL/6 * JGBF/Le
- skeleton phenotype
- abnormal osteoblast physiology (MGI Ref ID J:111462)
- osteoblasts exhibit hypercalcification compared with wild-type cell
- however, hypercalcification in osteoblasts can be reversed by soluble Enpp1 and Spp1
- other phenotype
- calcinosis (MGI Ref ID J:110028)
- aortic media exhibit calcification and chondrogenic differentiation unlike wild-type aortas
This mouse can be used to support research in many areas including:Ankank related
Dermatology Research
Skin and Hair Texture Defects
Developmental Biology Research
Growth Defects
Growth Defects (homozygous)
Skeletal Defects
Immunology and Inflammation Research
Immunodeficiency Associated with Other Defects
Inflammation
Mouse/Human Gene Homologs
craniometaphyseal dysplasia, autosomal dominant
Genes & Alleles
Gene & Allele Information
| Allele Symbol | A | ||
|---|---|---|---|
| Allele Name | wild type agouti | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | dark-bellied agouti; | ||
| Strain of Origin | various | ||
| Gene Symbol and Name | a, nonagouti | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | AGSW; AGTI; AGTIL; ASP; As; MGC126092; MGC126093; SHEP9; agouti; agouti signal protein; agouti suppressor; | ||
| General Note | The A allele is usually regarded as a wild-type allele. Hairs are black with a subapical yellow band. This black-yellow-black pattern is referred to as agouti. The general appearance is yellowish brown, slightly lighter on the belly than on the back. | ||
| Molecular Note | This allele, often referred to as wild-type, comprises a novel 131 amino acid protein encoded in a gene comprising four exons, three coding, spanning 18kb. Unique changes in this gene account for all other alleles that have been molecularly characterized. The expression of this allele is almost always dominant to other alleles of this gene. [MGI Ref ID J:3523] | ||
| Allele Symbol | Aw-J | ||
| Allele Name | white bellied agouti Jackson | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | AWJ; | ||
| Strain of Origin | C57BL/6J | ||
| Gene Symbol and Name | a, nonagouti | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | AGSW; AGTI; AGTIL; ASP; As; MGC126092; MGC126093; SHEP9; agouti; agouti signal protein; agouti suppressor; | ||
| Allele Symbol | Ankank | ||
| Allele Name | progressive ankylosis | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | ank; | ||
| Strain of Origin | JGBF/Le | ||
| Gene Symbol and Name | Ank, progressive ankylosis | ||
| Chromosome | 15 | ||
| Gene Common Name(s) | CCAL2; CMDJ; CPPDD; D15Ertd221e; DNA segment, Chr 15, ERATO Doi 221, expressed; FLJ27166; HANK; MANK; mKIAA1581; | ||
| General Note | Development of the joint disorder studied in the joints of the forefeet is characterized by an initial distention of joints with a milky fluid containing large macrophage-like mononuclear cells and suspended calcium hydroxyapatite, accompanied by proliferation of the synovial cells with subsequent roughness of the cartilaginous articular surfaces and eventual fusion of the articular cartilages, and by formation of periarticular cartilage bridges with subsequent ossification leading to complete joint fusion. The Ank disease resembles calcium hydroxyapatite-associated arthropathies in man although it is considerably more severe (J:7672).Light and electron microscopic studies of homozygous mutant mice mice show limb joint changes similar to human ankylosing spondylitis (OMIM 106300) (J:23576). Intervertebral disks are extensively mineralized with depositions of hydroxyapatite crystals, also resembling ankylosing spondylitis (J:751). | ||
| Molecular Note | A single nucleotide G to T substitution is predicted to result in a substitution at codon 440 from Glu to a stop codon in the encoded protein. [MGI Ref ID J:63420] | ||
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)
Hakim FT; Brown KS; Oppenheim JJ. 1986. Hereditary joint disorder in progressive ankylosis (ank/ank) mice. II. Effect of high-dose hydrocortisone treatment on inflammation and intraarticular calcium hydroxyapatite deposits. Arthritis Rheum 29(1):114-23. [PubMed: 3004514] [MGI Ref ID J:109949]
Hakim FT; Cranley R; Brown KS; Eanes ED; Harne L; Oppenheim JJ. 1984. Hereditary joint disorder in progressive ankylosis (ank/ank) mice. I. Association of calcium hydroxyapatite deposition with inflammatory arthropathy. Arthritis Rheum 27(12):1411-20. [PubMed: 6095872] [MGI Ref ID J:7672]
Ho AM; Johnson MD; Kingsley DM. 2000. Role of the mouse ank gene in control of tissue calcification and arthritis [see comments] Science 289(5477):265-70. [PubMed: 10894769] [MGI Ref ID J:63420]
Krug HE. 1998. Fibroblasts from mice with progessive ankylosis proliferate excessively in response to transforming growth factor-beta 1. J Investig Med 46(4):134-9. [PubMed: 9635372] [MGI Ref ID J:109902]
Krug HE; Mahowald ML; Clark C. 1989. Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. III. Proliferative spleen cell response to T cell mitogens. Clin Exp Immunol 78(1):97-101. [PubMed: 2805429] [MGI Ref ID J:109935]
Krug HE; Taurog JD. 2000. HLA-B27 has no effect on the phenotypic expression of progressive ankylosis in ank/ank mice J Rheumatol 27(5):1257-9. [PubMed: 10813297] [MGI Ref ID J:62431]
Krug HE; Wietgrefe MM; Ytterberg SR; Taurog JD; Mahowald ML. 1997. Murine progressive ankylosis is not immunologically mediated. J Rheumatol 24(1):115-22. [PubMed: 9002021] [MGI Ref ID J:109905]
Mahowald ML; Krug H; Halverson P. 1989. Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. II. Light and electron microscopic findings. J Rheumatol 16(1):60-6. [PubMed: 2541245] [MGI Ref ID J:23576]
Nurnberg P; Thiele H; Chandler D; Hohne W; Cunningham ML; Ritter H; Leschik G; Uhlmann K; Mischung C; Harrop K; Goldblatt J; Borochowitz ZU; Kotzot D; Westermann F; Mundlos S; Braun HS; Laing N; Tinschert S. 2001. Heterozygous mutations in ANKH, the human ortholog of the mouse progressive ankylosis gene, result in craniometaphyseal dysplasia. Nat Genet 28(1):37-41. [PubMed: 11326272] [MGI Ref ID J:69128]
Reichenberger E; Tiziani V; Watanabe S; Park L; Ueki Y; Santanna C; Baur ST; Shiang R; Grange DK; Beighton P; Gardner J; Hamersma H; Sellars S; Ramesar R; Lidral AC; Sommer A; Raposo do Amaral CM; Gorlin RJ; Mulliken JB; Olsen BR. 2001. Autosomal dominant craniometaphyseal dysplasia is caused by mutations in the transmembrane protein ANK. Am J Hum Genet 68(6):1321-6. [PubMed: 11326338] [MGI Ref ID J:109879]
Sampson HW. 1988. Ultrastructure of the mineralizing metacarpophalangeal joint of progressive ankylosis (ank/ank) mice. Am J Anat 182(3):257-69. [PubMed: 3213824] [MGI Ref ID J:109941]
Sampson HW. 1988. Spondyloarthropathy in progressive ankylosis (ank/ank) mice: morphological features. Spine 13(6):645-9. [PubMed: 3175755] [MGI Ref ID J:109942]
Sampson HW; Davis RW; Dufner DC. 1991. Spondyloarthropathy in progressive ankylosis mice: ultrastructural features of the intervertebral disk. Acta Anat (Basel) 141(1):36-41. [PubMed: 1659102] [MGI Ref ID J:751]
Sweet HO; Green MC. 1981. Progressive ankylosis, a new skeletal mutation in the mouse. J Hered 72(2):87-93. [PubMed: 7276519] [MGI Ref ID J:6580]
Additional References
A relatedAw-J relatedBlewitt ME; Vickaryous NK; Hemley SJ; Ashe A; Bruxner TJ; Preis JI; Arkell R; Whitelaw E. 2005. An N-ethyl-N-nitrosourea screen for genes involved in variegation in the mouse. Proc Natl Acad Sci U S A 102(21):7629-34. [PubMed: 15890782] [MGI Ref ID J:99816]
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]
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]
Czyzyk TA; Sikorski MA; Yang L; McKnight GS. 2008. Disruption of the RIIbeta subunit of PKA reverses the obesity syndrome of Agouti lethal yellow mice. Proc Natl Acad Sci U S A 105(1):276-81. [PubMed: 18172198] [MGI Ref ID J:131039]
Dickie MM. 1969. Mutations at the agouti locus in the mouse. J Hered 60(1):20-5. [PubMed: 5798139] [MGI Ref ID J:30922]
Dry FW. 1928. The agouti coloration of the mouse (Mus Musculus) and the rat (Mus Norvegicus). J Genet 20:131-144. [MGI Ref ID J:46318]
Guido V, and The Mouse Mutant Resource (MMR) at The Jackson Laboratory. 2002. Two new mutations of white bellied agouti, w-46J and w-47J MGI Direct Data Submission :. [MGI Ref ID J:77218]
Jackson IJ; Budd PS; Keighren M; McKie L. 2007. Humanized MC1R transgenic mice reveal human specific receptor function. Hum Mol Genet 16(19):2341-8. [PubMed: 17652101] [MGI Ref ID J:129904]
Mather K; North SB. 1940. Umbrous: a case of dominance modification in mice. J Genet 40:229-41. [MGI Ref ID J:280]
Perry WL; Copeland NG; Jenkins NA. 1994. The molecular basis for dominant yellow agouti coat color mutations. Bioessays 16(10):705-7. [PubMed: 7980472] [MGI Ref ID J:21244]
Quevedo WC Jr.; Chase HB. 1958. An analysis of the light mutation of coat color in mice. J Morphol 102:329-345. [MGI Ref ID J:13094]
Silvers WK. 1979. The Coat Colors of Mice; A Model for Mammalian Gene Action and Interaction. In: The Coat Colors of Mice. Springer-Verlag, New York. [MGI Ref ID J:78801]
Ankank relatedAberg T; Wang XP; Kim JH; Yamashiro T; Bei M; Rice R; Ryoo HM; Thesleff I. 2004. Runx2 mediates FGF signaling from epithelium to mesenchyme during tooth morphogenesis. Dev Biol 270(1):76-93. [PubMed: 15136142] [MGI Ref ID J:92174]
Barsh GS; Epstein CJ. 1989. Physical and genetic characterization of a 75-kilobase deletion associated with al, a recessive lethal allele at the mouse agouti locus. Genetics 121(4):811-8. [PubMed: 2566558] [MGI Ref ID J:9799]
Baurle J; Vogten H; Grusser-Cornehls U. 1998. Course and targets of the calbindin D-28k subpopulation of primary vestibular afferents. J Comp Neurol 402(1):111-28. [PubMed: 9831049] [MGI Ref ID J:118430]
Boran T; Lesot H; Peterka M; Peterkova R. 2005. Increased apoptosis during morphogenesis of the lower cheek teeth in tabby/EDA mice. J Dent Res 84(3):228-33. [PubMed: 15723861] [MGI Ref ID J:112546]
Chinta SJ; Rane A; Yadava N; Andersen JK; Nicholls DG; Polster BM. 2009. Reactive oxygen species regulation by AIF- and complex I-depleted brain mitochondria. Free Radic Biol Med 46(7):939-47. [PubMed: 19280713] [MGI Ref ID J:145908]
Cui CY; Hashimoto T; Grivennikov SI; Piao Y; Nedospasov SA; Schlessinger D. 2006. Ectodysplasin regulates the lymphotoxin-beta pathway for hair differentiation. Proc Natl Acad Sci U S A 103(24):9142-7. [PubMed: 16738056] [MGI Ref ID J:111051]
Cui CY; Kunisada M; Esibizione D; Grivennikov SI; Piao Y; Nedospasov SA; Schlessinger D. 2007. Lymphotoxin-beta regulates periderm differentiation during embryonic skin development. Hum Mol Genet 16(21):2583-90. [PubMed: 17673451] [MGI Ref ID J:129949]
Dickie MM. 1969. Mutations at the agouti locus in the mouse. J Hered 60(1):20-5. [PubMed: 5798139] [MGI Ref ID J:30922]
Esibizione D; Cui CY; Schlessinger D. 2008. Candidate EDA targets revealed by expression profiling of primary keratinocytes from Tabby mutant mice. Gene 427(1-2):42-6. [PubMed: 18848976] [MGI Ref ID J:143603]
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]
Granholm DE; Reese RN; Granholm NH. 1995. Agouti alleles influence thiol concentrations in hair follicles and extrafollicular tissues of mice (Ay/a, AwJ/AwJ, a/a). Pigment Cell Res 8(6):302-6. [PubMed: 8789738] [MGI Ref ID J:31403]
Jones JM; Huang JD; Mermall V; Hamilton BA; Mooseker MS; Escayg A; Copeland NG; Jenkins NA; Meisler MH. 2000. The mouse neurological mutant flailer expresses a novel hybrid gene derived by exon shuffling between Gnb5 and Myo5a. Hum Mol Genet 9(5):821-8. [PubMed: 10749990] [MGI Ref ID J:61324]
Kappenman KE; Dvoracek MA; Harvison GA; Fuller BB; Granholm NH. 1992. Tyrosinase abundance and activity in murine hairbulb melanocytes of agouti mutants (C57BL/6J-a/a, Ay/a, and AwJ/AwJ). Pigment Cell Res Suppl 2:79-83. [PubMed: 1409442] [MGI Ref ID J:1295]
Katoh A; Yoshida T; Himeshima Y; Mishina M; Hirano T. 2005. Defective control and adaptation of reflex eye movements in mutant mice deficient in either the glutamate receptor delta2 subunit or Purkinje cells. Eur J Neurosci 21(5):1315-26. [PubMed: 15813941] [MGI Ref ID J:101081]
Knapp PE; Adjan VV; Hauser KF. 2009. Cell-specific loss of kappa-opioid receptors in oligodendrocytes of the dysmyelinating jimpy mouse. Neurosci Lett 451(2):114-8. [PubMed: 19110031] [MGI Ref ID J:146365]
Lee M; Kim A; Chua SC Jr; Obici S; Wardlaw SL. 2007. Transgenic MSH overexpression attenuates the metabolic effects of a high-fat diet. Am J Physiol Endocrinol Metab 293(1):E121-31. [PubMed: 17374695] [MGI Ref ID J:126508]
Lu W; Tsirka SE. 2002. Partial rescue of neural apoptosis in the Lurcher mutant mouse through elimination of tissue plasminogen activator. Development 129(8):2043-50. [PubMed: 11934869] [MGI Ref ID J:111363]
Mayer TC; Fishbane JL. 1972. Mesoderm-ectoderm interaction in the production of the agouti pigmentation pattern in mice. Genetics 71(2):297-303. [PubMed: 4558326] [MGI Ref ID J:5288]
Mitsumori K; Yasuhara K; Mori I; Hayashi S; Shimo T; Onodera H; Nomura T; Hayashi Y. 1998. Pulmonary fibrosis caused by N-methyl-N-nitrosourethane inhibits lung tumorigenesis by urethane in transgenic mice carrying the human prototype c-Ha-ras gene. Cancer Lett 129(2):181-90. [PubMed: 9719460] [MGI Ref ID J:52138]
Monroe DG; Wipf LP; Diggins MR; Matthees DP; Granholm NH. 1998. Agouti-related maturation and tissue distribution of alpha-Melanocyte Stimulating Hormone in wild-type (AwJ/AwJ) and mutant (Ay/a,a/a) mice. Pigment Cell Res 11(5):310-3. [PubMed: 9877102] [MGI Ref ID J:52183]
Mullen RJ. 1974. A<w-J> - white-bellied agouti-J Mouse News Lett 50:38. [MGI Ref ID J:64104]
Mustonen T; Ilmonen M; Pummila M; Kangas AT; Laurikkala J; Jaatinen R; Pispa J; Gaide O; Schneider P; Thesleff I; Mikkola ML. 2004. Ectodysplasin A1 promotes placodal cell fate during early morphogenesis of ectodermal appendages. Development 131(20):4907-19. [PubMed: 15371307] [MGI Ref ID J:128256]
O'donnell SM; Hansberger MW; Connolly JL; Chappell JD; Watson MJ; Pierce JM; Wetzel JD; Han W; Barton ES; Forrest JC; Valyi-Nagy T; Yull FE; Blackwell TS; Rottman JN; Sherry B; Dermody TS. 2005. Organ-specific roles for transcription factor NF-kappaB in reovirus-induced apoptosis and disease. J Clin Invest 115(9):2341-2350. [PubMed: 16100570] [MGI Ref ID J:100906]
Peng J; Wu Z; Wu Y; Hsu M; Stevenson FF; Boonplueang R; Roffler-Tarlov SK; Andersen JK. 2002. Inhibition of caspases protects cerebellar granule cells of the weaver mouse from apoptosis and improves behavioral phenotype. J Biol Chem 277(46):44285-91. [PubMed: 12221097] [MGI Ref ID J:119427]
Peng J; Xie L; Stevenson FF; Melov S; Di Monte DA; Andersen JK. 2006. Nigrostriatal dopaminergic neurodegeneration in the weaver mouse is mediated via neuroinflammation and alleviated by minocycline administration. J Neurosci 26(45):11644-51. [PubMed: 17093086] [MGI Ref ID J:114943]
Poole TW. 1975. Dermal-epidermal interactions and the action of alleles at the agouti locus in the mouse. Dev Biol 42(2):203-10. [PubMed: 1090472] [MGI Ref ID J:5519]
Probst FJ; Cooper ML; Cheung SW; Justice MJ. 2008. Genotype, phenotype, and karyotype correlation in the XO mouse model of Turner Syndrome. J Hered 99(5):512-7. [PubMed: 18499648] [MGI Ref ID J:138994]
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Yamago G; Takata Y; Furuta I; Urase K; Momoi T; Huh N. 2001. Suppression of hair follicle development inhibits induction of sonic hedgehog, patched, and patched-2 in hair germs in mice. Arch Dermatol Res 293(9):435-41. [PubMed: 11758785] [MGI Ref ID J:116953]
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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.
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Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
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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 |
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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
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Supply Details
| Standard Supply | Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information. |
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| Supply Notes |
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Control Information
| Control | ||
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| +/? sibling | ||
| 001203 C3FeB6F1/J A/Aw-J | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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